227 Matching Annotations
  1. Last 7 days
    1. GroupID: 11

      DiseaseAssertion: assumed VHL

      GroupSize: 9

      GroupNumberMales: N/A

      GroupNumberFemales: N/A

      GroupEthnicity: N/A

      GroupAgeRange: N/A

      GroupInfo: 9 of the 573 patients discussed in this paper were found to the mutation belonging to 3 families, all with this mutation

      GroupPresentingHPOs: HP:0006880; HP:0005584; HP:0009711 (cerebellar hemangioblastoma, renal cell carcinoma; retinal capillary hemangioma)

      GroupHPOFreeText: 7 patients had retinal angiomas diagnosed at a mean age of 23Y, and 3 patients had cerebellar hemangioblastomas diagnosed at a mean age of 29Y. 5 patients had RCCs with a mean age of diagnosis of 43Y.

      GroupNotHPOs: HP:0002666 (pheochromocytoma)

      GroupNotHPOFreeText: N/A

      GroupPreviousTesting: N/A

      PreviouslyPublished: N/A

      SupplementalData: Supplementary Table S1.

      Variant: p.Q73* (c.217C>T)

      CaseProblemVariantFreeText: N/A

      LegacyVariant: N/A

      ClinVarID: 223164 https://www.ncbi.nlm.nih.gov/clinvar/variation/223164/

      CAID: N/A

      gnomAD: N/A

      VariantEvidence: N/A

      MutationType: stop_gained

      CivicName: Q73* (c.217C>T)

      MultipleGeneVariants: N/A

    2. GroupID: 28

      Case: 24Y0M, Sex Unknown, Ethnicity Unknown

      DiseaseAssertion: retinal capillary hemangioma

      FamilyInfo: 1 of the 573 patients discussed in this paper were found to have this variant. This mutation was found in 1 VHL family with a single patient.

      CasePresentingHPOs: HP:0009711 (retinal capillary hemangioma) 

      CaseHPOFreeText: patient had retinal capillary hemangioma diagnosed at 24Y

      CaseNotHPOs: HP:0002666; HP:0006880; HP:0005584 (pheochromocytoma; cerebellar hemangioblastoma; renal cell carcinoma)

      CaseNotHPOFreeText: N/A

      CasePreviousTesting: N/A

      PreviouslyPublished: N/A

      SupplementalData: Supplementary Table S1.

      Variant: p.L153Tfs*21 (c.456dupA) 

      LegacyVariant: c.455_456insA

      CaseProblemVariantFreeText: c.455_456insA automaps to c.456dupA due to redundancy

      ClinVarID: N/A

      CAID: CA2499307154 http://reg.clinicalgenome.org/redmine/projects/registry/genboree_registry/by_caid?caid=CA2499307154

      gnomAD: N/A

      VariantEvidence: N/A

      MutationType: duplication

      CivicName: T152fs (c.455insA)

      MultipleGeneVariants: N/A

    3. GroupID: 18

      Case: 28Y0M, Sex Unknown, Ethnicity Unknown

      DiseaseAssertion: retinal capillary hemangioma

      FamilyInfo: 1 of the 573 patients discussed in this paper were found to have this variant. This mutation was found in 1 VHL family with a single patient.

      CasePresentingHPOs: HP:0009711 (retinal capillary hemangioma)

      CaseHPOFreeText: patient had retinal angiomas diagnosed at 28Y

      CaseNotHPOs: HP:0005584; HP:0002666; HP:0006880 (renal cell carcinoma; pheochromocytoma; cerebellar hemangioblastoma)

      CaseNotHPOFreeText: N/A

      CasePreviousTesting: N/A

      PreviouslyPublished: N/A

      SupplementalData: Supplementary Table S1.

      Variant: p.R113Efs*46 (c.337del)

      CaseProblemVariantFreeText: N/A

      LegacyVariant: N/A

      ClinVarID: N/A

      CAID: CA432420675 http://reg.clinicalgenome.org/redmine/projects/registry/genboree_registry/allele?hgvsOrDescriptor=NM_000551.3%3Ac.337del

      gnomAD: N/A

      VariantEvidence: N/A

      MutationType: minus_1_frameshift_variant

      CivicName: R113FS (c.337delC)

      MultipleGeneVariants: N/A

    4. GroupID: 22

      DiseaseAssertion: assumed VHL

      GroupSize: 3

      GroupNumberMales: N/A

      GroupNumberFemales: N/A

      GroupEthnicity: N/A

      GroupAgeRange: N/A

      GroupInfo: 3 of the 573 patients discussed in this paper were found to have the following mutation belonging to 1 family. 

      GroupPresentingHPOs: HP:0006880; HP:0009711; HP:0005584 (cerebellar hemangioblastoma, retinal capillary hemangioma; renal cell carcinoma)

      GroupHPOFreeText: 1 patient had retinal angiomas diagnosed at the age of 15Y, 1 had cerebellar hemangioblastomas diagnosed at 20Y, and 1 member had RCC diagnosed at 38Y.

      GroupNotHPOs: HP:0002666 (pheochromocytoma)

      GroupNotHPOFreeText: N/A

      GroupPreviousTesting: N/A

      PreviouslyPublished: N/A

      SupplementalData: Supplementary Table S1.

      Variant: p.H125Qfs*7 (c.374dupA)

      LegacyVariant: N/A

      CaseProblemVariantFreeText: N/A

      ClinVarID: N/A

      CAID: CA2499307153 http://reg.clinicalgenome.org/redmine/projects/registry/genboree_registry/by_caid?caid=CA2499307153

      gnomAD: N/A

      VariantEvidence: N/A

      MutationType: duplication

      CivicName: H125fs (c.374insA) 

      MultipleGeneVariants: N/A

    5. GroupID: 5

      DiseaseAssertion: assumed VHL

      GroupSize: 5

      GroupNumberMales: N/A

      GroupNumberFemales: N/A

      GroupEthnicity: N/A

      GroupAgeRange: N/A

      GroupInfo: 5 of the 573 patients discussed in this paper were found to the mutation belonging to 1 family. This mutation (c.176delC) was found in 1 VHL family with 5 patients.

      GroupPresentingHPOs: HP:0006880; HP:0005584; HP:0009711 (cerebellar hemangioblastoma, renal cell carcinoma; retinal capillary hemangioma)

      GroupHPOFreeText: 3 patients had retinal angiomas diagnosed at a mean age of 22Y, 4 patients had cerebellar hemangioblastomas diagnosed at a mean age of 24Y, and 2 patients had RCCs with a mean age of diagnosis of 60Y.

      GroupNotHPOs: HP:0002666 (pheochromocytoma)

      GroupNotHPOFreeText: N/A

      GroupPreviousTesting: N/A

      PreviouslyPublished: N/A

      SupplementalData: Supplementary Table S1.

      Variant: p.P59Rfs*8 (c.176delC)

      CaseProblemVariantFreeText: N/A

      LegacyVariant: N/A

      ClinVarID: N/A

      CAID: CA432536374 http://reg.clinicalgenome.org/redmine/projects/registry/genboree_registry/allele?hgvsOrDescriptor=NM_000551.3%3Ac.176delC

      gnomAD: N/A

      VariantEvidence: N/A

      MutationType: minus_1_frameshift_variant

      CivicName: P59fs (c.176delC)

      MultipleGeneVariants: N/A

    6. GroupID: 7

      DiseaseAssertion: assumed VHL

      GroupSize: 7

      GroupNumberMales: N/A

      GroupNumberFemales: N/A

      GroupEthnicity: N/A

      GroupAgeRange: N/A

      GroupInfo: 7 of the 573 patients discussed in this paper were found to the mutation belonging to 1 family. This mutation (c.194delC) was found in 1 VHL family with 7 patients.

      GroupPresentingHPOs: HP:0006880; HP:0005584; HP:0009711; HP:0002666 (cerebellar hemangioblastoma, renal cell carcinoma; retinal capillary hemangioma, pheochromocytoma)

      GroupHPOFreeText: 3 patients had retinal angiomas diagnosed at a mean age of 18Y, 2 patients had cerebellar hemangioblastomas diagnosed at a mean age of 33Y, and 2 patients had RCCs with a mean age of diagnosis of 30Y and one single patient had pheos diagnosed at age 20Y.

      GroupNotHPOs: N/A

      GroupNotHPOFreeText: N/A

      GroupPreviousTesting: N/A

      PreviouslyPublished: N/A

      SupplementalData: Supplementary Table S1.

      Variant: p.S65Wfs*2 (c.194delC)

      CaseProblemVariantFreeText: N/A

      LegacyVariant: N/A

      ClinVarID: N/A

      CAID: CA432536395 http://reg.clinicalgenome.org/redmine/projects/registry/genboree_registry/allele?hgvsOrDescriptor=NM_000551.3%3Ac.194del

      gnomAD: N/A

      VariantEvidence: N/A

      MutationType: minus_1_frameshift_variant

      CivicName: S65FS (c.194delC)

      MultipleGeneVariants: N/A

    7. GroupID: 85

      Case: 27Y0M, Sex Unknown, Ethnicity Unknown

      DiseaseAssertion: assumed VHL

      FamilyInfo: 1 of the 573 patients discussed in this paper were found to have this variant. This mutation (c.538A>G) was found in 1 VHL family with a single patient.

      CasePresentingHPOs: HP:0005584 (renal cell carcinoma)

      CaseHPOFreeText: patient had RCCs diagnosed at 27Y

      CaseNotHPOs: HP:0009711; HP:0006880; HP:0002666 (retinal capillary hemangioma; cerebellar hemangioblastoma; pheochromocytoma)

      CaseNotHPOFreeText: N/A

      CasePreviousTesting: N/A

      PreviouslyPublished: N/A

      SupplementalData: Supplementary Table S1.

      Variant: p.I180V (c.538A>G)

      CaseProblemVariantFreeText: N/A

      LegacyVariant: N/A

      ClinVarID: 161401 https://www.ncbi.nlm.nih.gov/clinvar/variation/161401/

      CAID: N/A

      gnomAD: 0.00001061 https://gnomad.broadinstitute.org/variant/3-10191545-A-G

      VariantEvidence: N/A

      MutationType: missense_variant;transition

      CivicName: I180V (c.538A>G)

      MultipleGeneVariants: N/A

    8. GroupID: 50

      DiseaseAssertion: assumed VHL

      GroupSize: 5

      GroupNumberMales: N/A

      GroupNumberFemales: N/A

      GroupEthnicity: N/A

      GroupAgeRange: N/A

      GroupInfo: 5 of the 573 patients discussed in this paper were found to have the following mutation belonging to 1 family

      GroupPresentingHPOs: HP:0005584; HP:0006880; HP:0009711 (renal cell carcinoma; cerebellar hemangioblastoma; retinal capillary hemangioma)

      GroupHPOFreeText: 4 patients had retinal angiomas diagnosed at a mean age of 27Y, and 3 had cerebellar hemangioblastomas diagnosed at a mean age of 32Y

      GroupNotHPOs: HP:0002666 (pheochromocytoma)

      GroupNotHPOFreeText: N/A

      GroupPreviousTesting: N/A

      PreviouslyPublished: N/A

      SupplementalData: Supplementary Table S1.

      Variant: p.R82_V84del (c.243_251delGCGCGTCGT)

      LegacyVariant: N/A

      CaseProblemVariantFreeText: N/A

      ClinVarID: N/A

      CAID: CA658820713 http://reg.clinicalgenome.org/redmine/projects/registry/genboree_registry/allele?hgvsOrDescriptor=NM_000551.3%3Ac.243_251del

      gnomAD: N/A

      VariantEvidence: N/A

      MutationType: inframe_deletion

      CivicName: R82_V84del (c.243_251del)

      MultipleGeneVariants: N/A

    9. GroupID: 36

      DiseaseAssertion: assumed VHL

      GroupSize: 4

      GroupNumberMales: N/A

      GroupNumberFemales: N/A

      GroupEthnicity: N/A

      GroupAgeRange: N/A

      GroupInfo: 4 of the 573 patients discussed in this paper were found to have the following mutation belonging to 3 families altogether.

      GroupPresentingHPOs: HP:0006880; HP:0005584; HP:0009711 (cerebellar hemangioblastoma; renal cell carcinoma; retinal capillary hemangioma)

      GroupHPOFreeText: all 4 patients had retinal angiomas diagnosed at a mean age of 30Y and cerebellar hemangioblastomas diagnosed with a mean age of 25Y, and 2 had RCC diagnosed at a mean age of 29Y

      GroupNotHPOs: HP:0002666 (pheochromocytoma)

      GroupNotHPOFreeText: N/A

      GroupPreviousTesting: N/A

      PreviouslyPublished: N/A

      SupplementalData: Supplementary Table S1.

      Variant: p.Y185* (c.555C>G)

      LegacyVariant: N/A

      CaseProblemVariantFreeText: N/A

      ClinVarID: 223233 https://www.ncbi.nlm.nih.gov/clinvar/variation/223233/

      CAID: N/A

      gnomAD: N/A

      VariantEvidence: N/A

      MutationType: stop_gained

      CivicName: Y185* (c.555C>G)

      MultipleGeneVariants: N/A

    10. GroupID: 4

      Case: 24Y0M, Sex Unknown, Ethnicity Unknown

      DiseaseAssertion: assumed VHL

      FamilyInfo: 1 of the 573 patients discussed in this paper were found to have this variant. This mutation (c.166dupG) was found in 1 VHL family with a single patient.

      CasePresentingHPOs: HP:0009711; HP:0006880 (retinal capillary hemangioma; cerebellar hemangioblastoma)

      CaseHPOFreeText: patient had cerebellar hemangioblastoma at 15Y and retinal capillary hemangioma at 24Y

      CaseNotHPOs: HP:0005584; HP:0002666 (renal cell carcinoma, pheochromocytoma)

      CaseNotHPOFreeText: N/A

      CasePreviousTesting: N/A

      PreviouslyPublished: N/A

      SupplementalData: Supplementary Table S1.

      Variant: p.A56Gfs*76 (c.166dupG)

      CaseProblemVariantFreeText: N/A

      LegacyVariant: N/A

      ClinVarID: N/A

      CAID: CA645524645 http://reg.clinicalgenome.org/redmine/projects/registry/genboree_registry/allele?hgvsOrDescriptor=NM_000551.3%3Ac.166dupG

      gnomAD: N/A

      VariantEvidence: N/A

      MutationType: duplication

      CivicName: A56fs (c.166dup)

      MultipleGeneVariants: N/A

    11. GroupID: 39

      Case: 45Y0M, Sex Unknown, Ethnicity Unknown

      DiseaseAssertion: assumed VHL

      FamilyInfo: 1 of the 573 patients discussed in this paper were found to have this variant. This mutation was found in 1 VHL family with a single patient.

      CasePresentingHPOs: HP:0009711; HP:0006880; HP:0005584 (retinal capillary hemangioma; cerebellar hemangioblastoma; renal cell carcinoma)

      CaseHPOFreeText: patient had retinal capillary hemangioma diagnosed at 45Y, cerebellar hemangioblastomas diagnosed at 24Y, and RCC at 45Y

      CaseNotHPOs: HP:0002666 (pheochromocytoma)

      CaseNotHPOFreeText: N/A

      CasePreviousTesting: N/A

      PreviouslyPublished: N/A

      SupplementalData: Supplementary Table S1.

      Variant: p.K196Rfs*59 (c.584_585delAG) 

      LegacyVariant: N/A

      CaseProblemVariantFreeText: This mutation also automaps to NM_000551.3:c.585_586delGA

      ClinVarID: 547831 https://www.ncbi.nlm.nih.gov/clinvar/variation/547831/

      CAID: N/A

      gnomAD: N/A

      VariantEvidence: N/A

      MutationType: minus_2_frameshift_variant

      CivicName: K196fs (c.584_585delAG)

      MultipleGeneVariants: N/A

    12. GroupID: 15

      Case: 23Y0M, Sex Unknown, Ethnicity Unknown

      DiseaseAssertion: assumed VHL

      FamilyInfo: 1 of the 573 patients discussed in this paper were found to have this variant. This mutation was found in 1 VHL family with a single patient.

      CasePresentingHPOs: HP:0009711; HP:0006880 (retinal capillary hemangioma; cerebellar hemangioblastoma)

      CaseHPOFreeText: patient had retinal angiomas at 21Y and cerebellar hemangioblastomas diagnosed at 23Y

      CaseNotHPOs: HP:0005584; HP:0002666 (renal cell carcinoma; pheochromocytoma)

      CaseNotHPOFreeText: N/A

      CasePreviousTesting: N/A

      PreviouslyPublished: N/A

      SupplementalData: Supplementary Table S1.

      Variant: p.F91* (c.272_273delinsAA)

      CaseProblemVariantFreeText: c.272T>A and c.273C>A results in c.272_273delinsAA

      LegacyVariant: N/A

      ClinVarID: CA2499307077 http://reg.clinicalgenome.org/redmine/projects/registry/genboree_registry/by_caid?caid=CA2499307077

      CAID: N/A

      gnomAD: N/A

      VariantEvidence: N/A

      MutationType: delins; stop_gained

      CivicName: F91* (c.272_273delinsAA)

      MultipleGeneVariants: N/A

    13. GroupID: 6

      Case: 31Y0M, Sex Unknown, Ethnicity Unknown

      DiseaseAssertion: assumed VHL

      FamilyInfo: 1 of the 573 patients discussed in this paper were found to have this variant. This mutation (c.182_185delCCGT) was found in 1 VHL family with a single patient.

      CasePresentingHPOs: HP:0009711; HP:0006880 (retinal capillary hemangioma; cerebellar hemangioblastoma)

      CaseHPOFreeText: patient had retinal capillary hemangioma diagnosed at 31Y and cerebellar hemangioblastoma diagnosed at 30Y

      CaseNotHPOs: HP:0005584; HP:0002666 (renal cell carcinoma; pheochromocytoma)

      CaseNotHPOFreeText: N/A

      CasePreviousTesting: N/A

      PreviouslyPublished: N/A

      SupplementalData: Supplementary Table S1.

      Variant: p.P61Rfs*5 (c.182_185delCCGT)

      CaseProblemVariantFreeText: N/A

      LegacyVariant: N/A

      ClinVarID: N/A

      CAID: CA658820712 http://reg.clinicalgenome.org/redmine/projects/registry/genboree_registry/allele?hgvsOrDescriptor=NM_000551.3%3Ac.182_185del

      gnomAD: N/A

      VariantEvidence: N/A

      MutationType: minus_1_frameshift_variant

      CivicName: P61FS (c.182_185delCCGT)

      MultipleGeneVariants: N/A

    14. GroupID: 53

      DiseaseAssertion: assumed VHL

      GroupSize: 8

      GroupNumberMales: N/A

      GroupNumberFemales: N/A

      GroupEthnicity: N/A

      GroupAgeRange: N/A

      GroupInfo: 8 of the 573 patients discussed in this paper were found to have identical variants. This mutation (S65W (c.194C>G)) was found in 1 VHL family with 8 patients.

      GroupPresentingHPOs: HP:0009711; HP:0006880; HP:0005584 (retinal capillary hemangioma, cerebellar hemangioblastoma, renal cell carcinoma)

      GroupHPOFreeText: 6 had retinal hemangioblastoma, 5 had cerebellar hemangioblastomas, and 1 had renal cell carcinoma. Mean ages for each diagnosis follows: 32 (RH), 39 (CHB), 56 (RCC - with one patient)

      GroupNotHPOs: HP:0002666 (pheochromcytoma)

      GroupNotHPOFreeText: N/A

      GroupPreviousTesting: N/A

      PreviouslyPublished: N/A

      SupplementalData: Supplementary Table S1.

      Variant: p.S65W (c.194C>G)

      CaseProblemVariantFreeText: N/A

      LegacyVariant: N/A

      ClinVarID: 43597 https://www.ncbi.nlm.nih.gov/clinvar/variation/43597/

      CAID: N/A

      gnomAD: N/A

      VariantEvidence: N/A

      MutationType: missense_variant;transversion

      CivicName: S65W (c.194C>G)

      MultipleGeneVariants: N/A

    Tags

    Annotators

    URL

    1. MLPA showed an exon 2 deletion in proband 6

      PatientID: 6

      KindredID: 6

      Case: 30Y0M, Sex unknown, Chinese

      DiseaseAssertion: VHL

      FamilyInfo: Their sister had the same deletion and presented with VHL disease type 1, and first presented with a CNS hemangioblastoma at age 21. A second sister had no mutation and was asymptomatic, and the proband's daughter had the same deletion, but was asymptomatic at the time of the study.

      CasePresentingHPOs: HP:0009715; HP:0010797; HP:0005584 (Papillary cystadenoma of the epididymis, hemangioblastoma, renal cell carcinoma)

      CaseHPOFreeText: CNS hemangioblastoma first presenting at age 15Y and RCC at age 22Y and EC (papillary cystadenoma of the epididymis) at 30Y

      CaseNotHPOs: HP:0002666 (pheochromocytoma)

      CaseNotHPOFreeText: N/A

      CasePreviousTesting: N/A

      PreviouslyPublished: N/A

      SupplementalData: N/A

      Variant: Exon 2 deletion

      CaseProblemVariantFreeText: N/A

      LegacyVariant: N/A

      ClinVarID: N/A

      CAID: N/A

      gnomAD: N/A

      VariantEvidence: N/A

      MutationType: exon_loss_variant

      CivicName: Exon 2 deletion

      MultipleGeneVariants: N/A

    2. c.239G>T [p.Ser80Ile]

      PatientID: Fetus 2 (of proband)

      KindredID: 9

      Case: Fetus, sex unknown, Chinese

      DiseaseAssertion: N/A

      FamilyInfo: Positive - Family history of RCC and Pheo; Parent had CNS hemangioblastoma presenting at 26Y. In prenatal diagnosis, two fetuses (1 & 2) were positive for the mutation.

      CasePresentingHPOs: N/A

      CaseHPOFreeText: N/A

      CaseNotHPOs: N/A

      CaseNotHPOFreeText: N/A

      CasePreviousTesting: N/A

      PreviouslyPublished: N/A

      SupplementalData: N/A

      Variant: p.S80I (c.239G>T)

      CaseProblemVariantFreeText: N/A

      LegacyVariant: N/A

      ClinVar: 625229 https://www.ncbi.nlm.nih.gov/clinvar/variation/625229/

      CAID: N/A

      gnomAD: N/A

      VariantEvidence: N/A

      MutationType: missense_variant; transversion

      CivicName: S80I (c.239G>T)

      MultipleGeneVariants: N/A

    3. c.319C>G [p.Arg107Gly]

      PatientID: 7

      KindredID: 7

      Case: 55Y0M, Sex unknown, Chinese

      DiseaseAssertion: VHL

      FamilyInfo: Positive -- Their father and brother both had the same germline mutation. Their father was screened after genetic testing and found to have a left RCC with lung metastasis at age 80, and their brother was asymptomatic.

      CasePresentingHPOs: HP:0010797 (hemangioblastoma)

      CaseHPOFreeText: CNS hemangioblastoma first presenting at 55Y

      CaseNotHPOs: HP:0005584; HP:0002666; HP:0009715 (renal cell carcinoma, pheochromocytoma, Papillary cystadenoma of the epididymis)

      CaseNotHPOFreeText: N/A

      CasePreviousTesting: N/A

      PreviouslyPublished: N/A

      SupplementalData: N/A

      Variant: p.R107G (c.319C>G)

      CaseProblemVariantFreeText: N/A

      LegacyVariant: N/A

      ClinVarID: 43599 https://www.ncbi.nlm.nih.gov/clinvar/variation/43599/

      CAID: N/A

      gnomAD: N/A

      VariantEvidence: N/A

      MutationType: missense_variant; transversion

      CivicName: R107G (c.319C>G)

      MultipleGeneVariants: N/A

    1. frameshift mutations (4/16)

      PatientID: 7

      KindredID: 7

      Case: 23Y0M, Sex Unknown, Argentinian

      DiseaseAssertion: VHL

      FamilyInfo: Thus far, it has not been possible to study the parents or close relatives of this patient.

      CasePresentingHPOs: HP:0009711; HP:0000107 (retinal capillary hemangioma; renal cyst)

      CaseHPOFreeText: Aged 22Y at diagnosis (genetic testing); fulfils type 1 VHL clinical diagnosis. Bilateral retinal hemangioblastomas diagnosed at 22Y, and renal cysts were diagnosed at 23Y (See Table 1 & 2).

      CaseNotHPOs: N/A

      CaseNotHPOFreeText: N/A

      CasePreviousTesting: N/A

      PreviouslyPublished: N/A

      SupplementalData: N/A

      Variant: p.Q132Hfs*45 (c.343_395dup)

      LegacyVariant: N/A

      CaseProblemVariantFreeText: N/A

      ClinVarID: N/A

      CAID: CA2497030272 http://reg.clinicalgenome.org/redmine/projects/registry/genboree_registry/by_caid?caid=CA2497030272

      gnomAD: N/A

      VariantEvidence: N/A

      MutationType: plus_2_frameshift_variant; duplication

      CivicName: Q132Hfs*45 (c.343_395dup)

      MultipleGeneVariants: N/A

    1. T152I missense mutation

      PatientID: None (mother)

      KindredID: 2

      Case: F, 48Y0M, Ethnicity Unknown

      DiseaseAssertion: asymptomatic

      FamilyInfo: Her 2 daughters were found to carry the same mutation. One daughter was asymptomatic too, while the other (aged 25Y) was operated on for a carotid body tumour.

      CasePresentingHPOs: None

      CaseHPOFreeText: N/A

      CaseNotHPOs: N/A

      CaseNotHPOFreeText: An extensive clinical/physical examination was conducted: laboratory tests (urinary metanephrine and normetanephrine, plasma chromogranin A), an ophthalmoscopic examination and radiological exams (NMR of the brain, CT scan of the thorax and the abdomen) - all tests were normal.

      CasePreviousTesting: N/A

      PreviouslyPublished: N/A

      SupplementalData: N/A

      Variant: p.T152I (c.455C>T)

      LegacyVariant: N/A

      CaseProblemVariantFreeText: N/A

      ClinVarID: N/A

      CAID: CA351754382 http://reg.clinicalgenome.org/redmine/projects/registry/genboree_registry/allele?hgvsOrDescriptor=NM_000551.3%3Ac.455C%3ET

      gnomAD: N/A

      VariantEvidence: N/A

      MutationType: missense_variant;transition

      CivicName: T152I (c.455C>T)

      MultipleGeneVariants: N/A

    1. 481C>T

      GroupID/ KindredID: 15

      Case: Age unknown, Sex unknown, Polish

      DiseaseAssertion: VHL

      FamilyInfo: This mutation (p.R161* (c.481C>T)) was found in Family No. 15 with 1 member affected.

      CasePresentingHPOs: HP:0009711; HP:0010797; HP:0005584 (retinal capillary hemangioma, hemangioblastoma, renal cell carcinoma)

      CaseHPOFreeText: N/A

      CaseNotHPOs: N/A

      CaseNotHPOFreeText: N/A

      CasePreviousTesting: N/A

      PreviouslyPublished: N/A

      SupplementalData: N/A

      Variant: p.R161* (c.481C>T)

      CaseProblemVariantFreeText: N/A

      LegacyVariant: N/A

      ClinVarID: 2217 https://www.ncbi.nlm.nih.gov/clinvar/variation/2217/

      CAID: N/A

      gnomAD: N/A

      VariantEvidence: N/A

      MutationType: stop_gained

      CivicName: R161* (c.481C>T)

      MultipleGeneVariants: N/A

    2. Complete deletion

      GroupID/ KindredID: 28

      PatientID: IV

      Case: 62Y0M, Sex unknown, Polish

      DiseaseAssertion: VHL

      FamilyInfo: Family 28 consisted of 4 members; one relative (age 27Y) was found with multiple cerebellar HABs at 25Y, and multiple spinal HABs, another was diagnosed with a single cerebellar HAB at 24Y, and a final relative (40Y), was diagnosed at 30Y with multiple cerebellar HABs, and multiple spinal HABs

      CasePresentingHPOs: HP:0006880 (cerebellar hemangioblastoma)

      CaseHPOFreeText: Patient was diagnosed with a single HAB at 62Y.

      GroupNotHPOs: HP:0009713; HP:0009711; HP:0005584 (spinal hemangioblastoma, retinal capillary hemangioma; renal cell carcinoma)

      CaseNotHPOFreeText: N/A

      CasePreviousTesting: N/A

      PreviouslyPublished: N/A

      SupplementalData: N/A

      Variant: complete deletion of VHL gene

      CaseProblemVariantFreeText: N/A

      LegacyVariant: N/A

      ClinVarID: N/A

      CAID: N/A

      gnomAD: N/A

      VariantEvidence: Haplotype analysis information in Table 3

      MutationType: deletion

      CivicName: deletion

      MultipleGeneVariants: N/A

    3. Complete deletion

      GroupID/ KindredID: 28

      PatientID: III

      Case: 40Y0M, Sex unknown, Polish

      DiseaseAssertion: VHL

      FamilyInfo: Family 28 consisted of 4 members; one relative (age 27Y) was found with multiple cerebellar HABs at 25Y, and multiple spinal HABs, another was diagnosed with a single cerebellar HAB at 24Y, and a final relative (62Y), diagnosed with a single HAB.

      CasePresentingHPOs: HP:0009713; HP:0006880 (spinal hemangioblastoma, cerebellar hemangioblastoma)

      CaseHPOFreeText: Patient was diagnosed at 30Y with multiple cerebellar HABs, and multiple spinal HABs

      GroupNotHPOs: HP:0009711; HP:0005584 (retinal capillary hemangioma; renal cell carcinoma)

      CaseNotHPOFreeText: N/A

      CasePreviousTesting: N/A

      PreviouslyPublished: N/A

      SupplementalData: N/A

      Variant: complete deletion of VHL gene

      CaseProblemVariantFreeText: N/A

      LegacyVariant: N/A

      ClinVarID: N/A

      CAID: N/A

      gnomAD: N/A

      VariantEvidence: Haplotype analysis information in Table 3

      MutationType: deletion

      CivicName: deletion

      MultipleGeneVariants: N/A

    4. Complete deletion

      GroupID/ KindredID: 28

      PatientID: I

      Case: 27Y0M, Sex unknown, Polish

      DiseaseAssertion: VHL

      FamilyInfo: Family 28 consisted of 4 members; one relative (age 24Y) diagnosed with a single cerebellar HAB, another (40Y) diagnosed at 30Y with multiple cerebellar HABs, and multiple spinal HABs, and a final relative (62Y), diagnosed with a single HAB.

      CasePresentingHPOs: HP:0009713; HP:0006880 (spinal hemangioblastoma, cerebellar hemangioblastoma)

      CaseHPOFreeText: Patient was found with multiple cerebellar HABs at 25Y, and multiple spinal HABs

      GroupNotHPOs: HP:0009711; HP:0005584 (retinal capillary hemangioma; renal cell carcinoma)

      CaseNotHPOFreeText: N/A

      CasePreviousTesting: N/A

      PreviouslyPublished: N/A

      SupplementalData: N/A

      Variant: complete deletion of VHL gene

      CaseProblemVariantFreeText: N/A

      LegacyVariant: N/A

      ClinVarID: N/A

      CAID: N/A

      gnomAD: N/A

      VariantEvidence: Haplotype analysis information in Table 3

      MutationType: deletion

      CivicName: deletion

      MultipleGeneVariants: N/A

    5. 226_228delTTC

      GroupID/ KindredID: 7

      DiseaseAssertion: VHL

      GroupSize: 2

      GroupNumberMales: N/A

      GroupNumberFemales: N/A

      GroupEthnicity: Polish

      GroupAgeRange: N/A

      GroupInfo: Familial VHL stated; 2 family members recorded with this mutation.

      GroupPresentingHPOs: HP:0009711; HP:0010797 (retinal capillary hemangioma, hemangioblastoma)

      GroupHPOFreeText: 1 patient was tallied with a retinal capillary hemangioma and both (2) with cHemangioblastomas.

      GroupNotHPOs: HP:0005584 (renal cell carcinoma)

      GroupNotHPOFreeText: None of the patients were recorded to have RCC

      GroupPreviousTesting: N/A

      PreviouslyPublished: 32179488

      SupplementalData: N/A

      Variant: p.F76del (c.226_228delTTC)

      CaseProblemVariantFreeText: NM_000551.3:c.226_228delTTC automaps to updated c.227_229delTCT

      LegacyVariant: N/A

      ClinVarID: N/A

      CAID: CA357012 http://reg.clinicalgenome.org/redmine/projects/registry/genboree_registry/allele?hgvsOrDescriptor=NM_000551.3%3Ac.226_228delTTC

      gnomAD: N/A

      VariantEvidence: N/A

      MutationType: inframe_deletion

      CivicName: F76del (c.227_229del)

      MultipleGeneVariants: N/A

    6. The VHL gene product (pVHL) has two macromolecular sites, α and β domains, which can bind different proteins. pVHL bound to elongin B, C/cullin/Rbx1 acts as an E3 ubiquitin ligase and targets proteins for degradation.22 Similarly, hypoxia inducible proteins are regulated by complex pVHL/elongin B and C that requires direct binding of hypoxia inducible factor (HIF) to the β domain and targets HIF for ubiquitination catalysed by the α domain.23 The VHL protein also plays a role in extracellular matrix formation and is necessary for cell cycle exit.24,25 Germline VHL mutations cause different protein defects that result in the clinical heterogeneity of VHL disease. VHL type 1 disease (without phaeochromocytoma) is associated with mutations predicted to cause complete unravelling of protein structure (missense mutations mapping to VHL protein hydrophobic core, protein truncating mutations, and partial gene deletions). VHL type 2 (with phaeochromocytoma) is caused by missense mutations which map to protein binding sites of pVHL and are predicted to cause local protein defects.22 Specific phaeochromocytoma associated missense mutations confer different risks of HAB and RCC, being responsible for the occurrence of subcategories VHL type 2A (VHL without RCC), 2B (VHL with RCC), and 2C (phaeochromocytoma only).15 Phenotypic expression of VHL disease is also influenced by genetic modifiers.26
    7. 226_228delTTC

      GroupID/ KindredID: 5

      DiseaseAssertion: VHL

      GroupSize: 3

      GroupNumberMales: N/A

      GroupNumberFemales: N/A

      GroupEthnicity: Polish

      GroupAgeRange: N/A

      GroupInfo: Familial VHL stated; 3 family members recorded with this mutation.

      GroupPresentingHPOs: HP:0009711; HP:0010797 (retinal capillary hemangioma, hemangioblastoma)

      GroupHPOFreeText: all 3 patients were tallied with retinal capillary hemangiomas and 2 with cHemangioblastomas. These phenotypes could be paired with the same or different members in this family as it was not clear.

      GroupNotHPOs: HP:0005584 (renal cell carcinoma)

      GroupNotHPOFreeText: None of the patients were recorded to have RCC

      GroupPreviousTesting: N/A

      PreviouslyPublished: 32179488

      SupplementalData: N/A

      Variant: p.F76del (c.226_228delTTC)

      CaseProblemVariantFreeText: NM_000551.3:c.226_228delTTC automaps to updated c.227_229delTCT

      LegacyVariant: N/A

      ClinVarID: N/A

      CAID: CA357012 http://reg.clinicalgenome.org/redmine/projects/registry/genboree_registry/allele?hgvsOrDescriptor=NM_000551.3%3Ac.226_228delTTC

      gnomAD: N/A

      VariantEvidence: N/A

      MutationType: inframe_deletion

      CivicName: F76del (c.227_229del)

      MultipleGeneVariants: N/A

    8. 226_228delTTC

      GroupID/ KindredID: 6

      Case: Age unknown, Sex unknown, Polish

      DiseaseAssertion: VHL

      FamilyInfo: This mutation was found in Family No. 6 with 1 member affected.

      CasePresentingHPOs: HP:0009711; HP:0010797 (retinal capillary hemangioma, hemangioblastoma)

      CaseHPOFreeText: N/A

      CaseNotHPOs: HP:0005584 (renal cell carcinoma)

      CaseNotHPOFreeText: N/A

      CasePreviousTesting: N/A

      PreviouslyPublished: 32179488

      SupplementalData: N/A

      Variant: p.F76del (c.226_228delTTC)

      CaseProblemVariantFreeText: NM_000551.3:c.226_228delTTC automaps to updated c.227_229delTCT

      LegacyVariant: N/A

      ClinVarID: N/A

      CAID: CA357012 http://reg.clinicalgenome.org/redmine/projects/registry/genboree_registry/allele?hgvsOrDescriptor=NM_000551.3%3Ac.226_228delTTC

      gnomAD: N/A

      VariantEvidence: N/A

      MutationType: inframe_deletion

      CivicName: F76del (c.227_229del)

      MultipleGeneVariants: N/A

    9. 24Exon 3 deletion (8.5 kb abnormal band on QSA)*

      GroupID/ KindredID: 24

      DiseaseAssertion: VHL

      GroupSize: 2

      GroupNumberMales: N/A

      GroupNumberFemales: N/A

      GroupEthnicity: Polish

      GroupAgeRange: N/A

      GroupInfo: Familial VHL stated; 2 family members recorded with this deletion.

      GroupPresentingHPOs: HP:0010797; HP:0009711; HP:0005584 (hemangioblastoma; retinal capillary hemangioma; renal cell carcinoma)

      GroupHPOFreeText: Both (2) patients had hemangioblastomas, and RCC, and 1 had retinal capillary hemangioma

      GroupNotHPOs: N/A

      GroupNotHPOFreeText: N/A

      GroupPreviousTesting: N/A

      PreviouslyPublished: N/A

      SupplementalData: N/A

      Variant: Exon 3 deletion

      CaseProblemVariantFreeText: Patients were both found with an Exon 3 deletion (and 8.5 kb abnormal band on QSA)

      LegacyVariant: N/A

      ClinVarID: N/A

      CAID: N/A

      gnomAD: N/A

      VariantEvidence: N/A

      MutationType: exon_loss_variant

      CivicName: Exon 3 Deletion

      MultipleGeneVariants: N/A

    10. Exon 1deletion

      GroupID/ KindredID: 19 / S 1

      DiseaseAssertion: VHL

      GroupSize: 2

      GroupNumberMales: N/A

      GroupNumberFemales: N/A

      GroupEthnicity: Polish

      GroupAgeRange: N/A

      GroupInfo: Familial VHL stated; 2 family members recorded with this deletion.

      GroupPresentingHPOs: HP:0010797; HP:0009711; HP:0005584 (hemangioblastoma; retinal capillary hemangioma; renal cell carcinoma)

      GroupHPOFreeText: Both (2) patients had RCC, 1 had hemangioblastomas and 1 had retinal capillary hemangioma. These phenotypes couldn’t be paired as it was not clear.

      GroupNotHPOs: N/A

      GroupNotHPOFreeText: N/A

      GroupPreviousTesting: N/A

      PreviouslyPublished: N/A

      SupplementalData: N/A

      Variant: Exon 1 deletion

      CaseProblemVariantFreeText: N/A

      LegacyVariant: N/A

      ClinVarID: N/A

      CAID: N/A

      gnomAD: N/A

      VariantEvidence: N/A

      MutationType: exon_loss_variant

      CivicName: Exon 1 Deletion

      MultipleGeneVariants: N/A

    11. Exon 3 deletion

      GroupID/ KindredID: 23 / S 5

      Case: Age unknown, Sex unknown, Polish

      DiseaseAssertion: VHL

      FamilyInfo: This deletion was found in Family No. 23 with 1 member affected. No other family info was given

      CasePresentingHPOs: HP:0009711; HP:0005584; HP:0010797 (retinal capillary hemangioma, renal cell carcinoma, hemangioblastoma)

      CaseHPOFreeText: N/A

      CaseNotHPOs: N/A

      CaseNotHPOFreeText: N/A

      CasePreviousTesting: N/A

      PreviouslyPublished: N/A

      SupplementalData: N/A

      Variant: Exon 3 deletion

      CaseProblemVariantFreeText: N/A

      LegacyVariant: N/A

      ClinVarID: N/A

      CAID: N/A

      gnomAD: N/A

      VariantEvidence: N/A

      MutationType: exon_loss_variant

      CivicName: Exon 3 Deletion

      MultipleGeneVariants: N/A

    12. Complete deletion

      GroupID/ KindredID: 28

      PatientID: II

      Case: 24Y0M, Sex unknown, Polish

      DiseaseAssertion: VHL

      FamilyInfo: Family 28 consisted of 4 members; one relative (age 27Y) was found with multiple cerebellar HABs at 25Y, and multiple spinal HABs, another (40Y) diagnosed at 30Y with multiple cerebellar HABs, and multiple spinal HABs, and a final relative (62Y), diagnosed with a single HAB.

      CasePresentingHPOs: HP:0006880 (cerebellar hemangioblastoma)

      CaseHPOFreeText: Patient was diagnosed with a single cerebellar HAB at 24Y

      GroupNotHPOs: HP:0009713; HP:0009711; HP:0005584 (spinal hemangioblastoma, retinal capillary hemangioma; renal cell carcinoma)

      CaseNotHPOFreeText: N/A

      CasePreviousTesting: N/A

      PreviouslyPublished: N/A

      SupplementalData: N/A

      Variant: complete deletion of VHL gene

      CaseProblemVariantFreeText: N/A

      LegacyVariant: N/A

      ClinVarID: N/A

      CAID: N/A

      gnomAD: N/A

      VariantEvidence: Haplotype analysis information in Table 3

      MutationType: deletion

      CivicName: deletion

      MultipleGeneVariants: N/A

    13. Exon 3 deletion

      GroupID/ KindredID: 23 / S 5

      Case: Age unknown, Sex unknown, Polish

      DiseaseAssertion: VHL

      FamilyInfo: This deletion was found in Family No. 23 with 1 member affected. No other family info was given

      CasePresentingHPOs: HP:0009711; HP:0005584; HP:0010797 (retinal capillary hemangioma, renal cell carcinoma, hemangioblastoma)

      CaseHPOFreeText: N/A

      CaseNotHPOs: N/A

      CaseNotHPOFreeText: N/A

      CasePreviousTesting: N/A

      PreviouslyPublished: N/A

      SupplementalData: N/A

      Variant: Exon 3 deletion

      CaseProblemVariantFreeText: N/A

      LegacyVariant: N/A

      ClinVarID: N/A

      CAID: N/A

      gnomAD: N/A

      VariantEvidence: N/A

      MutationType: exon_loss_variant

      CivicName: Exon 3 Deletion

      MultipleGeneVariants: N/A

    14. Complete deletion

      GroupID/ KindredID: 28

      PatientID: II

      Case: 24Y0M, Sex unknown, Polish

      DiseaseAssertion: VHL

      FamilyInfo: Family 28 consisted of 4 members; one relative (age 27Y) was found with multiple cerebellar HABs at 25Y, and multiple spinal HABs, another (40Y) diagnosed at 30Y with multiple cerebellar HABs, and multiple spinal HABs, and a final relative (62Y), diagnosed with a single HAB.

      CasePresentingHPOs: HP:0006880 (cerebellar hemangioblastoma)

      CaseHPOFreeText: Patient was diagnosed with a single cerebellar HAB at 24Y

      GroupNotHPOs: HP:0009713; HP:0009711; HP:0005584 (spinal hemangioblastoma, retinal capillary hemangioma; renal cell carcinoma)

      CaseNotHPOFreeText: N/A

      CasePreviousTesting: N/A

      PreviouslyPublished: N/A

      SupplementalData: N/A

      Variant: complete deletion of VHL gene

      CaseProblemVariantFreeText: N/A

      LegacyVariant: N/A

      ClinVarID: N/A

      CAID: N/A

      gnomAD: N/A

      VariantEvidence: Haplotype analysis information in Table 3

      MutationType: deletion

      CivicName: deletion

      MultipleGeneVariants: N/A

    1. PMID: 21528239

      GroupID/ KindredID: B

      DiseaseAssertion: assumed VHL

      GroupSize: 3

      GroupNumberMales: 1

      GroupNumberFemales: 2

      GroupEthnicity: N/A

      GroupAgeRange: N/A

      GroupInfo: 3 members: mother (I:1) and her two children, II:1 (M) and II:2 (F) - Each proved to hold the mutation. II:2 was a predicted asymptomatic carrier. The mother (proband) was considered to carry a new mutation.

      GroupPresentingHPOs: HP:0005584; HP:0006880 (renal cell carcinoma; cerebellar hemangioblastoma)

      GroupHPOFreeText: The mother (I:1) had RCC and a cerebellar hemangioblastoma. Her son II:1 had a cerebellar hemangioblastoma.

      GroupNotHPOs: N/A

      GroupNotHPOFreeText: The daughter (II:2) is devoid of know manifestations

      GroupPreviousTesting: N/A

      PreviouslyPublished: N/A

      SupplementalData: N/A

      Variant: p.N174KFS*29 (c.519insAA)

      LegacyVariant: p.174FS (c.732insAA)

      CaseProblemVariantFreeText: c.519insAA corrects to NM_000551.3:c.520_521dupAA

      ClinVarID: N/A

      CAID: CA2573051315 https://reg.clinicalgenome.org/redmine/projects/registry/genboree_registry/by_caid?caid=CA2573051315

      gnomAD: N/A

      VariantEvidence: N/A

      MutationType: plus_2_frameshift_variant; duplication

      CivicName: N174FS*29 (c.519insAA)

      MultipleGeneVariants: N/A

    2. PMID: 21528239

      GroupID/ KindredID: A

      DiseaseAssertion: assumed VHL

      GroupSize: 8

      GroupNumberMales: 2

      GroupNumberFemales: 6

      GroupEthnicity: N/A

      GroupAgeRange: N/A

      GroupInfo: The kindred comprised of 21 individuals over 4 generations. The following members have a confirmed mutation: I:1 (F, deceased), II:2 (F, deceased), III:2 (F, deceased), III:4 (M), III:6 (F), IV:4 (F), IV:6 (M), IV:7 (F, is predicted to be affected). The 3 deceased members had died from VHL related tumors. Another 3 were suffering from VHL, another developed RCC an cHB, and 1 was a VHL carrier. All 8 members had this mutation

      GroupPresentingHPOs: HP:0005584; HP:0006880; HP:0009711; HP:0030421 (renal cell carcinoma; cerebellar hemangioblastoma; retinal capillary hemangioma; epidymidal tumor)

      GroupHPOFreeText: 5 members had RCC, 5 had multiple cerebellar hemangioblastomas, 2 had retinal capillary hemangioma and 1 had an epidymidal tumor.

      GroupNotHPOs: HP:0002666 (pheochromocytoma)

      GroupNotHPOFreeText: None of the eight VHL carriers of the first kindred had developed pheochromocytoma, and this kindred clearly presents VHL disease type 1

      GroupPreviousTesting: N/A

      PreviouslyPublished: 7700111

      SupplementalData: N/A

      Variant: p.S183Cfs*19 (c.548delC)

      LegacyVariant: p.183 (c.761delC)

      CaseProblemVariantFreeText: N/A

      ClinVarID: N/A

      CAID: CA658795184 https://reg.clinicalgenome.org/redmine/projects/registry/genboree_registry/allele?hgvsOrDescriptor=NM_000551.3%3Ac.548delC

      gnomAD: N/A

      VariantEvidence: N/A

      MutationType: minus_1_frameshift_variant

      CivicName: S183fs (c.548delC)

      MultipleGeneVariants: N/A

    1. PatientID: II-16

      KindredID: 1

      Case: M, Age unknown (deceased), Ethnicity Unknown

      DiseaseAssertion: asymptomatic

      FamilyInfo: Large multigenerational family with a history of both VHL and spinocerebellar ataxia type 2 (SCA2). Screening for clinical and genetic diagnostics were gathered as well as thorough information on non-living members. See family pedigree (Fig. 1).

      CasePresentingHPOs: None

      CaseHPOFreeText: VHL found by genetic testing not clinical findings.

      CaseNotHPOs: N/A

      CaseNotHPOFreeText: N/A

      CasePreviousTesting: N/A

      PreviouslyPublished: N/A

      SupplementalData: N/A

      Variant: p.E160Sfs*10 (c.477delA)

      LegacyVariant: c.688delA

      CaseProblemVariantFreeText: c.477del, p.Glu160Serfs10 should be used. Details: 477del same as 475delA bc that codon is AAA so doesn't matter which A gets deleted: there is an A at 475 476 477 so for HGVS we say that 477 (the latter) is deleted since that follows HGVS nomenclature. Thus use c.477del: p.Glu160Serfs10

      ClinVarID: 182959 https://www.ncbi.nlm.nih.gov/clinvar/variation/182959/

      CAID: N/A

      gnomAD: N/A

      VariantEvidence: N/A

      MutationType: minus_1_frameshift_variant

      CivicName: E160fs (c.477del)

      MultipleGeneVariants: N/A

    2. PatientID: III-23

      KindredID: 1

      Case: M, Age unknown, Ethnicity Unknown

      DiseaseAssertion: asymptomatic

      FamilyInfo: Large multigenerational family with a history of both VHL and spinocerebellar ataxia type 2 (SCA2). Screening for clinical and genetic diagnostics were gathered as well as thorough information on non-living members. His mom and grandmother appeared to have the VHL mutation. See family pedigree (Fig. 1).

      CasePresentingHPOs: None

      CaseHPOFreeText: VHL found by genetic testing not clinical findings.

      CaseNotHPOs: N/A

      CaseNotHPOFreeText: N/A

      CasePreviousTesting: N/A

      PreviouslyPublished: N/A

      SupplementalData: N/A

      Variant: p.E160Sfs*10 (c.477delA)

      LegacyVariant: c.688delA

      CaseProblemVariantFreeText: c.477del, p.Glu160Serfs10 should be used. Details: 477del same as 475delA bc that codon is AAA so doesn't matter which A gets deleted: there is an A at 475 476 477 so for HGVS we say that 477 (the latter) is deleted since that follows HGVS nomenclature. Thus use c.477del: p.Glu160Serfs10

      ClinVarID: 182959 https://www.ncbi.nlm.nih.gov/clinvar/variation/182959/

      CAID: N/A

      gnomAD: N/A

      VariantEvidence: N/A

      MutationType: minus_1_frameshift_variant

      CivicName: E160fs (c.477del)

      MultipleGeneVariants: N/A

    3. PatientID: III-40

      KindredID: 1

      Case: F, Age unknown (deceased), Ethnicity Unknown

      DiseaseAssertion: asymptomatic

      FamilyInfo: Large multigenerational family with a history of both VHL and spinocerebellar ataxia type 2 (SCA2). Screening for clinical and genetic diagnostics were gathered as well as thorough information on non-living members. Her dad and grandmother appeared to have the VHL mutation. See family pedigree (Fig. 1).

      CasePresentingHPOs: None

      CaseHPOFreeText: VHL found by genetic testing not clinical findings.

      CaseNotHPOs: N/A

      CaseNotHPOFreeText: N/A

      CasePreviousTesting: N/A

      PreviouslyPublished: N/A

      SupplementalData: N/A

      Variant: p.E160Sfs*10 (c.477delA)

      LegacyVariant: c.688delA

      CaseProblemVariantFreeText: c.477del, p.Glu160Serfs10 should be used. Details: 477del same as 475delA bc that codon is AAA so doesn't matter which A gets deleted: there is an A at 475 476 477 so for HGVS we say that 477 (the latter) is deleted since that follows HGVS nomenclature. Thus use c.477del: p.Glu160Serfs10

      ClinVarID: 182959 https://www.ncbi.nlm.nih.gov/clinvar/variation/182959/

      CAID: N/A

      gnomAD: N/A

      VariantEvidence: N/A

      MutationType: minus_1_frameshift_variant

      CivicName: E160fs (c.477del)

      MultipleGeneVariants: N/A

    4. PatientID: III-40

      KindredID: 1

      Case: F, Age unknown (deceased), Ethnicity Unknown

      DiseaseAssertion: asymptomatic

      FamilyInfo: Large multigenerational family with a history of both VHL and spinocerebellar ataxia type 2 (SCA2). Screening for clinical and genetic diagnostics were gathered as well as thorough information on non-living members. Her dad and grandmother appeared to have the VHL mutation. See family pedigree (Fig. 1).

      CasePresentingHPOs: None

      CaseHPOFreeText: VHL found by genetic testing not clinical findings.

      CaseNotHPOs: N/A

      CaseNotHPOFreeText: N/A

      CasePreviousTesting: N/A

      PreviouslyPublished: N/A

      SupplementalData: N/A

      Variant: p.E160Sfs*10 (c.477delA)

      LegacyVariant: c.688delA

      CaseProblemVariantFreeText: c.477del, p.Glu160Serfs10 should be used. Details: 477del same as 475delA bc that codon is AAA so doesn't matter which A gets deleted: there is an A at 475 476 477 so for HGVS we say that 477 (the latter) is deleted since that follows HGVS nomenclature. Thus use c.477del: p.Glu160Serfs10

      ClinVarID: 182959 https://www.ncbi.nlm.nih.gov/clinvar/variation/182959/

      CAID: N/A

      gnomAD: N/A

      VariantEvidence: N/A

      MutationType: minus_1_frameshift_variant

      CivicName: E160fs (c.477del)

      MultipleGeneVariants: N/A

    1. 1 c.191G>C p.Arg64Pro p.R64P Familial VHL

      PatientID: III-4

      KindredID: 1

      Case: 34Y0M, Sex and Ethnicity Unknown

      DiseaseAssertion: pheochromocytoma

      FamilyInfo: Family suggesting incomplete penetrance of a VHL gene germline mutation. Mutation (p.R64P) was found in a family with 6 patients total with three generations. The earliest patient described (I-1) presented with renal cell carcinoma (age at diagnosis 48 years), 1 of their 6 children (II-1) at age 59 had no typical VHL manifestations after annual clinical monitoring and suggest non-penetrance in the patient; the second of 6 children (II-3), then aged 51, had bilateral pheochromocytoma diagnosed age 14. Their only child (III-5) had a paraganglioma with an age of diagnosis of 29 years, and a renal cyst. Patient II-1 had 4 children - one (III-1; aged 40) who presented as a carrier with no typical VHL manifestations after annual clinical monitoring; and another 32 years old presenting with pheochromocytoma. (See Figure 2 for pedigree)

      CasePresentingHPOs: HP:0002666 (pheochromocytoma)

      CaseHPOFreeText: Bilateral pheochromocytoma diagnosed at age 34

      CaseNotHPOs: N/A

      CaseNotHPOFreeText: Unclear as to whether testing for other manifestations was conducted

      CasePreviousTesting: N/A

      PreviouslyPublished: Previously reported, HGMD (Human Gene Mutation Database: http://uwcmml1s.uwcm.ac.uk/uwcm/mg/search/120488.html)

      SupplementalData: N/A

      Variant: p.R64P (c.191G>C)

      CaseProblemVariantFreeText: N/A

      LegacyVariant: N/A

      ClinVarID: 2226 https://www.ncbi.nlm.nih.gov/clinvar/variation/2226/

      CAID: CA020089 http://reg.clinicalgenome.org/redmine/projects/registry/genboree_registry/allele?hgvsOrDescriptor=NM_000551.3%3Ac.191G%3EC

      gnomAD: N/A

      VariantEvidence: N/A

      MutationType: missense_variant;transversion

      CivicName: R64P (c.191G>C)

      MultipleGeneVariants: N/A

    2. 3 c.194C>G p.Ser65Trp p.S65W Familial VHL

      PatientID: None

      KindredID: 3

      Case: Age, Sex, Ethnicity Unknown

      DiseaseAssertion: VHL

      FamilyInfo: Familial VHL

      CasePresentingHPOs: HP:0009711; HP:0010797; HP:0001737; HP:0005584; HP:0000107 (retinal capillary hemangioma, hemangioblastoma, pancreatic cysts, renal cell carcinoma, renal cyst)

      CaseHPOFreeText: N/A

      CaseNotHPOs: HP:0002666 (pheochromocytoma)

      CaseNotHPOFreeText: N/A

      CasePreviousTesting: N/A

      PreviouslyPublished: Previously reported, HGMD (Human Gene Mutation Database: http://uwcmml1s.uwcm.ac.uk/uwcm/mg/search/120488.html)

      SupplementalData: N/A

      Variant: p.S65W (c.194C>G)

      CaseProblemVariantFreeText: N/A

      LegacyVariant: N/A

      ClinVarID: 43597 https://www.ncbi.nlm.nih.gov/clinvar/variation/43597/

      CAID: CA020099 http://reg.clinicalgenome.org/redmine/projects/registry/genboree_registry/allele?hgvsOrDescriptor=NM_000551.3%3Ac.194C%3EG

      gnomAD: N/A

      VariantEvidence: N/A

      MutationType: missense_variant;transversion

      CivicName: S65W (c.194C>G)

      MultipleGeneVariants: N/A

    3. 23 c.583C>T p.Gln195X p.Q195X Familial VHL

      GroupID/ KindredID: 23

      DiseaseAssertion: VHL

      GroupSize: 2

      GroupNumberMales: N/A

      GroupNumberFemales: N/A

      GroupEthnicity: N/A

      GroupAgeRange: N/A

      GroupInfo: Described are 2 patients with this familial VHL mutation. They belong to family 23 and have the germline VHL mutation of c.583C>T

      GroupPresentingHPOs: HP:0009711; HP:0010797; HP:0002666 (retinal capillary hemangioma, hemangioblastoma, pheochromocytoma)

      GroupHPOFreeText: 2 familial patients affected; 2 rHAB (retinal hemangioblastoma), 1 cHAB (central nervous system hemangioblastoma), 1 pheochromocytoma.

      GroupNotHPOs: HP:0005584; HP:0001737 (renal cell carcinoma, pancreatic cysts)

      GroupNotHPOFreeText: None have the above manifestations

      GroupPreviousTesting: N/A

      PreviouslyPublished: Previously reported, HGMD (Human Gene Mutation Database: http://uwcmml1s.uwcm.ac.uk/uwcm/mg/search/120488.html)

      SupplementalData: N/A

      Variant: p.Q195* (c.583C>T)

      CaseProblemVariantFreeText: N/A

      LegacyVariant: N/A

      ClinVar: 428794 https://www.ncbi.nlm.nih.gov/clinvar/variation/428794/

      CAID: N/A

      gnomAD: N/A

      VariantEvidence: N/A

      MutationType: stop_gained

      CivicName: Q195* (c.583C>T)

      MultipleGeneVariants: N/A

    4. 20 c.481C>T p.Arg161X p.R161X Familial VHL

      GroupID/ KindredID: 20

      Case: Age, Sex, Ethnicity Unknown

      DiseaseAssertion: VHL

      FamilyInfo: Familial VHL; One registrant belonging to family 20 has the germline VHL mutation of c.481C>T.

      CasePresentingHPOs: HP:0009711; HP:0000107; HP:0001737 (retinal capillary hemangioma, renal cyst, pancreatic cysts)

      CaseHPOFreeText: N/A

      CaseNotHPOs: HP:0010797; HP:0002666; HP:0005584 (hemangioblastoma, pheochromocytoma, renal cell carcinoma)

      CaseNotHPOFreeText: N/A

      CasePreviousTesting: N/A

      PreviouslyPublished: Previously reported, HGMD (Human Gene Mutation Database: http://uwcmml1s.uwcm.ac.uk/uwcm/mg/search/120488.html)

      SupplementalData: N/A

      Variant: p.R161* (c.481C>T)

      CaseProblemVariantFreeText: N/A

      LegacyVariant: N/A

      ClinVarID: 2217 https://www.ncbi.nlm.nih.gov/clinvar/variation/2217/

      CAID: N/A

      gnomAD: N/A

      VariantEvidence: N/A

      MutationType: stop_gained

      CivicName: R161* (c.481C>T)

      MultipleGeneVariants: N/A

    5. 15 c.500G>A p.Arg167Gln p.R167Q Familial VHL

      GroupID/ KindredID: 15

      DiseaseAssertion: VHL

      GroupSize: 5

      GroupNumberMales: N/A

      GroupNumberFemales: N/A

      GroupEthnicity: N/A

      GroupAgeRange: N/A

      GroupInfo: Described are 5 patients with this familial VHL mutation. They belong to family 15 and have the germline VHL mutation of c.500G>A.

      GroupPresentingHPOs: HP:0009711; HP:0010797; HP:0005584; HP:0000107; HP:0001737; HP:0002666; HP:0030393 (retinal capillary hemangioma, hemangioblastoma, renal cell carcinoma, renal cyst, pancreatic cysts, pheochromocytoma, endolymphatic sac tumor)

      GroupHPOFreeText: of the totalling 5 members, 3 have rHAB, 3 have cHAB, 3 have renal cysts, 2 have RCC, 2 patients suspected (deafness, tinnitius, or vertigo) for an endolymphatic sac tumor (ELST), 1 has a pheochromocytoma and 1 has a pancreatic cyst. Additionally an adnexal papillary tumor of probable mesonephric origin (APMO) was recorded in this cohort.

      GroupNotHPOs: N/A

      GroupNotHPOFreeText: N/A

      GroupPreviousTesting: N/A

      PreviouslyPublished: Previously reported, HGMD (Human Gene Mutation Database: http://uwcmml1s.uwcm.ac.uk/uwcm/mg/search/120488.html)

      SupplementalData: N/A

      Variant: p.R167Q (c.500G>A)

      CaseProblemVariantFreeText: N/A

      LegacyVariant: N/A

      ClinVarID: 2216 https://www.ncbi.nlm.nih.gov/clinvar/variation/2216/

      CAID: N/A

      gnomAD: N/A

      VariantEvidence: N/A

      MutationType: missense_variant;transition

      CivicName: R167Q (c.500G>A)

      MultipleGeneVariants: N/A

    1. A149S (34) 

      301 were enrolled in a prospective clinical protocol to evaluate the natural history of vHL-associated pancreatic lesions (NCT00062166). Of these, 69 patients with pancreatic manifestations of vHL disease and missense VHL mutations were included in the current study. Individual patient phenotype was not described, but overall of the 60 patients, 57 had RCC, 41 had CNS hemangioblastomas, 28 had retinal hemangioblastoma, 23 had pheochromocytoma. 36/69 patients were female and the mean age was 50.5 years old.All patients underwent genetic testing using Sanger sequencing and Southern Blotting. Four patients were listed with this missense mutation, c.445G>T.

    2. F136S (33) 

      301 were enrolled in a prospective clinical protocol to evaluate the natural history of vHL-associated pancreatic lesions (NCT00062166). Of these, 69 patients with pancreatic manifestations of vHL disease and missense VHL mutations were included in the current study. Individual patient phenotype was not described, but overall of the 60 patients, 57 had RCC, 41 had CNS hemangioblastomas, 28 had retinal hemangioblastoma, 23 had pheochromocytoma. 36/69 patients were female and the mean age was 50.5 years old. All patients underwent genetic testing using Sanger sequencing and Southern Blotting. Three patients were listed with this missense mutation, c.407T>C.

    3. P86S (26) 4 

      GroupID: None

      DiseaseAssertion: VHL

      GroupSize: 4

      GroupNumberMales:N/A

      GroupNumberFemales:N/A

      GroupEthnicity: N/A

      GroupAgeRange: ≥12

      GroupInfo: The four patients were grouped by mutation.

      GroupPresentingHPOs: HP:0001732 (abnormality of the pancreas)

      GroupHPOFreeText: N/A

      GroupNotHPOs:N/A

      GroupNotHPOFreeText: N/A

      GroupPreviousTesting: N/A

      PreviouslyPublished: N/A

      SupplementalData: N/A

      Variant: p.P86S (c.256C>T)

      LegacyVariant:N/A

      CaseProblemVariantFreeText: N/A

      ClinVarID: 178692 https://www.ncbi.nlm.nih.gov/clinvar/variation/178692/

      CAID: N/A

      gnomAD: N/A

      VariantEvidence:N/A

      MutationType: missense_variant;transition

      CivicName: P86S (c.256C>T)

      MultipleGeneVariants: N/A

    4. R167L 2 

      GroupID: None

      DiseaseAssertion: VHL

      GroupSize:2

      GroupNumberMales:N/A

      GroupNumberFemales:N/A

      GroupEthnicity: N/A

      GroupAgeRange: ≥12

      GroupInfo: The two patients were grouped by mutation.

      GroupPresentingHPOs: HP:0001732 (abnormality of the pancreas)

      GroupHPOFreeText: N/A

      GroupNotHPOs:N/A

      GroupNotHPOFreeText: N/A

      GroupPreviousTesting: N/A

      PreviouslyPublished: N/A

      SupplementalData: N/A

      Variant: p.R167L(c.500G>T)

      LegacyVariant: N/A

      CaseProblemVariantFreeText: N/A

      ClinVarID: 526685 https://www.ncbi.nlm.nih.gov/clinvar/variation/526685/

      CAID:N/A

      gnomAD: N/A

      VariantEvidence: N/A

      MutationType: missense_variant;transversion

      CivicName:R167L(c.500G>T)

      MultipleGeneVariants: N/A

    5. S65W (22, 23) 2 

      GroupID: None

      DiseaseAssertion: VHL

      GroupSize: 2

      GroupNumberMales:N/A

      GroupNumberFemales:N/A

      GroupEthnicity: N/A

      GroupAgeRange: ≥12

      GroupInfo: The two patients were grouped by mutation.

      GroupPresentingHPOs: HP:0001732 (abnormality of the pancreas)

      GroupHPOFreeText: N/A

      GroupNotHPOs:N/A

      GroupNotHPOFreeText: N/A

      GroupPreviousTesting: N/A

      PreviouslyPublished: N/A

      SupplementalData: N/A

      Variant: p.S65W(c.194C>G)

      GroupProblemVariantFreeText: N/A

      LegacyVariant: N/A

      ClinVarID:43597 https://www.ncbi.nlm.nih.gov/clinvar/variation/43597/

      CAID:N/A

      gnomAD: N/A

      VariantEvidence: N/A

      MutationType:missense_variant;transversion

      CivicName: S65W(c.194C>G)

      MultipleGeneVariants: N/A

    6. L158P (35) 6 

      GroupID: None

      DiseaseAssertion: VHL

      GroupSize: 6

      GroupNumberMales:N/A

      GroupNumberFemales:N/A

      GroupEthnicity: N/A

      GroupAgeRange: ≥12

      GroupInfo: The six patients were grouped by mutation.

      GroupPresentingHPOs: HP:0001732 (abnormality of the pancreas)

      GroupHPOFreeText: N/A

      GroupNotHPOs:N/A

      GroupNotHPOFreeText: N/A

      GroupPreviousTesting: N/A

      PreviouslyPublished: N/A

      SupplementalData: N/A

      Variant: p.L158P (c.473T>C)

      CaseProblemVariantFreeText: N/A

      LegacyVariant: N/A

      ClinVarID: 182980 https://www.ncbi.nlm.nih.gov/clinvar/variation/182980/

      CAID: N/A

      gnomAD: N/A

      VariantEvidence: N/A

      MutationType: missense_variant;transition

      CivicName: L158P (c.473T>C)

      MultipleGeneVariants: N/A

    7. G93V (28) 1 

      GroupID:N/A

      Case: Sex Unknown, Age Unknown, Ethnicity Unknown

      DiseaseAssertion: VHL

      FamilyInfo: N/A

      CohortInfo: 301 were enrolled to evaluate the natural history of vHL-associated pancreatic lesions. Of these, 69 patients with pancreatic manifestations of vHL disease and missense VHL mutations were included in the current study.

      CasePresentingHPOs: HP:0001732 (abnormality of the pancreas)

      CaseHPOFreeText: N/A

      CaseNotHPOs: N/A

      CaseNotHPOFreeText: N/A

      CasePreviousTesting: N/A

      PreviouslyPublished: N/A

      SupplementalData: N/A

      Variant: p.G93V (c.278G>T)

      LegacyVariant: N/A

      CaseProblemVariantFreeText: N/A

      ClinVarID: 625232 https://www.ncbi.nlm.nih.gov/clinvar/variation/625232/

      CAID: N/A

      gnomAD: N/A

      VariantEvidence: N/A

      MutationType: missense_variant;transversion

      CivicName:G93V(c.278G>T)

      MultipleGeneVariants: N/A

    8. A149S (34) 4 

      GroupID: None

      DiseaseAssertion: VHL

      GroupSize: 4

      GroupNumberMales:N/A

      GroupNumberFemales:N/A

      GroupEthnicity: N/A

      GroupAgeRange: ≥12

      GroupInfo: The four patients were grouped by mutation.

      GroupPresentingHPOs: HP:0001732 (abnormality of the pancreas)

      GroupHPOFreeText: N/A

      GroupNotHPOs:N/A

      GroupNotHPOFreeText: N/A

      GroupPreviousTesting: N/A

      PreviouslyPublished: N/A

      SupplementalData: N/A

      Variant: p.A149S (c.445G>T)

      LegacyVariant:N/A

      CaseProblemVariantFreeText: N/A

      ClinVarID:127829 https://www.ncbi.nlm.nih.gov/clinvar/variation/127829/

      CAID: N/A

      gnomAD: N/A

      VariantEvidence: N/A

      MutationType: missense_variant;transversion

      CivicName: A149S (c.445G>T)

      MultipleGeneVariants: N/A

    9. W88R (27) 

      301 were enrolled in a prospective clinical protocol to evaluate the natural history of vHL-associated pancreatic lesions (NCT00062166). Of these, 69 patients with pancreatic manifestations of vHL disease and missense VHL mutations were included in the current study. Individual patient phenotype was not described, but overall of the 60 patients, 57 had RCC, 41 had CNS hemangioblastomas, 28 had retinal hemangioblastoma, 23 had pheochromocytoma. 36/69 patients were female and the mean age was 50.5 years old. All patients underwent genetic testing using Sanger sequencing and Southern Blotting. One patient was listed with this missense mutation, c.262T>A.

    10. A149S (34) 4 

      GroupID: None

      DiseaseAssertion: VHL

      GroupSize: 4

      GroupNumberMales:N/A

      GroupNumberFemales:N/A

      GroupEthnicity: N/A

      GroupAgeRange: ≥12

      GroupInfo: The four patients were grouped by mutation.

      GroupPresentingHPOs: HP:0001732 (abnormality of the pancreas)

      GroupHPOFreeText: N/A

      GroupNotHPOs:N/A

      GroupNotHPOFreeText: N/A

      GroupPreviousTesting: N/A

      PreviouslyPublished: N/A

      SupplementalData: N/A

      Variant: p.A149S (c.445G>T)

      LegacyVariant:N/A

      CaseProblemVariantFreeText: N/A

      ClinVarID:127829 https://www.ncbi.nlm.nih.gov/clinvar/variation/127829/

      CAID: N/A

      gnomAD: N/A

      VariantEvidence: N/A

      MutationType: missense_variant;transversion

      CivicName: A149S (c.445G>T)

      MultipleGeneVariants: N/A

    11. W88R (27) 

      301 were enrolled in a prospective clinical protocol to evaluate the natural history of vHL-associated pancreatic lesions (NCT00062166). Of these, 69 patients with pancreatic manifestations of vHL disease and missense VHL mutations were included in the current study. Individual patient phenotype was not described, but overall of the 60 patients, 57 had RCC, 41 had CNS hemangioblastomas, 28 had retinal hemangioblastoma, 23 had pheochromocytoma. 36/69 patients were female and the mean age was 50.5 years old. All patients underwent genetic testing using Sanger sequencing and Southern Blotting. One patient was listed with this missense mutation, c.262T>A.

    1. GroupID/ KindredID: F26

      Case: Sex unknown, 31Y0M, Spanish

      DiseaseAssertion: assumed VHL

      FamilyInfo: Noted of familial antecedents of phaeochromocytoma and CNS hemangioblastoma.

      CasePresentingHPOs: HP:0009711; HP:0000107 (retinal capillary hemangioma, renal cysts)

      CaseHPOFreeText: Age of onset is 31Y0M.

      CaseNotHPOs: HP:0006770; HP:0002666; HP:0006880; HP:0001737 (clear cell renal cell carcinoma, pheochromocytoma, cerebellar hemangioblastoma, pancreatic cysts, retinal capillary hemangioma)

      CaseNotHPOFreeText: N/A

      CasePreviousTesting: N/A

      PreviouslyPublished: N/A

      SupplementalData: N/A

      Variant: p.D121G (c.362A>G)

      LegacyVariant: N/A

      CaseProblemVariantFreeText: N/A

      ClinVarID: 223200 https://www.ncbi.nlm.nih.gov/clinvar/variation/223200/

      CAID: N/A

      gnomAD: N/A

      VariantEvidence: N/A

      MutationType: missense_variant; transition

      CivicName: D121G (c.362A>G)

      MultipleGeneVariants: N/A

    2. GroupID/ KindredID: F61

      Case: Sex unknown, 15Y0M, Spanish

      DiseaseAssertion: assumed VHL

      FamilyInfo: familial antecedents found of clear cell RCC

      CasePresentingHPOs: HP:0009711; HP:0002666; HP:0000107 (retinal capillary hemangioma, pheochromocytoma, renal cysts)

      CaseHPOFreeText: Unilateral pheo. Age of onset is 15Y0M.

      CaseNotHPOs: HP:0006880; HP:0006770; HP:0001737 (cerebellar hemangioblastoma, clear cell renal cell carcinoma, pancreatic cysts)

      CaseNotHPOFreeText: N/A

      CasePreviousTesting: N/A

      PreviouslyPublished: N/A

      SupplementalData: N/A

      Variant: p.C162Y (c.485G>A)

      LegacyVariant: N/A

      CaseProblemVariantFreeText: N/A

      ClinVarID: 223225 https://www.ncbi.nlm.nih.gov/clinvar/variation/223225/

      CAID: N/A

      gnomAD: N/A

      VariantEvidence: N/A

      MutationType: missense_variant; transition

      CivicName: C162Y (c.485G>A)

      MultipleGeneVariants: N/A

    3. GroupID/ KindredID: F9

      Case: Sex unknown, 20Y0M, Spanish

      DiseaseAssertion: assumed VHL

      FamilyInfo: None. Microsatellites were used to exclude nonpaternity, and the de novo character of the mutation was demonstrated in this patient. Paper says its confirmed however only discuss nonpaternity.

      CasePresentingHPOs: HP:0009711; HP:0006880; HP:0001737 (retinal capillary hemangioma, cerebellar hemangioblastoma, pancreatic cysts)

      CaseHPOFreeText: Cerebellar hemangioblastoma was found with multiple lesions. Age of onset is 20Y0M.

      CaseNotHPOs: N/A

      CaseNotHPOFreeText: N/A

      CasePreviousTesting: N/A

      PreviouslyPublished: N/A

      SupplementalData: N/A

      Variant: p.R161* (c.481C>T)

      CaseProblemVariantFreeText: N/A

      LegacyVariant: N/A

      ClinVarID: 2217 https://www.ncbi.nlm.nih.gov/clinvar/variation/2217/

      CAID: N/A

      gnomAD: N/A

      VariantEvidence: N/A

      MutationType: stop_gained

      CivicName: R161* (c.481C>T)

      MultipleGeneVariants: N/A

    4. GroupID/ KindredID: F56

      Case: Sex unknown, 45Y0M, Spanish

      DiseaseAssertion: assumed VHL

      FamilyInfo: Noted of familial antecedents with 2 affected family members. (See Table 2).

      CasePresentingHPOs: HP:0009711; HP:0006880; HP:0000107 (retinal capillary hemangioma, cerebellar hemangioblastoma, renal cyst)

      CaseHPOFreeText: Age of onset is 45Y0M.

      CaseNotHPOs: HP:0006770; HP:0002666 (clear cell renal cell carcinoma, pheochromocytoma)

      CaseNotHPOFreeText: N/A

      CasePreviousTesting: N/A

      PreviouslyPublished: N/A

      SupplementalData: N/A

      Variant: p.R167Q (c.500G>A)

      LegacyVariant: N/A

      CaseProblemVariantFreeText: N/A

      ClinVar: 2216 https://www.ncbi.nlm.nih.gov/clinvar/variation/2216/

      CAID: N/A

      gnomAD: 0.000003977 https://gnomad.broadinstitute.org/variant/3-10191507-G-A

      VariantEvidence:N/A

      MutationType: missense_variant;transition

      CivicName: R167Q (c.500G>A)

      MultipleGeneVariants: N/A

    5. GroupID/ KindredID: F64

      Case: Sex unknown, 24Y0M, Spanish

      DiseaseAssertion: assumed VHL

      FamilyInfo: None

      CasePresentingHPOs: HP:0009711; HP:0002666; HP:0001737 (retinal capillary hemangioma, pheochromocytoma, clear cell renal cell carcinoma, pancreatic cysts)

      CaseHPOFreeText: Bilateral pheo was found. Age of onset is 24Y0M.

      CaseNotHPOs: HP:0006770; HP:0000107; HP:0006880 (clear cell renal cell carcinoma, renal cysts, cerebellar hemangioblastoma)

      CaseNotHPOFreeText: N/A

      CasePreviousTesting: N/A

      PreviouslyPublished: N/A

      SupplementalData: N/A

      Variant: p.R167W (c.499C>T)

      LegacyVariant: N/A

      CaseProblemVariantFreeText: N/A

      ClinVarID: 2218 https://www.ncbi.nlm.nih.gov/clinvar/variation/2218/

      CAID: N/A

      gnomAD: 0.000007954 https://gnomad.broadinstitute.org/variant/3-10191506-C-T

      VariantEvidence: N/A

      MutationType: missense_variant; transition

      CivicName: R167W (c.499C>T)

      MultipleGeneVariants: N/A

    6. GroupID/ KindredID: F54

      Case: Sex unknown, 31Y0M, Spanish

      DiseaseAssertion: assumed VHL

      FamilyInfo: None.

      CasePresentingHPOs: HP:0006880; HP:0000107; HP:0001737 (cerebellar hemangioblastoma, renal cysts, pancreatic cysts)

      CaseHPOFreeText: Age of onset is 31Y0M.

      CaseNotHPOs: HP:0006770; HP:0002666; HP:0009711 (clear cell renal cell carcinoma, pheochromocytoma, retinal capillary hemangioma)

      CaseNotHPOFreeText: N/A

      CasePreviousTesting: N/A

      PreviouslyPublished: N/A

      SupplementalData: N/A

      Variant: p.F76del (c.227_229del)

      LegacyVariant: g.941_943delTCT

      CaseProblemVariantFreeText: Patient was reported with the g. (genomic) coding positions. The g.941_943delTCT variant worked out to correspond with c.227_229delTCT.

      ClinVarID: N/A

      CAID: CA357012 http://reg.clinicalgenome.org/redmine/projects/registry/genboree_registry/allele?hgvsOrDescriptor=NM_000551.3%3Ac.227_229del

      gnomAD: N/A

      VariantEvidence: N/A

      MutationType: inframe_deletion

      CivicName: F76del (c.227_229del)

      MultipleGeneVariants: N/A

    7. GroupID/ KindredID: F41

      Case: Sex unknown, 22Y0M, Spanish

      DiseaseAssertion: assumed VHL

      FamilyInfo: familial antecedents found; unknown of any additional features to index case relatives

      CasePresentingHPOs: HP:0009711; HP:0006770; HP:0006880; HP:0000107; HP:0001737 (retinal capillary hemangioma, clear cell renal cell carcinoma, cerebellar hemangioblastoma, renal cysts, pancreatic cysts)

      CaseHPOFreeText: Multiple lesions were found with the patient’s cerebellar hemangioma. Unilateral ccRCC. Age of onset is 22Y0M.

      CaseNotHPOs: HP:0002666 (pheochromocytoma)

      CaseNotHPOFreeText: N/A

      CasePreviousTesting: N/A

      PreviouslyPublished: N/A

      SupplementalData: N/A

      Variant: p.L128R (c.383T>G)

      LegacyVariant: N/A

      CaseProblemVariantFreeText: N/A

      ClinVarID: N/A

      CAID: CA351753891 http://reg.clinicalgenome.org/redmine/projects/registry/genboree_registry/allele?hgvsOrDescriptor=NM_000551.3%3Ac.383T%3EG

      gnomAD: N/A

      VariantEvidence: N/A

      MutationType: missense_variant; transversion

      CivicName: L128R (c.383T>G)

      MultipleGeneVariants: N/A

    8. GroupID/ KindredID: F11

      Case: Sex unknown, 32Y0M, Spanish

      DiseaseAssertion: assumed VHL

      FamilyInfo: familial antecedents found; unknown of any additional features to index case relatives

      CasePresentingHPOs: HP:0002666; HP:0009711 (pheochromocytoma, retinal capillary hemangioma)

      CaseHPOFreeText: Multiple lesions were found with the patient’s retinal hemangioma. Bilateral pheo. Age of onset is 32Y0M.

      CaseNotHPOs: HP:0006770; HP:0000107; HP:0006880; HP:0001737 (clear cell renal cell carcinoma, renal cysts, cerebellar hemangioblastoma, pancreatic cysts)

      CaseNotHPOFreeText: N/A

      CasePreviousTesting: N/A

      PreviouslyPublished: N/A

      SupplementalData: N/A

      Variant: p.Y175N (c.523T>A)

      LegacyVariant: N/A

      CaseProblemVariantFreeText: N/A

      ClinVarID: N/A

      CAID: CA351756226 http://reg.clinicalgenome.org/redmine/projects/registry/genboree_registry/allele?hgvsOrDescriptor=NM_000551.3%3Ac.523T%3EA

      gnomAD: N/A

      VariantEvidence: N/A

      MutationType: missense_variant; transversion

      CivicName: Y175N (c.523T>A)

      MultipleGeneVariants: N/A

    Tags

    Annotators

    URL

    1. In a study of 426 unrelated VHL patients, 111 were discovered to have alterations in the VHL gene. 18 novel variants were identified in VHL patients, but none were present in 200 unaffected control individuals. DNA samples from peripheral blood leukocytes underwent polymerase chain reaction (PCR) amplification, denaturing high-performance liquid chromatography (DHPLC), and direct sequence analysis of the entire coding sequence and intron-exon boundaries. This missense mutation, c.191G>C, was found in a 26 year old VHL patient with pheochromocytoma and no family history (index case 123). Only supporting evidence for pathogenicity because patient's phenotype is highly specific for a disease with a single genetic etiology.

    2. In a study of 426 unrelated VHL patients, 111 were discovered to have alterations in the VHL gene. 18 novel variants were identified in VHL patients, but none were present in 200 unaffected control individuals. DNA samples from peripheral blood leukocytes underwent polymerase chain reaction (PCR) amplification, denaturing high-performance liquid chromatography (DHPLC), and direct sequence analysis of the entire coding sequence and intron-exon boundaries. This splice site variant, c.463+1G>T, was found in an asymptomatic 8 year-old with family history of VHL disease (index case 242).

    3. In a study of 426 unrelated VHL patients, 111 were discovered to have alterations in the VHL gene. 18 novel variants were identified in VHL patients, but none were present in 200 unaffected control individuals. DNA samples from peripheral blood leukocytes underwent polymerase chain reaction (PCR) amplification, denaturing high-performance liquid chromatography (DHPLC), and direct sequence analysis of the entire coding sequence and intron-exon boundaries. This nonsense mutation, c.481C>T, was found in 3 VHL patients. The 17-year-old VHL patient only had hemangioblastomas of the central nervous system (CNS) (index case 218). The 24-year-old VHL patient had CNS hemangioblastomas and clear cell renal cell carcinoma (index case 46). The 29-year-old VHL patient had CNS and retinal capillary hemangioma and pheochromocytoma (index case 79). ACMG code as follows: There is very strong evidence for pathogenicity in the form of a nonsense variant in a gene where loss-of-function is a known mechanism of disease.

    4. PatientID: 218

      KindredID: 218

      Case: Sex Unknown, 17Y0M, Ethnicity Unknown

      DiseaseAssertion: VHL

      FamilyInfo: Positive VHL family history.

      CasePresentingHPOs: HP:0010797 (hemangioblastoma )

      CaseHPOFreeText: N/A

      CaseNotHPOs: HP:0009711, HP:0001737, HP:0002666, HP:0000107, HP:0006770 (retinal capillary hemangioma, pancreatic cyst, pheochromocytoma, renal cyst, clear cell renal cell carcinoma)

      CaseNotHPOFreeText: N/A

      CasePreviousTesting: N/A

      PreviouslyPublished: N/A

      SupplementalData: Table S1, S2, S3.

      Variant: p.R161* (c.481C>T)

      LegacyVariant: N/A

      CaseProblemVariantFreeText: N/A

      ClinVarID: 2217 https://www.ncbi.nlm.nih.gov/clinvar/variation/2217/

      CAID: CA020408 http://reg.clinicalgenome.org/redmine/projects/registry/genboree_registry/allele?hgvsOrDescriptor=NM_000551.3%3Ac.481C%3ET

      gnomAD: N/A

      VariantEvidence: N/A

      MutationType: stop_gained

      CivicName: R161*(c.481C>T)

      MultipleGeneVariants: N/A

    5. PatientID: 152

      KindredID: 152

      Case: Sex Unknown, 24Y0M, Ethnicity Unknown

      DiseaseAssertion: VHL

      FamilyInfo: None

      CasePresentingHPOs: HP:0009711, HP:0001737, HP:0000107 (retinal capillary hemangioma, pancreatic cyst, renal cyst)

      CaseHPOFreeText: N/A

      CaseNotHPOs: HP:0002666, HP:0010797, HP:0006770 (pheochromocytoma, hemangioblastoma, clear cell renal cell carcinoma)

      CaseNotHPOFreeText: N/A

      CasePreviousTesting: N/A

      PreviouslyPublished: N/A

      SupplementalData: Table S1, S2, S3.

      Variant: p.N78S(c.233A>G)

      CaseProblemVariantFreeText: N/A

      LegacyVariant: N/A

      ClinVarID: 93326 https://www.ncbi.nlm.nih.gov/clinvar/variation/93326/

      CAID: CA020131 http://reg.clinicalgenome.org/redmine/projects/registry/genboree_registry/allele?hgvsOrDescriptor=NM_000551.3%3Ac.233A%3EG

      gnomAD: N/A

      VariantEvidence: N/A

      MutationType:missense_variant;transition

      CivicName: N78S(c.233A>G)

      MultipleGeneVariants: N/A

    6. PatientID: 194

      KindredID: 194

      Case: Sex Unknown, 46Y0M, Ethnicity Unknown

      DiseaseAssertion: VHL

      FamilyInfo: N/A

      CasePresentingHPOs: HP:0010797; HP:0001732; HP:0002666; HP:0000107 (Hemangioblastoma, Abnormality of the pancreas, Pheochromocytoma, Renal cyst)

      CaseHPOFreeText: CNS hemangioblastoma, pancreatic cyst or tumor, pheochromocytoma and renal cystic lesion.

      CaseNotHPOs: HP:0009711; HP:0006770 (Retinal capillary hemangioma, Clear cell renal cell carcinoma)

      CaseNotHPOFreeText: N/A

      CasePreviousTesting: N/A

      PreviouslyPublished: N/A

      SupplementalData: Table S1, S2 and S3

      Variant: p.P59Rfs*8 (c.176del)

      LegacyVariant: N/A

      CaseProblemVariantFreeText: N/A

      ClinVarID: N/A

      CAID: CA432536374, https://reg.clinicalgenome.org/redmine/projects/registry/genboree_registry/allele?hgvsOrDescriptor=NM_000551.3%3Ac.176del

      gnomAD: N/A

      VariantEvidence: N/A

      MutationType: deletion; minus_1_frameshift_variant

      CivicName: P59fs (c.176delC)

      MultipleGeneVariants: N/A

    7. PatientID: 259

      KindredID: 259

      Case: Sex Unknown, 29Y0M, Ethnicity Unknown

      DiseaseAssertion: VHL

      FamilyInfo: None.

      CasePresentingHPOs: HP:0001737, HP:0009711 (pancreatic cysts, retinal capillary hemangioma)

      CaseHPOFreeText: N/A

      CaseNotHPOs:HP:0002666, HP:0006770, HP:0000107, HP:0010797 (pheochromocytoma, clear cell renal cell carcinoma, renal cyst, hemangioblastoma)

      CaseNotHPOFreeText: N/A

      CasePreviousTesting: N/A

      PreviouslyPublished: N/A

      SupplementalData: Table S1, S2, S3.

      Variant: p.R167Q(c.500G>A)

      LegacyVariant: N/A

      CaseProblemVariantFreeText: N/A

      ClinVarID: 2216 https://www.ncbi.nlm.nih.gov/clinvar/variation/2216/

      CAID: CA020454 http://reg.clinicalgenome.org/redmine/projects/registry/genboree_registry/allele?hgvsOrDescriptor=NM_000551.3%3Ac.500G%3EA

      gnomAD: 0.000003977 https://gnomad.broadinstitute.org/variant/3-10191507-G-A

      VariantEvidence: N/A

      MutationType: missense_variant;transition

      CivicName: R167Q(c.500G>A)

      MultipleGeneVariants: N/A

    8. PatientID: 78

      KindredID: 78

      Case: Sex Unknown, 29Y0M, Ethnicity Unknown

      DiseaseAssertion: VHL

      FamilyInfo: Family history noted but details not specified.

      CasePresentingHPOs: HP:0001732 (Abnormality of the pancreas)

      CaseHPOFreeText: Pancreatic cysts or tumors.

      CaseNotHPOs: HP:0006770; HP:0002666; HP:0010797; HP:0009711; HP:0000107 (Clear cell renal cell carcinoma, Pheochromocytoma, Hemangioblastoma, Retinal capillary hemangioma, Renal cyst)

      CaseNotHPOFreeText: N/A

      CasePreviousTesting: N/A

      PreviouslyPublished: N/A

      SupplementalData: Table S1, S2 and S3

      Variant: p.C162W (c.486C>G)

      LegacyVariant: N/A

      CaseProblemVariantFreeText: N/A

      ClinVarID: 223227, https://www.ncbi.nlm.nih.gov/clinvar/variation/223227/

      CAID: N/A

      gnomAD: N/A

      VariantEvidence: N/A

      MutationType: missense_variant;transversion

      CivicName: C162W (c.486C>G)

      MultipleGeneVariants: N/A

    9. PatientID: 45

      KindredID: 45

      Case: Sex Unknown, 33Y0M, Ethnicity Unknown

      DiseaseAssertion: VHL

      FamilyInfo: None

      CasePresentingHPOs: HP:0001737, HP:0010797 ( pancreatic cysts, hemangioblastoma)

      CaseHPOFreeText: N/A

      CaseNotHPOs: HP:0002666, HP:0006770, HP:0009711, HP:0000107 (pheochromocytoma, clear cell renal cell carcinoma, retinal capillary hemangioma, renal cyst)

      CaseNotHPOFreeText: N/A

      CasePreviousTesting: N/A

      PreviouslyPublished: N/A

      SupplementalData: Table S1, S2, S3.

      Variant: p.N78S(c.233A>G)

      CaseProblemVariantFreeText: N/A

      LegacyVariant: N/A

      ClinVarID: 93326 https://www.ncbi.nlm.nih.gov/clinvar/variation/93326/

      CAID: CA020131 http://reg.clinicalgenome.org/redmine/projects/registry/genboree_registry/allele?hgvsOrDescriptor=NM_000551.3%3Ac.233A%3EG

      gnomAD: N/A

      VariantEvidence: N/A

      MutationType:missense_variant;transition

      CivicName: N78S(c.233A>G)

      MultipleGeneVariants: N/A

    10. PatientID: 262

      KindredID: 262

      Case: Sex Unknown, 54Y0M, Ethnicity Unknown

      DiseaseAssertion: VHL

      FamilyInfo: Positive family history for VHL.

      CasePresentingHPOs: HP:0009711, HP:0010797 (retinal capillary hemangioma, hemangioblastoma)

      CaseHPOFreeText: N/A

      CaseNotHPOs: HP:0001737, HP:0002666, HP:0006770, HP:0000107 (pancreatic cysts, pheochromocytoma, clear cell renal cell carcinoma, renal cyst)

      CaseNotHPOFreeText: N/A

      CasePreviousTesting: N/A

      PreviouslyPublished: N/A

      SupplementalData: Table S1, S2, S3.

      Variant: p.Q195* (c.583C>T)

      CaseProblemVariantFreeText: N/A

      LegacyVariant: N/A

      ClinVarID: 428794 https://www.ncbi.nlm.nih.gov/clinvar/variation/428794/

      CAID: CA70052558 http://reg.clinicalgenome.org/redmine/projects/registry/genboree_registry/allele?hgvsOrDescriptor=NM_000551.3%3Ac.583C%3ET

      gnomAD: N/A

      VariantEvidence: N/A

      MutationType: stop_gained

      CivicName: Q195* (c.583C>T)

      MultipleGeneVariants: N/A

    11. PatientID: 207

      KindredID: 207

      Case: Sex Unknown, 30Y0M, Ethnicity Unknown

      DiseaseAssertion: VHL

      FamilyInfo: Family history noted but details not specified.

      CasePresentingHPOs: HP:0010797 (Hemangioblastoma)

      CaseHPOFreeText: CNS hemangioblastoma.

      CaseNotHPOs: HP:0001732; HP:0002666; HP:0009711; HP:0006770; HP:0000107 (Abnormality of the pancreas, Pheochromocytoma, Retinal capillary hemangioma, Clear cell renal cell carcinoma, Renal cyst)

      CaseNotHPOFreeText: N/A

      CasePreviousTesting: N/A

      PreviouslyPublished: N/A

      SupplementalData: Table S1, S2 and S3

      Variant: p.F136S (c.407T>C)

      LegacyVariant: N/A

      CaseProblemVariantFreeText: N/A

      ClinVarID: 496064, https://www.ncbi.nlm.nih.gov/clinvar/variation/496064/

      CAID: N/A

      gnomAD: 0.000003976, https://gnomad.broadinstitute.org/variant/3-10188264-T-C?dataset=gnomad_r2_1

      VariantEvidence: N/A

      MutationType: missense_variant;transition

      CivicName: F136S (c.407T>C)

      MultipleGeneVariants: N/A

    12. PatientID: 53

      KindredID: 53

      Case: Sex Unknown, 37Y0M, Ethnicity Unknown

      DiseaseAssertion: VHL

      FamilyInfo: Family history noted but details not specified.

      CasePresentingHPOs: HP:0009711; HP:0002666 (Retinal capillary hemangioma, Pheochromocytoma)

      CaseHPOFreeText: N/A

      CaseNotHPOs: HP:0006770; HP:0001732; HP:0010797; HP:0000107 (Clear cell renal cell carcinoma, Abnormality of the pancreas, Hemangioblastoma, Renal cyst)

      CaseNotHPOFreeText: N/A

      CasePreviousTesting: N/A

      PreviouslyPublished: N/A

      SupplementalData: Table S1, S2 and S3

      Variant: p.V170G (c.509T>G)

      LegacyVariant: N/A

      CaseProblemVariantFreeText: N/A

      ClinVarID: N/A

      CAID: CA351756196, https://reg.clinicalgenome.org/redmine/projects/registry/genboree_registry/allele?hgvsOrDescriptor=NM_000551.3%3Ac.509T%3EG

      gnomAD: N/A

      VariantEvidence: N/A

      MutationType: missense_variant;transversion

      CivicName: V170G (c.509T>G)

      MultipleGeneVariants: N/A

    13. PatientID: 4

      KindredID: 4

      Case: Sex Unknown, 26Y0M, Ethnicity Unknown

      DiseaseAssertion: VHL

      FamilyInfo: N/A

      CasePresentingHPOs: HP:0000107; HP:0009711; HP:0002666; HP:0010797 (Renal cyst, Retinal capillary hemangioma, Pheochromocytoma, Hemangioblastoma)

      CaseHPOFreeText: CNS hemangioblastoma, pheochromocytoma, renal cystic lesion and retinal hemangioblastoma.

      CaseNotHPOs: HP:0006770; HP:0001732 (Clear cell renal cell carcinoma, Abnormality of the pancreas)

      CaseNotHPOFreeText: N/A

      CasePreviousTesting: N/A

      PreviouslyPublished: N/A

      SupplementalData: Table S1, S2 and S3

      Variant: p.S80I (c.239G>T)

      LegacyVariant: N/A

      CaseProblemVariantFreeText: N/A

      ClinVarID: 625229, https://www.ncbi.nlm.nih.gov/clinvar/variation/625229/

      CAID: N/A

      gnomAD: N/A

      VariantEvidence: N/A

      MutationType: missense_variant;transversion

      CivicName: S80I (c.239G>T)

      MultipleGeneVariants: N/A

    14. PatientID: 160

      KindredID: 160

      Case: Sex Unknown, 14Y0M, Ethnicity Unknown

      DiseaseAssertion: VHL

      FamilyInfo: N/A

      CasePresentingHPOs: HP:0009711; HP:0002666; HP:0000107; HP:0001732 (Retinal capillary hemangioma, Pheochromocytoma, Renal cyst, Abnormality of the pancreas)

      CaseHPOFreeText: Retinal hemangioblastoma, pheochromocytoma, renal cystic lesion and pancreatic cyst or tumor.

      CaseNotHPOs: HP:0006770; HP:0010797 (Clear cell renal cell carcinoma, Hemangioblastoma)

      CaseNotHPOFreeText: N/A

      CasePreviousTesting: N/A

      PreviouslyPublished: N/A

      SupplementalData: Table S1, S2 and S3

      Variant: p.L178P (c.533T>C)

      LegacyVariant: N/A

      CaseProblemVariantFreeText: N/A

      ClinVarID: 428795, https://www.ncbi.nlm.nih.gov/clinvar/variation/428795/

      CAID: N/A

      gnomAD: N/A

      VariantEvidence: Variant noted as c.533C>T/p.L178P which was assumed to be c.533T>C.

      MutationType: missense_variant;transition

      CivicName: L178P (c.533T>C)

      MultipleGeneVariants: N/A

    15. PatientID: 105

      KindredID: 105

      Case: Sex Unknown, 33Y0M, Ethnicity Unknown

      DiseaseAssertion: VHL

      FamilyInfo: Family history noted but no details provided.

      CasePresentingHPOs: HP:0000107; HP:0009711; HP:0010797; HP:0001732 (Renal cyst, Retinal capillary hemangioma, Hemangioblastoma, Abnormality of the pancreas)

      CaseHPOFreeText: CNS hemangioblastoma, pancreatic cyst or tumor, renal cystic lesion and retinal hemangioblastoma.

      CaseNotHPOs: HP:0006770; HP:0002666 (Clear cell renal cell carcinoma, Pheochromocytoma)

      CaseNotHPOFreeText: N/A

      CasePreviousTesting: N/A

      PreviouslyPublished: N/A

      SupplementalData: Table S1, S2 and S3

      Variant: p.P86A (c.256C>G)

      LegacyVariant: N/A

      CaseProblemVariantFreeText: N/A

      ClinVarID: 93327, https://www.ncbi.nlm.nih.gov/clinvar/variation/93327/

      CAID: N/A

      gnomAD: N/A

      VariantEvidence: N/A

      MutationType: missense_variant;transversion

      CivicName: P86A (c.256C>G)

      MultipleGeneVariants: N/A

    16. PatientID: 249

      KindredID: 249

      Case: Sex Unknown, 32Y0M, Ethnicity Unknown

      DiseaseAssertion: VHL

      FamilyInfo: None.

      CasePresentingHPOs: HP:0006770, HP:0000107 (clear cell renal cell carcinoma, renal cyst)

      CaseHPOFreeText: N/A

      CaseNotHPOs: HP:0009711,HP:0010797, HP:0001737, HP:0002666 ( retinal capillary hemangioma, hemangioblastoma, pancreatic cyst, pheochromocytoma )

      CaseNotHPOFreeText: N/A

      CasePreviousTesting: N/A

      PreviouslyPublished: N/A

      SupplementalData: Table S1, S2, S3.

      Variant: p.P86L(c.257C>T)

      LegacyVariant: N/A

      CaseProblemVariantFreeText: N/A

      ClinVarID: 182977 https://www.ncbi.nlm.nih.gov/clinvar/variation/182977/

      CAID: CA020186 http://reg.clinicalgenome.org/redmine/projects/registry/genboree_registry/allele?hgvsOrDescriptor=NM_000551.3%3Ac.257C%3ET

      gnomAD: N/A

      VariantEvidence: N/A

      MutationType: missense_variant;transition

      CivicName: P86L(c.257C>T)

      MultipleGeneVariants: N/A

    Tags

    Annotators

    URL

    1. , VHL, RET, and MAX germline and somatic mutations have been reported in 3–25%, 13–9%, 5–5%, and 1–3% of tumours, respectively [33]. Recently activating mutations in HIF2A and HRAS were reported in a subset of these tumours [6, 7, 19, 20]. Whilst HIF2A mutations may be found in multiple tumours from patients without a detectable germline mutation (suggesting low level constitutional mosaicism) or occasionally as a germline mutation [5], to date HRAS mutations have only been detected as somatic changes (germline HRAS mutations are associated with Costello syndrome but PCC/PGL/HNPGL are apparently not a feature of this disorder) [34].
    2. P9PCC VHL c.292T>C

      PatientID: P9

      KindredID: 6

      Case: Sex Unknown, Age Unknown, Ethnicity Unknown

      DiseaseAssertion: pheochromocytoma

      FamilyInfo: N/A

      CasePresentingHPOs: HP:0002666 (pheochromocytoma)

      CaseHPOFreeText: N/A

      CaseNotHPOs: N/A

      CaseNotHPOFreeText: N/A

      CasePreviousTesting: N/A

      PreviouslyPublished: N/A

      SupplementalData: N/A

      Variant: p.Y98H (c.292T>C)

      LegacyVariant: N/A

      CaseProblemVariantFreeText: N/A

      ClinVar: 2223 https://www.ncbi.nlm.nih.gov/clinvar/variation/2223/

      CAID: N/A

      gnomAD: 0.00001343 https://gnomad.broadinstitute.org/variant/3-10183823-T-C

      VariantEvidence: N/A

      MutationType: missense_variant;transition

      CivicName: Y98H (c.292T>C)

      MultipleGeneVariants: N/A

    3. P7PCC VHL c.292T>C

      PatientID: P7

      KindredID: 4

      Case: Sex Unknown, Age Unknown, Ethnicity Unknown

      DiseaseAssertion: pheochromocytoma

      FamilyInfo: N/A

      CasePresentingHPOs: HP:0002666 (pheochromocytoma)

      CaseHPOFreeText: N/A

      CaseNotHPOs: N/A

      CaseNotHPOFreeText: N/A

      CasePreviousTesting: N/A

      PreviouslyPublished: N/A

      SupplementalData: N/A

      Variant: p.Y98H (c.292T>C)

      LegacyVariant: N/A

      CaseProblemVariantFreeText: N/A

      ClinVar: 2223 https://www.ncbi.nlm.nih.gov/clinvar/variation/2223/

      CAID: N/A

      gnomAD: 0.00001343 https://gnomad.broadinstitute.org/variant/3-10183823-T-C

      VariantEvidence: N/A

      MutationType: missense_variant;transition

      CivicName: Y98H (c.292T>C)

      MultipleGeneVariants: N/A

    4. P6PCC VHL c.292T>C

      PatientID: P6

      KindredID: 3

      Case: Sex Unknown, Age Unknown, Ethnicity Unknown

      DiseaseAssertion: pheochromocytoma

      FamilyInfo: N/A

      CasePresentingHPOs: HP:0002666 (pheochromocytoma)

      CaseHPOFreeText: N/A

      CaseNotHPOs: N/A

      CaseNotHPOFreeText: N/A

      CasePreviousTesting: N/A

      PreviouslyPublished: N/A

      SupplementalData: N/A

      Variant: p.Y98H (c.292T>C)

      LegacyVariant: N/A

      CaseProblemVariantFreeText: N/A

      ClinVar: 2223 https://www.ncbi.nlm.nih.gov/clinvar/variation/2223/

      CAID: N/A

      gnomAD: 0.00001343 https://gnomad.broadinstitute.org/variant/3-10183823-T-C

      VariantEvidence: N/A

      MutationType: missense_variant;transition

      CivicName: Y98H (c.292T>C)

      MultipleGeneVariants: N/A

    5. P5PCC VHL c.292T>C

      PatientID: P5

      KindredID: 2

      Case: Sex Unknown, Age Unknown, Ethnicity Unknown

      DiseaseAssertion: pheochromocytoma

      FamilyInfo: N/A

      CasePresentingHPOs: HP:0002666 (pheochromocytoma)

      CaseHPOFreeText: N/A

      CaseNotHPOs: N/A

      CaseNotHPOFreeText: N/A

      CasePreviousTesting: N/A

      PreviouslyPublished: N/A

      SupplementalData: N/A

      Variant: p.Y98H (c.292T>C)

      LegacyVariant: N/A

      CaseProblemVariantFreeText: N/A

      ClinVar: 2223 https://www.ncbi.nlm.nih.gov/clinvar/variation/2223/

      CAID: N/A

      gnomAD: 0.00001343 https://gnomad.broadinstitute.org/variant/3-10183823-T-C

      VariantEvidence: N/A

      MutationType: missense_variant;transition

      CivicName: Y98H (c.292T>C)

      MultipleGeneVariants: N/A

    1. germline missense mutation at nucleotide 505 (T to C) of the VHL tumor suppressor gene in 14, apparently unrelated, VHL type 2A families from the Black Forest region of Germany.

      GroupID/ KindredID: VHL 34

      DiseaseAssertion: assumed VHL

      GroupSize: 2

      GroupNumberMales: N/A

      GroupNumberFemales: N/A

      GroupEthnicity: German

      GroupAgeRange: N/A

      FamilyInfo: 2 affected members belong to this VHL family. Diagnosis of VHL was clinically confirmed in the index person and VHL type could not be determined due to the small size of the pedigree. One representative affected member was analyzed with this mutation, and VHL was diagnosed clinically in this index person. It is unclear as to whether the additional patients had this precise mutation, although assumed.

      GroupPresentingHPOs: HP:0010797; HP:0005584 (hemangioblastoma, renal cell carcinoma)

      GroupHPOFreeText: both (2) individuals had RCC, where as only one had a CNS hemangioblastoma.

      GroupNotHPOs: HP:0009711; HP:0002666; HP:0001737; HP:0009715 (retinal capillary hemangioma, pheochromocytoma, pancreatic cysts, papillary cystadenoma of the epididymis)

      GroupNotHPOFreeText: No patients had the above tumors

      GroupPreviousTesting: N/A

      PreviouslyPublished: 11134110, 9681856, 11850829

      SupplementalData: N/A

      Variant: p.Y98H (c.292T>C)

      LegacyVariant: p.Y98H (c.505T>C)

      CaseProblemVariantFreeText: N/A

      ClinVar: 2223 https://www.ncbi.nlm.nih.gov/clinvar/variation/2223/

      CAID: N/A

      gnomAD: 0.00001343 https://gnomad.broadinstitute.org/variant/3-10183823-T-C

      VariantEvidence: N/A

      MutationType: missense_variant;transition

      CivicName: Y98H (c.292T>C)

      MultipleGeneVariants: N/A

    2. germline missense mutation at nucleotide 505 (T to C) of the VHL tumor suppressor gene in 14, apparently unrelated, VHL type 2A families from the Black Forest region of Germany.

      GroupID/ KindredID: VHL 1

      DiseaseAssertion: assumed VHL

      GroupSize: 2

      GroupNumberMales: N/A

      GroupNumberFemales: N/A

      GroupEthnicity: German

      GroupAgeRange: N/A

      FamilyInfo: 2 affected members belong to this VHL type 2A family. One representative affected member was analyzed with this mutation, and VHL was diagnosed clinically in this index person. It is unclear as to whether the second patient had this precise mutation, although assumed.

      GroupPresentingHPOs: HP:0009711; HP:0002666 (retinal capillary hemangioma, pheochromocytoma)

      GroupHPOFreeText: both individuals had Pheos, whereas only 1 person had a retinal capillary hemangioma.

      GroupNotHPOs: HP:0010797; HP:0005584; HP:0001737; HP:0009715 (hemangioblastoma, renal cell carcinoma, pancreatic cysts, papillary cystadenoma of the epididymis)

      GroupNotHPOFreeText: No patients had the above tumors

      GroupPreviousTesting: N/A

      PreviouslyPublished: 11134110, 9681856, 11850829

      SupplementalData: N/A

      Variant: p.Y98H (c.292T>C)

      LegacyVariant: p.Y98H (c.505T>C)

      CaseProblemVariantFreeText: N/A

      ClinVar: 2223 https://www.ncbi.nlm.nih.gov/clinvar/variation/2223/

      CAID: N/A

      gnomAD: 0.00001343 https://gnomad.broadinstitute.org/variant/3-10183823-T-C

      VariantEvidence: N/A

      MutationType: missense_variant;transition

      CivicName: Y98H (c.292T>C)

      MultipleGeneVariants: N/A

    1. Expression study of the new VHL isoforms in patients' cellsRNA sequencing (RNA-seq) analysis of patients' LCLs and tumors demonstrated that genomic variants in E1′ were associated with an upregulation of transcripts containing the E1′ cryptic exon compared with controls (Figure 3A; supplemental Figure 8). In addition, the mutated allele was preferentially expressed (>70%), suggesting a causal relationship between the genetic variants and E1′ retention (supplemental Figure 8C).Figure 3. Expression study of the new VHL transcript isoforms in patient cells. (A) Sashimi plots from RNA-seq data obtained from samples (LCLs or pheochromocytomas [Pheo]) of 3 patients from F8. The positions of the different VHL exons are indicated, with the maximal number of reads indicated at the right. Splice junctions are denoted by the horizontal links, with details provided in supplemental Figure 8. (B) TaqMan quantification of the different VHL isoforms from samples of F8 performed using probes specific to VHL E1-E2, the translated sequence upstream E1′, or E1-E1′ junctions. Relative gene expression was normalized to LCL control (C1) fixed at 1 (mean results of technical duplicates). (C) TaqMan quantification of the different VHL isoforms in LCLs (established from 2 independent controls and from patients of F1, F2, and F8) cultured in the absence or presence of puromycin (puro), an inhibitor of nonsense-mediated mRNA decay. TaqMan probes were specific to the VHL E1-E1′ or E1-E2 junction. The graph resumes experiments performed on LCLs cultured independently 3 times and quantified in duplicate. Data are represented as the mean ± standard error of the mean. (D) RT-PCR using primers specific for E1 and E3 was performed on mRNA extracted from LCLs established from controls and patients of F6 (carrying the mutation c.340+574A>T that targets the SA site of E1′). Patient with erythrocytosis is indicated in red. On the right, the spliced isoforms are schematically represented. **P < .05, ***P < .01 based on Student t test. *Denotes larger fragments that contained E1′ spliced with E1, but with 15 nucleotides deleted (represented in red) by the use of an alternative SA site (sequences of the cloned bands are detailed in supplemental Figure 10).Download : Download high-res image (230KB)Download : Download full-size imageFigure 3. Expression study of the new VHL transcript isoforms in patient cells. (A) Sashimi plots from RNA-seq data obtained from samples (LCLs or pheochromocytomas [Pheo]) of 3 patients from F8. The positions of the different VHL exons are indicated, with the maximal number of reads indicated at the right. Splice junctions are denoted by the horizontal links, with details provided in supplemental Figure 8. (B) TaqMan quantification of the different VHL isoforms from samples of F8 performed using probes specific to VHL E1-E2, the translated sequence upstream E1′, or E1-E1′ junctions. Relative gene expression was normalized to LCL control (C1) fixed at 1 (mean results of technical duplicates). (C) TaqMan quantification of the different VHL isoforms in LCLs (established from 2 independent controls and from patients of F1, F2, and F8) cultured in the absence or presence of puromycin (puro), an inhibitor of nonsense-mediated mRNA decay. TaqMan probes were specific to the VHL E1-E1′ or E1-E2 junction. The graph resumes experiments performed on LCLs cultured independently 3 times and quantified in duplicate. Data are represented as the mean ± standard error of the mean. (D) RT-PCR using primers specific for E1 and E3 was performed on mRNA extracted from LCLs established from controls and patients of F6 (carrying the mutation c.340+574A>T that targets the SA site of E1′). Patient with erythrocytosis is indicated in red. On the right, the spliced isoforms are schematically represented. **P < .05, ***P < .01 based on Student t test. *Denotes larger fragments that contained E1′ spliced with E1, but with 15 nucleotides deleted (represented in red) by the use of an alternative SA site (sequences of the cloned bands are detailed in supplemental Figure 10).We performed quantitative RT-PCR using TaqMan probes specific for the different splicing junctions or for the region upstream of E1′ (location of probes shown in Figure 1C), which showed a strong upregulation of a unique isoform containing E1′ spliced with E1 in LCLs and tumors from patients of F8 compared with controls (Figure 3B). The study therefore focused on the isoform E1-E1′. Transcripts that retained E1′ spliced with E1 contained (in-frame with E1) a premature termination codon (Figure 1C) and could likely be targeted for degradation according to nonsense-mediated mRNA decay (NMD) mechanisms. We therefore investigated the expression of transcripts that contained E1 spliced with E1′ in the absence or presence of puromycin, an inhibitor of NMD. Without puromycin, higher levels of expression were seen in samples with mutated E1′ (Figure 3C) compared with samples containing WT E1′. Exposure to puromycin resulted in a profound induction of isoforms containing E1 spliced with E1′ vs other isoforms (Figure 3C; supplemental Figure 9). These results indicated that isoforms with E1-E1′ junction were degraded by NMD and may have failed to produce proteins. We performed RT-PCR on LCL samples of F6 carrying the mutation in the SA site, using primers in VHL exons E1 and E3. We observed fragments of larger size in samples from patients carrying the mutation, which were highly visible in the presence of puromycin (Figure 3D). Cloning and sequencing of these fragments demonstrated a dysregulated splicing of E1′ with the use of an alternative SA site located 15 nucleotides downstream (supplemental Figure 10).To measure the impact of the splicing dysregulation on pVHL expression, we performed an immunoblot with an antibody able to recognize the amino acids encoded by E1 and therefore able to detect the different pVHL isoforms.8 The antibody detected overexpressed exogenous X1 protein after transfection of the plasmid encoding X1 (Figure 4A). However, it failed to detect the endogenous protein, even in patients' samples that overexpressed the mRNA containing E1-E1′. Instead, the immunoblots showed a lower expression of all the VHL protein isoforms in patients with mutated E1′ (Figures 4A-B).Figure 4. Functional studies of mutations in VHL E1′. (A-B) Immunoblot analysis of patient LCLs. A representative immunoblot (A) and quantification of 3 different immunoblots (B) are presented. Relative gene expression was normalized to glyceraldehyde-3-phosphate dehydrogenase (GAPDH) expression, and results obtained with LCL control (C1) were fixed at 100%. Data are represented as the mean ± standard error of the mean. A VHL antibody that recognized VHL E1 was able to detect the hypothetical X1 protein. In the most left lane, control LCLs were transfected with an expression vector containing the coding sequence for X1; 5 µg of proteins were blotted vs 45 µg for other samples to avoid signal saturation with overexpressed X1. Patients with erythrocytosis are indicated in red. (C) Functional hypoxia response element (HRE)–dependent reporter assays were performed in 786-O cells (ie, VHL− cells that constitutively express HIF-2α). The results are expressed as relative firefly luciferase activity with Renilla luciferase as an internal control; 1.0 unit denotes the basal activity of endogenous HIF-2α using the HRE luciferase reporter plasmid. The ability of WT and mutated X1 to downregulate firefly luciferase activity (related to HIF activity) was compared with pVHL and in competition with pVHL. An immunoblot using an antibody specific to the hemagglutinin tag (HA) was used to detect HA-VHL and HA-X1. X1-L128V+L138P corresponds to a potential impact of the c.340+648T>C and c.340+617C>G mutations on the hypothetical X1 protein. Three independent experiments were performed. (D) Characterization of VHL E1′ retention by the minigene experiment (representative picture of agarose gel; n = 3). RT-PCR was performed on mRNA obtained from cell lines transfected with a minigene construct containing VHL E1′ (WT or mutated) flanked by large intronic sequences cloned between the SERPING1 exons (exons A and B, targeted by the RT-PCR primers). The plasmids were transfected, and the expression of the spliced chimeric transcripts (containing EA and EB ± E1′) was analyzed. Two WT constructs containing E1′ were used; 1 contained the single-nucleotide polymorphism c.340+1150T>C (rs779808). Bands corresponding to EA and EB spliced together or with VHL E1′ are indicated on the right. *P < .05, **P < .01, ***P < .001, ****P < .0001 based on Student t test. †Corresponds to unspecific bands verified by sequencing. The minigene experiment performed with the construction carrying the mutation c.340+574A>T (that targets the SA site of E1′ in F6) confirmed the use of an alternative SA site (right panel) with the deletion of 15 nucleotides (represented in red). ns, not significant.Download : Download high-res image (204KB)Download : Download full-size imageFigure 4. Functional studies of mutations in VHL E1′. (A-B) Immunoblot analysis of patient LCLs. A representative immunoblot (A) and quantification of 3 different immunoblots (B) are presented. Relative gene expression was normalized to glyceraldehyde-3-phosphate dehydrogenase (GAPDH) expression, and results obtained with LCL control (C1) were fixed at 100%. Data are represented as the mean ± standard error of the mean. A VHL antibody that recognized VHL E1 was able to detect the hypothetical X1 protein. In the most left lane, control LCLs were transfected with an expression vector containing the coding sequence for X1; 5 µg of proteins were blotted vs 45 µg for other samples to avoid signal saturation with overexpressed X1. Patients with erythrocytosis are indicated in red. (C) Functional hypoxia response element (HRE)–dependent reporter assays were performed in 786-O cells (ie, VHL− cells that constitutively express HIF-2α). The results are expressed as relative firefly luciferase activity with Renilla luciferase as an internal control; 1.0 unit denotes the basal activity of endogenous HIF-2α using the HRE luciferase reporter plasmid. The ability of WT and mutated X1 to downregulate firefly luciferase activity (related to HIF activity) was compared with pVHL and in competition with pVHL. An immunoblot using an antibody specific to the hemagglutinin tag (HA) was used to detect HA-VHL and HA-X1. X1-L128V+L138P corresponds to a potential impact of the c.340+648T>C and c.340+617C>G mutations on the hypothetical X1 protein. Three independent experiments were performed. (D) Characterization of VHL E1′ retention by the minigene experiment (representative picture of agarose gel; n = 3). RT-PCR was performed on mRNA obtained from cell lines transfected with a minigene construct containing VHL E1′ (WT or mutated) flanked by large intronic sequences cloned between the SERPING1 exons (exons A and B, targeted by the RT-PCR primers). The plasmids were transfected, and the expression of the spliced chimeric transcripts (containing EA and EB ± E1′) was analyzed. Two WT constructs containing E1′ were used; 1 contained the single-nucleotide polymorphism c.340+1150T>C (rs779808). Bands corresponding to EA and EB spliced together or with VHL E1′ are indicated on the right. *P < .05, **P < .01, ***P < .001, ****P < .0001 based on Student t test. †Corresponds to unspecific bands verified by sequencing. The minigene experiment performed with the construction carrying the mutation c.340+574A>T (that targets the SA site of E1′ in F6) confirmed the use of an alternative SA site (right panel) with the deletion of 15 nucleotides (represented in red). ns, not significant.Functional characterization of the mutated VHL E1′Because the hypoxia pathway represents the major pathway involved in the genesis of secondary erythrocytosis and VHL disease,13, 14, 1528 we performed functional studies of the hypothetical WT or mutated X1 proteins using hypoxia response element–dependent reporter assays. These functional tests failed to reveal any substantial effects of X1 on this pathway, either alone or in competition with pVHL (Figure 4C; supplemental Figure 11). We next focused our study on a potential impact of the E1′ variants on splicing by performing splicing reporter minigene assays in various cell lines. The experiments showed that splicing of WT E1′ was barely detected (Figure 4D). Interestingly, higher molecular weight bands corresponding to the expected spliced isoforms containing E1′ appeared in the presence of the mutations. Cloning and sequencing of the isoforms confirmed a retention of E1′ at the expected splicing sites. The level of expression of this upper isoform, specific to E1′ inclusion, was higher for mutations associated with cancers than for those with erythrocytosis, independently of the cell lines. Notably, the combination of both variants associated with cancer had a more pronounced effect than each variant individually (the single-nucleotide polymorphism showing very low effect), suggesting a synergistic effect of the variants on splicing (supplemental Figure 12). In silico analysis of c.340+617C>G consistently predicted a severe alteration of splicing by the creation of an exonic splicing enhancer site (supplemental Figure 13).The minigene experiment performed with mutated E1′ at the SA site (F6) confirmed the inclusion of E1′ during splicing (Figure 4D, right panel), using the same downstream alternative SA site identified in mRNA extracted from patients' LCLs (supplemental Figure 10).Synonymous mutations in VHL E2 induce exon skippingWe then focused our study on the synonymous heterozygous D143D mutation in E2, identified in the proband of F1. This mutation was also identified in the homozygous state in 2 patients with erythrocytosis (F9 and F10; Figure 5A; Table 1). The mRNA extracted from LCLs established from the different members of these 2 families was reverse transcribed and sequenced. Comparison of chromatograms obtained by sequencing of DNA vs cDNA displayed a weaker peak of the mutated allele in cDNA, reflecting a decreased expression of the mRNA transcripts carrying the mutation.Download : Download high-res image (221KB)Download : Download full-size imageFigure 5. Genetic and expression study of synonymous mutations in VHL E2. (A-B) Pedigree and sequence chromatograms of germline DNA, tumor (pheochromocytoma) DNA, or cDNA prepared from 2 families (F9 and F10) with erythrocytosis (A) and 2 families (F11 and F12) with VHL disease (B). (C) Results of RT-PCR using mRNA extracted from LCLs (F9 and F10) and leukocytes and tumor material (pheochromocytoma) (F11 and F12). (D) TaqMan quantification of the different VHL isoforms in LCLs (established from patients of F9, F10, and F11) cultured in the absence or presence of puromycin. TaqMan probes are specific to the VHL E1-E2 or E1-E3 junction. Relative gene expression was normalized to LCL control (C1). (E) Immunoblot analysis of patient LCLs. Patients with erythrocytosis are indicated in red. A representative immunoblot (upper panel) and quantification of 4 different immunoblots are displayed (lower panel). Relative gene expression was normalized to glyceraldehyde-3-phosphate dehydrogenase (GAPDH) expression, and results obtained with C1 were fixed at 100%. Data are represented as the mean ± standard error of the mean. *P < .05, **P < .01, ***P < .001, ****P < .0001 based on Student t test. CNS, central nervous system.A different synonymous mutation in E2, c.414A>G p.Pro138Pro (P138P), was identified in 2 families (F11 and F12) with VHL disease (Figure 5B). This heterozygous mutation segregated with the disease in 3 generations. Sequencing of DNA extracted from the pheochromocytoma of F11-III.1 showed a loss of the WT allele in the tumor, demonstrating loss of heterozygosity as currently described in classical VHL disease.Suspecting an effect of the synonymous mutations on splicing, we next assessed the expression of the VHL transcripts in patients' samples by RT-PCR (Figure 5C). We found a significant change in the ratio of expressed VHL isoforms, with a higher expression of the E1-E3 transcripts in LCLs of patients homozygous for D143D and in the pheochromocytoma with P138P mutation. These results suggest an effect of the mutation on splicing regulatory elements, leading to E2 skipping. In silico analysis of the synonymous mutations indicated a potential effect on exonic splicing enhancer motifs (supplemental Figure 14).To specifically quantify the different VHL isoforms, we performed quantitative RT-PCR on LCLs using TaqMan probes complementary to the VHL E1-E2 or E1-E3 junction (Figure 5D). All mutated samples displayed an increase of the isoform with skipped E2 (E1-E3). The patients carrying a homozygous D143D mutation presented a severe decrease of the WT isoform expression level. These results demonstrated that synonymous mutations in E2 affected mRNA isoform production.To evaluate a potential impact on protein expression, we performed a western blot analysis. We did not observe any overexpression of the pVHL172 isoform as expected from mRNA quantification studies. However, in patients homozygous for D143D, we detected a strong downregulation of all the pVHL isoforms, which was also observed to a lesser extent in LCL samples from heterozygous patients (Figure 5E).Proportion of VHL E2 skipping is correlated with disease severity in minigene experimentsTo study the impact of the synonymous E2 mutations on splicing in different cell lines, we performed minigene assays. We tested the implications of the D143D and P138P mutations on splicing in addition to the nearby mutations described in patients with erythrocytosis (P138L and G144R).4,6,29 Indeed, these mutations may also affect splicing rather than VHL protein function. We first evaluated the loss of function of these mutants by reporter assays. We found that these could downregulate HIF in a manner similar to the WT protein, in contrast to VHL proteins lacking E2 (pVHLΔE2), which are described as nonfunctional in terms of their regulation of HIF activity8, 9, 1012 (Figure 6A). Minigene experiments were performed in a variety of cell lines relevant to the studied diseases, using LCLs as control (Figure 6B). We demonstrated that all mutations caused E2 skipping in LCLs. In other cell lines, these experiments demonstrated a major impact on the VHL E2 splicing of the P138P mutation, which is associated with cancer. The mutations P138L, D143D, and G144R, which are all associated with erythrocytosis, displayed a weaker effect on splicing, with slight variations among cell lines but with a stronger effect in the erythroid cell line (UT7 cultured with erythropoietin).Figure 6. Functional study of synonymous mutations in VHL E2. (A) Functional hypoxia response element (HRE)–dependent reporter assays were performed in 786-O cells to evaluate the impact of VHL mutations in E2 (P138L and G144R) on VHL protein activity. The VHL protein lacking E2 (pVHL172/VHLΔE2) was used as a negative control. The results are expressed as firefly luciferase activity relative to Renilla luciferase as an internal control; 1.0 unit denotes the basal activity of endogenous HIF-2α using the HRE luciferase reporter plasmid. Immunoblots using an antibody specific for the hemagglutinin tag (HA) were used to detect HA-VHL. (B) Characterization of VHL E2 skipping by minigene analyses. Minigene experiments were performed in a variety of cell lines relevant to the studied diseases: renal (293T, 786-O, and HK2), pheochromocytoma (pheo; PC12), erythroid cell line (UT7 cultured with erythropoietin), and LCL. RT-PCR was performed on mRNA obtained from cell lines transfected with a minigene construct containing VHL E2 flanked by intronic sequences cloned between the SERPING1 exons (exons A and B; targeted by the RT-PCR primers). Bands corresponding to EA and EB spliced together or with VHL E2 are indicated on the right. (C) Sashimi plots from RNA-seq data. The positions of the different VHL exons are indicated, with the maximum number of reads for each exon indicated at the right. Splice junctions are denoted by the horizontal links, with details provided in supplemental Figure 15A. (D) Heatmap of pheochromocytoma transcriptome data. A comparison of transcriptome data for the pheochromocytoma from patient F11 III.1 (with P138P mutation) vs Affymetrix data from the largest available cohort of paragangliomas/pheochromocytomas (recruited by the French COMETE network) that identified homogeneous molecular subgroups associated with susceptibility genes (Burnichon et al30).Download : Download high-res image (254KB)Download : Download full-size imageFigure 6. Functional study of synonymous mutations in VHL E2. (A) Functional hypoxia response element (HRE)–dependent reporter assays were performed in 786-O cells to evaluate the impact of VHL mutations in E2 (P138L and G144R) on VHL protein activity. The VHL protein lacking E2 (pVHL172/VHLΔE2) was used as a negative control. The results are expressed as firefly luciferase activity relative to Renilla luciferase as an internal control; 1.0 unit denotes the basal activity of endogenous HIF-2α using the HRE luciferase reporter plasmid. Immunoblots using an antibody specific for the hemagglutinin tag (HA) were used to detect HA-VHL. (B) Characterization of VHL E2 skipping by minigene analyses. Minigene experiments were performed in a variety of cell lines relevant to the studied diseases: renal (293T, 786-O, and HK2), pheochromocytoma (pheo; PC12), erythroid cell line (UT7 cultured with erythropoietin), and LCL. RT-PCR was performed on mRNA obtained from cell lines transfected with a minigene construct containing VHL E2 flanked by intronic sequences cloned between the SERPING1 exons (exons A and B; targeted by the RT-PCR primers). Bands corresponding to EA and EB spliced together or with VHL E2 are indicated on the right. (C) Sashimi plots from RNA-seq data. The positions of the different VHL exons are indicated, with the maximum number of reads for each exon indicated at the right. Splice junctions are denoted by the horizontal links, with details provided in supplemental Figure 15A. (D) Heatmap of pheochromocytoma transcriptome data. A comparison of transcriptome data for the pheochromocytoma from patient F11 III.1 (with P138P mutation) vs Affymetrix data from the largest available cohort of paragangliomas/pheochromocytomas (recruited by the French COMETE network) that identified homogeneous molecular subgroups associated with susceptibility genes (Burnichon et al30).Splicing dysregulation of VHL is causal in the development of diseaseRNA-seq confirmed that the synonymous mutations were not silent but instead induced potent E2 skipping (Figure 6C; supplemental Figure 15A). Additional transcriptome analyses of the pheochromocytoma carrying P138P showed an upregulation of HIF target genes (typically seen in VHL-related pheochromocytomas) compared with the pheochromocytoma carrying a RET mutation (supplemental Figure 15B).30 We then reanalyzed our independent cohort of pheochromocytomas30 using RNA-seq data from both tumors. After unsupervised classification, we observed a segregation of the P138P pheochromocytoma with other VHL-related tumors (C1B cluster), whereas the control pheochromocytoma bearing the RET mutation was grouped with other RET-related tumors (Figure 6D).
    2. Expression study of the new VHL isoforms in patients' cellsRNA sequencing (RNA-seq) analysis of patients' LCLs and tumors demonstrated that genomic variants in E1′ were associated with an upregulation of transcripts containing the E1′ cryptic exon compared with controls (Figure 3A; supplemental Figure 8). In addition, the mutated allele was preferentially expressed (>70%), suggesting a causal relationship between the genetic variants and E1′ retention (supplemental Figure 8C).Figure 3. Expression study of the new VHL transcript isoforms in patient cells. (A) Sashimi plots from RNA-seq data obtained from samples (LCLs or pheochromocytomas [Pheo]) of 3 patients from F8. The positions of the different VHL exons are indicated, with the maximal number of reads indicated at the right. Splice junctions are denoted by the horizontal links, with details provided in supplemental Figure 8. (B) TaqMan quantification of the different VHL isoforms from samples of F8 performed using probes specific to VHL E1-E2, the translated sequence upstream E1′, or E1-E1′ junctions. Relative gene expression was normalized to LCL control (C1) fixed at 1 (mean results of technical duplicates). (C) TaqMan quantification of the different VHL isoforms in LCLs (established from 2 independent controls and from patients of F1, F2, and F8) cultured in the absence or presence of puromycin (puro), an inhibitor of nonsense-mediated mRNA decay. TaqMan probes were specific to the VHL E1-E1′ or E1-E2 junction. The graph resumes experiments performed on LCLs cultured independently 3 times and quantified in duplicate. Data are represented as the mean ± standard error of the mean. (D) RT-PCR using primers specific for E1 and E3 was performed on mRNA extracted from LCLs established from controls and patients of F6 (carrying the mutation c.340+574A>T that targets the SA site of E1′). Patient with erythrocytosis is indicated in red. On the right, the spliced isoforms are schematically represented. **P < .05, ***P < .01 based on Student t test. *Denotes larger fragments that contained E1′ spliced with E1, but with 15 nucleotides deleted (represented in red) by the use of an alternative SA site (sequences of the cloned bands are detailed in supplemental Figure 10).Download : Download high-res image (230KB)Download : Download full-size imageFigure 3. Expression study of the new VHL transcript isoforms in patient cells. (A) Sashimi plots from RNA-seq data obtained from samples (LCLs or pheochromocytomas [Pheo]) of 3 patients from F8. The positions of the different VHL exons are indicated, with the maximal number of reads indicated at the right. Splice junctions are denoted by the horizontal links, with details provided in supplemental Figure 8. (B) TaqMan quantification of the different VHL isoforms from samples of F8 performed using probes specific to VHL E1-E2, the translated sequence upstream E1′, or E1-E1′ junctions. Relative gene expression was normalized to LCL control (C1) fixed at 1 (mean results of technical duplicates). (C) TaqMan quantification of the different VHL isoforms in LCLs (established from 2 independent controls and from patients of F1, F2, and F8) cultured in the absence or presence of puromycin (puro), an inhibitor of nonsense-mediated mRNA decay. TaqMan probes were specific to the VHL E1-E1′ or E1-E2 junction. The graph resumes experiments performed on LCLs cultured independently 3 times and quantified in duplicate. Data are represented as the mean ± standard error of the mean. (D) RT-PCR using primers specific for E1 and E3 was performed on mRNA extracted from LCLs established from controls and patients of F6 (carrying the mutation c.340+574A>T that targets the SA site of E1′). Patient with erythrocytosis is indicated in red. On the right, the spliced isoforms are schematically represented. **P < .05, ***P < .01 based on Student t test. *Denotes larger fragments that contained E1′ spliced with E1, but with 15 nucleotides deleted (represented in red) by the use of an alternative SA site (sequences of the cloned bands are detailed in supplemental Figure 10).We performed quantitative RT-PCR using TaqMan probes specific for the different splicing junctions or for the region upstream of E1′ (location of probes shown in Figure 1C), which showed a strong upregulation of a unique isoform containing E1′ spliced with E1 in LCLs and tumors from patients of F8 compared with controls (Figure 3B). The study therefore focused on the isoform E1-E1′. Transcripts that retained E1′ spliced with E1 contained (in-frame with E1) a premature termination codon (Figure 1C) and could likely be targeted for degradation according to nonsense-mediated mRNA decay (NMD) mechanisms. We therefore investigated the expression of transcripts that contained E1 spliced with E1′ in the absence or presence of puromycin, an inhibitor of NMD. Without puromycin, higher levels of expression were seen in samples with mutated E1′ (Figure 3C) compared with samples containing WT E1′. Exposure to puromycin resulted in a profound induction of isoforms containing E1 spliced with E1′ vs other isoforms (Figure 3C; supplemental Figure 9). These results indicated that isoforms with E1-E1′ junction were degraded by NMD and may have failed to produce proteins. We performed RT-PCR on LCL samples of F6 carrying the mutation in the SA site, using primers in VHL exons E1 and E3. We observed fragments of larger size in samples from patients carrying the mutation, which were highly visible in the presence of puromycin (Figure 3D). Cloning and sequencing of these fragments demonstrated a dysregulated splicing of E1′ with the use of an alternative SA site located 15 nucleotides downstream (supplemental Figure 10).To measure the impact of the splicing dysregulation on pVHL expression, we performed an immunoblot with an antibody able to recognize the amino acids encoded by E1 and therefore able to detect the different pVHL isoforms.8 The antibody detected overexpressed exogenous X1 protein after transfection of the plasmid encoding X1 (Figure 4A). However, it failed to detect the endogenous protein, even in patients' samples that overexpressed the mRNA containing E1-E1′. Instead, the immunoblots showed a lower expression of all the VHL protein isoforms in patients with mutated E1′ (Figures 4A-B).Figure 4. Functional studies of mutations in VHL E1′. (A-B) Immunoblot analysis of patient LCLs. A representative immunoblot (A) and quantification of 3 different immunoblots (B) are presented. Relative gene expression was normalized to glyceraldehyde-3-phosphate dehydrogenase (GAPDH) expression, and results obtained with LCL control (C1) were fixed at 100%. Data are represented as the mean ± standard error of the mean. A VHL antibody that recognized VHL E1 was able to detect the hypothetical X1 protein. In the most left lane, control LCLs were transfected with an expression vector containing the coding sequence for X1; 5 µg of proteins were blotted vs 45 µg for other samples to avoid signal saturation with overexpressed X1. Patients with erythrocytosis are indicated in red. (C) Functional hypoxia response element (HRE)–dependent reporter assays were performed in 786-O cells (ie, VHL− cells that constitutively express HIF-2α). The results are expressed as relative firefly luciferase activity with Renilla luciferase as an internal control; 1.0 unit denotes the basal activity of endogenous HIF-2α using the HRE luciferase reporter plasmid. The ability of WT and mutated X1 to downregulate firefly luciferase activity (related to HIF activity) was compared with pVHL and in competition with pVHL. An immunoblot using an antibody specific to the hemagglutinin tag (HA) was used to detect HA-VHL and HA-X1. X1-L128V+L138P corresponds to a potential impact of the c.340+648T>C and c.340+617C>G mutations on the hypothetical X1 protein. Three independent experiments were performed. (D) Characterization of VHL E1′ retention by the minigene experiment (representative picture of agarose gel; n = 3). RT-PCR was performed on mRNA obtained from cell lines transfected with a minigene construct containing VHL E1′ (WT or mutated) flanked by large intronic sequences cloned between the SERPING1 exons (exons A and B, targeted by the RT-PCR primers). The plasmids were transfected, and the expression of the spliced chimeric transcripts (containing EA and EB ± E1′) was analyzed. Two WT constructs containing E1′ were used; 1 contained the single-nucleotide polymorphism c.340+1150T>C (rs779808). Bands corresponding to EA and EB spliced together or with VHL E1′ are indicated on the right. *P < .05, **P < .01, ***P < .001, ****P < .0001 based on Student t test. †Corresponds to unspecific bands verified by sequencing. The minigene experiment performed with the construction carrying the mutation c.340+574A>T (that targets the SA site of E1′ in F6) confirmed the use of an alternative SA site (right panel) with the deletion of 15 nucleotides (represented in red). ns, not significant.Download : Download high-res image (204KB)Download : Download full-size imageFigure 4. Functional studies of mutations in VHL E1′. (A-B) Immunoblot analysis of patient LCLs. A representative immunoblot (A) and quantification of 3 different immunoblots (B) are presented. Relative gene expression was normalized to glyceraldehyde-3-phosphate dehydrogenase (GAPDH) expression, and results obtained with LCL control (C1) were fixed at 100%. Data are represented as the mean ± standard error of the mean. A VHL antibody that recognized VHL E1 was able to detect the hypothetical X1 protein. In the most left lane, control LCLs were transfected with an expression vector containing the coding sequence for X1; 5 µg of proteins were blotted vs 45 µg for other samples to avoid signal saturation with overexpressed X1. Patients with erythrocytosis are indicated in red. (C) Functional hypoxia response element (HRE)–dependent reporter assays were performed in 786-O cells (ie, VHL− cells that constitutively express HIF-2α). The results are expressed as relative firefly luciferase activity with Renilla luciferase as an internal control; 1.0 unit denotes the basal activity of endogenous HIF-2α using the HRE luciferase reporter plasmid. The ability of WT and mutated X1 to downregulate firefly luciferase activity (related to HIF activity) was compared with pVHL and in competition with pVHL. An immunoblot using an antibody specific to the hemagglutinin tag (HA) was used to detect HA-VHL and HA-X1. X1-L128V+L138P corresponds to a potential impact of the c.340+648T>C and c.340+617C>G mutations on the hypothetical X1 protein. Three independent experiments were performed. (D) Characterization of VHL E1′ retention by the minigene experiment (representative picture of agarose gel; n = 3). RT-PCR was performed on mRNA obtained from cell lines transfected with a minigene construct containing VHL E1′ (WT or mutated) flanked by large intronic sequences cloned between the SERPING1 exons (exons A and B, targeted by the RT-PCR primers). The plasmids were transfected, and the expression of the spliced chimeric transcripts (containing EA and EB ± E1′) was analyzed. Two WT constructs containing E1′ were used; 1 contained the single-nucleotide polymorphism c.340+1150T>C (rs779808). Bands corresponding to EA and EB spliced together or with VHL E1′ are indicated on the right. *P < .05, **P < .01, ***P < .001, ****P < .0001 based on Student t test. †Corresponds to unspecific bands verified by sequencing. The minigene experiment performed with the construction carrying the mutation c.340+574A>T (that targets the SA site of E1′ in F6) confirmed the use of an alternative SA site (right panel) with the deletion of 15 nucleotides (represented in red). ns, not significant.Functional characterization of the mutated VHL E1′Because the hypoxia pathway represents the major pathway involved in the genesis of secondary erythrocytosis and VHL disease,13, 14, 1528 we performed functional studies of the hypothetical WT or mutated X1 proteins using hypoxia response element–dependent reporter assays. These functional tests failed to reveal any substantial effects of X1 on this pathway, either alone or in competition with pVHL (Figure 4C; supplemental Figure 11). We next focused our study on a potential impact of the E1′ variants on splicing by performing splicing reporter minigene assays in various cell lines. The experiments showed that splicing of WT E1′ was barely detected (Figure 4D). Interestingly, higher molecular weight bands corresponding to the expected spliced isoforms containing E1′ appeared in the presence of the mutations. Cloning and sequencing of the isoforms confirmed a retention of E1′ at the expected splicing sites. The level of expression of this upper isoform, specific to E1′ inclusion, was higher for mutations associated with cancers than for those with erythrocytosis, independently of the cell lines. Notably, the combination of both variants associated with cancer had a more pronounced effect than each variant individually (the single-nucleotide polymorphism showing very low effect), suggesting a synergistic effect of the variants on splicing (supplemental Figure 12). In silico analysis of c.340+617C>G consistently predicted a severe alteration of splicing by the creation of an exonic splicing enhancer site (supplemental Figure 13).The minigene experiment performed with mutated E1′ at the SA site (F6) confirmed the inclusion of E1′ during splicing (Figure 4D, right panel), using the same downstream alternative SA site identified in mRNA extracted from patients' LCLs (supplemental Figure 10).Synonymous mutations in VHL E2 induce exon skippingWe then focused our study on the synonymous heterozygous D143D mutation in E2, identified in the proband of F1. This mutation was also identified in the homozygous state in 2 patients with erythrocytosis (F9 and F10; Figure 5A; Table 1). The mRNA extracted from LCLs established from the different members of these 2 families was reverse transcribed and sequenced. Comparison of chromatograms obtained by sequencing of DNA vs cDNA displayed a weaker peak of the mutated allele in cDNA, reflecting a decreased expression of the mRNA transcripts carrying the mutation.Download : Download high-res image (221KB)Download : Download full-size imageFigure 5. Genetic and expression study of synonymous mutations in VHL E2. (A-B) Pedigree and sequence chromatograms of germline DNA, tumor (pheochromocytoma) DNA, or cDNA prepared from 2 families (F9 and F10) with erythrocytosis (A) and 2 families (F11 and F12) with VHL disease (B). (C) Results of RT-PCR using mRNA extracted from LCLs (F9 and F10) and leukocytes and tumor material (pheochromocytoma) (F11 and F12). (D) TaqMan quantification of the different VHL isoforms in LCLs (established from patients of F9, F10, and F11) cultured in the absence or presence of puromycin. TaqMan probes are specific to the VHL E1-E2 or E1-E3 junction. Relative gene expression was normalized to LCL control (C1). (E) Immunoblot analysis of patient LCLs. Patients with erythrocytosis are indicated in red. A representative immunoblot (upper panel) and quantification of 4 different immunoblots are displayed (lower panel). Relative gene expression was normalized to glyceraldehyde-3-phosphate dehydrogenase (GAPDH) expression, and results obtained with C1 were fixed at 100%. Data are represented as the mean ± standard error of the mean. *P < .05, **P < .01, ***P < .001, ****P < .0001 based on Student t test. CNS, central nervous system.A different synonymous mutation in E2, c.414A>G p.Pro138Pro (P138P), was identified in 2 families (F11 and F12) with VHL disease (Figure 5B). This heterozygous mutation segregated with the disease in 3 generations. Sequencing of DNA extracted from the pheochromocytoma of F11-III.1 showed a loss of the WT allele in the tumor, demonstrating loss of heterozygosity as currently described in classical VHL disease.Suspecting an effect of the synonymous mutations on splicing, we next assessed the expression of the VHL transcripts in patients' samples by RT-PCR (Figure 5C). We found a significant change in the ratio of expressed VHL isoforms, with a higher expression of the E1-E3 transcripts in LCLs of patients homozygous for D143D and in the pheochromocytoma with P138P mutation. These results suggest an effect of the mutation on splicing regulatory elements, leading to E2 skipping. In silico analysis of the synonymous mutations indicated a potential effect on exonic splicing enhancer motifs (supplemental Figure 14).To specifically quantify the different VHL isoforms, we performed quantitative RT-PCR on LCLs using TaqMan probes complementary to the VHL E1-E2 or E1-E3 junction (Figure 5D). All mutated samples displayed an increase of the isoform with skipped E2 (E1-E3). The patients carrying a homozygous D143D mutation presented a severe decrease of the WT isoform expression level. These results demonstrated that synonymous mutations in E2 affected mRNA isoform production.To evaluate a potential impact on protein expression, we performed a western blot analysis. We did not observe any overexpression of the pVHL172 isoform as expected from mRNA quantification studies. However, in patients homozygous for D143D, we detected a strong downregulation of all the pVHL isoforms, which was also observed to a lesser extent in LCL samples from heterozygous patients (Figure 5E).Proportion of VHL E2 skipping is correlated with disease severity in minigene experimentsTo study the impact of the synonymous E2 mutations on splicing in different cell lines, we performed minigene assays. We tested the implications of the D143D and P138P mutations on splicing in addition to the nearby mutations described in patients with erythrocytosis (P138L and G144R).4,6,29 Indeed, these mutations may also affect splicing rather than VHL protein function. We first evaluated the loss of function of these mutants by reporter assays. We found that these could downregulate HIF in a manner similar to the WT protein, in contrast to VHL proteins lacking E2 (pVHLΔE2), which are described as nonfunctional in terms of their regulation of HIF activity8, 9, 1012 (Figure 6A). Minigene experiments were performed in a variety of cell lines relevant to the studied diseases, using LCLs as control (Figure 6B). We demonstrated that all mutations caused E2 skipping in LCLs. In other cell lines, these experiments demonstrated a major impact on the VHL E2 splicing of the P138P mutation, which is associated with cancer. The mutations P138L, D143D, and G144R, which are all associated with erythrocytosis, displayed a weaker effect on splicing, with slight variations among cell lines but with a stronger effect in the erythroid cell line (UT7 cultured with erythropoietin).Figure 6. Functional study of synonymous mutations in VHL E2. (A) Functional hypoxia response element (HRE)–dependent reporter assays were performed in 786-O cells to evaluate the impact of VHL mutations in E2 (P138L and G144R) on VHL protein activity. The VHL protein lacking E2 (pVHL172/VHLΔE2) was used as a negative control. The results are expressed as firefly luciferase activity relative to Renilla luciferase as an internal control; 1.0 unit denotes the basal activity of endogenous HIF-2α using the HRE luciferase reporter plasmid. Immunoblots using an antibody specific for the hemagglutinin tag (HA) were used to detect HA-VHL. (B) Characterization of VHL E2 skipping by minigene analyses. Minigene experiments were performed in a variety of cell lines relevant to the studied diseases: renal (293T, 786-O, and HK2), pheochromocytoma (pheo; PC12), erythroid cell line (UT7 cultured with erythropoietin), and LCL. RT-PCR was performed on mRNA obtained from cell lines transfected with a minigene construct containing VHL E2 flanked by intronic sequences cloned between the SERPING1 exons (exons A and B; targeted by the RT-PCR primers). Bands corresponding to EA and EB spliced together or with VHL E2 are indicated on the right. (C) Sashimi plots from RNA-seq data. The positions of the different VHL exons are indicated, with the maximum number of reads for each exon indicated at the right. Splice junctions are denoted by the horizontal links, with details provided in supplemental Figure 15A. (D) Heatmap of pheochromocytoma transcriptome data. A comparison of transcriptome data for the pheochromocytoma from patient F11 III.1 (with P138P mutation) vs Affymetrix data from the largest available cohort of paragangliomas/pheochromocytomas (recruited by the French COMETE network) that identified homogeneous molecular subgroups associated with susceptibility genes (Burnichon et al30).Download : Download high-res image (254KB)Download : Download full-size imageFigure 6. Functional study of synonymous mutations in VHL E2. (A) Functional hypoxia response element (HRE)–dependent reporter assays were performed in 786-O cells to evaluate the impact of VHL mutations in E2 (P138L and G144R) on VHL protein activity. The VHL protein lacking E2 (pVHL172/VHLΔE2) was used as a negative control. The results are expressed as firefly luciferase activity relative to Renilla luciferase as an internal control; 1.0 unit denotes the basal activity of endogenous HIF-2α using the HRE luciferase reporter plasmid. Immunoblots using an antibody specific for the hemagglutinin tag (HA) were used to detect HA-VHL. (B) Characterization of VHL E2 skipping by minigene analyses. Minigene experiments were performed in a variety of cell lines relevant to the studied diseases: renal (293T, 786-O, and HK2), pheochromocytoma (pheo; PC12), erythroid cell line (UT7 cultured with erythropoietin), and LCL. RT-PCR was performed on mRNA obtained from cell lines transfected with a minigene construct containing VHL E2 flanked by intronic sequences cloned between the SERPING1 exons (exons A and B; targeted by the RT-PCR primers). Bands corresponding to EA and EB spliced together or with VHL E2 are indicated on the right. (C) Sashimi plots from RNA-seq data. The positions of the different VHL exons are indicated, with the maximum number of reads for each exon indicated at the right. Splice junctions are denoted by the horizontal links, with details provided in supplemental Figure 15A. (D) Heatmap of pheochromocytoma transcriptome data. A comparison of transcriptome data for the pheochromocytoma from patient F11 III.1 (with P138P mutation) vs Affymetrix data from the largest available cohort of paragangliomas/pheochromocytomas (recruited by the French COMETE network) that identified homogeneous molecular subgroups associated with susceptibility genes (Burnichon et al30).Splicing dysregulation of VHL is causal in the development of diseaseRNA-seq confirmed that the synonymous mutations were not silent but instead induced potent E2 skipping (Figure 6C; supplemental Figure 15A). Additional transcriptome analyses of the pheochromocytoma carrying P138P showed an upregulation of HIF target genes (typically seen in VHL-related pheochromocytomas) compared with the pheochromocytoma carrying a RET mutation (supplemental Figure 15B).30 We then reanalyzed our independent cohort of pheochromocytomas30 using RNA-seq data from both tumors. After unsupervised classification, we observed a segregation of the P138P pheochromocytoma with other VHL-related tumors (C1B cluster), whereas the control pheochromocytoma bearing the RET mutation was grouped with other RET-related tumors (Figure 6D).
    3. F6, II.1c.492G>T/c.340+574A>T*VHL p.Gln164His/SA2014/6 moM15.6496.91167Splenomegaly—

      PatientID: II.1

      KindredID: F6

      Case: M, 0Y6M, Ethnicity Unknown

      DiseaseAssertion: Splenomegaly

      FamilyInfo: N/A

      CasePresentingHPOs: HP:0001744 (Splenomegaly)

      CaseHPOFreeText: Diagnosed with splenomegaly at age 6 months (DOB: 2014).

      CaseNotHPOs: N/A

      CaseNotHPOFreeText: N/A

      CasePreviousTesting: N/A

      PreviouslyPublished: N/A

      SupplementalData: N/A

      Variant: p.Q164H (c.492G>T)

      LegacyVariant: N/A

      CaseProblemVariantFreeText: N/A

      ClinVarID: 456566, https://www.ncbi.nlm.nih.gov/clinvar/variation/456566/

      CAID: N/A

      gnomAD: N/A

      VariantEvidence: Variants are heterozygous.

      MutationType: missense_variant;transversion

      CivicName: Q164H (c.492G>T) and c.340+574A>T

      MultipleGeneVariants: Germline, VHL, c.340+574A>T

    4. F8c.340+617C>G + c.340+648T>C†/WTX1 p.Leu128Val+ X1 p.Leu138Pro/WTNNNNVHL disease—

      PatientID: I.2

      KindredID: F8

      Case: M, Age Unknown, Ethnicity Unknown

      DiseaseAssertion: VHL

      FamilyInfo: 6/10 genetically tested family members across two generations were found to harbor the c.340+648T>C and c.340+617C>G germline mutations of the VHL gene. Patient I.2 presented with retinal capillary hemangioma, pheochromocytoma (pheo) and renal cell carcinoma. Patient I.3 presented with CNS hemangioblastoma and pheo. Patient II.1 presented with pheo. Patients II.2, II.6 and II.7 presented with retinal capillary hemangioma.

      CasePresentingHPOs: HP:0005584; HP:0009711; HP:0002666 (Renal cell carcinoma, Retinal capillary hemangioma, Pheochromocytoma)

      CaseHPOFreeText: Presented with renal cell carcinoma, retinal capillary hemangioma and pheochromocytoma. Tumors detected at ages 15, 46 and 52.

      CaseNotHPOs: N/A

      CaseNotHPOFreeText: N/A

      CasePreviousTesting: N/A

      PreviouslyPublished: N/A

      SupplementalData: N/A

      Variant: c.340+648T>C

      LegacyVariant: N/A

      CaseProblemVariantFreeText: N/A

      ClinVarID: 827583, https://www.ncbi.nlm.nih.gov/clinvar/variation/827583/

      CAID: N/A

      gnomAD: N/A

      VariantEvidence: These variants segregated in 6 patients of this family who developed VHL disease and were absent in 4 healthy tested descendants, indicating their presence on a single disease-associated allele. Sequencing of tumor DNA did not display loss of heterozygosity, suggesting that a WT VHL deletion (as observed in classic VHL disease) may not be a prerequisite in cells of patients with this specific VHL genotype.

      MutationType: missense_variant;transition; splice_site_variant

      CivicName: c.340+617C>G and c.340+648T>C

      MultipleGeneVariants: Germline, VHL, c.340+617C>G

    5. F8c.340+617C>G + c.340+648T>C†/WTX1 p.Leu128Val+ X1 p.Leu138Pro/WTNNNNVHL disease

      PatientID: II.6

      KindredID: F8

      Case: F, Age Unknown, Ethnicity Unknown

      DiseaseAssertion: VHL

      FamilyInfo: 6/10 genetically tested family members across two generations were found to harbor the c.340+648T>C and c.340+617C>G germline mutations of the VHL gene. Patient I.2 presented with retinal capillary hemangioma, pheochromocytoma (pheo) and renal cell carcinoma. Patient I.3 presented with CNS hemangioblastoma and pheo. Patient II.1 presented with pheo. Patients II.2, II.6 and II.7 presented with retinal capillary hemangioma.

      CasePresentingHPOs: HP:0009711 (Retinal capillary hemangioma)

      CaseHPOFreeText: Presented with retinal capillary hemangioma. Tumor detected at age 16.

      CaseNotHPOs: N/A

      CaseNotHPOFreeText: N/A

      CasePreviousTesting: N/A

      PreviouslyPublished: N/A

      SupplementalData: N/A

      Variant: c.340+648T>C

      LegacyVariant: N/A

      CaseProblemVariantFreeText: N/A

      ClinVarID: 827583, https://www.ncbi.nlm.nih.gov/clinvar/variation/827583/

      CAID: N/A

      gnomAD: N/A

      VariantEvidence: These variants segregated in 6 patients of this family who developed VHL disease and were absent in 4 healthy tested descendants, indicating their presence on a single disease-associated allele. Sequencing of tumor DNA did not display loss of heterozygosity, suggesting that a WT VHL deletion (as observed in classic VHL disease) may not be a prerequisite in cells of patients with this specific VHL genotype.

      MutationType: missense_variant;transition; splice_site_variant

      CivicName: c.340+617C>G and c.340+648T>C

      MultipleGeneVariants: Germline, VHL, c.340+617C>G

    6. F3, II.1c.598C>T/c.340+770T>CVHL p.Arg200Trp/X1 p.Ser179Pro?2003/4 moM17.9547.560

      PatientID: II.1

      KindredID: 3

      Case: M, 0Y4M, Ethnicity Unknown

      DiseaseAssertion: Polycythemia

      FamilyInfo: The patient had an affected brother (II.2) with the same mutation and polycythemia. Biologic material from parents were unavailable but Chuvash core haplotype analysis demonstrated that all patients were compound heterozygous, with 1 mutation being inherited from each parent. See Figure 2B for family pedigree.

      CohortInfo: Patients with Chuvash polycythemia for whom VHL R200W had been found in a heterozygous state.

      CasePresentingHPOs: HP:0001901 (Polycythemia)

      CaseHPOFreeText: N/A

      CaseNotHPOs: N/A

      CaseNotHPOFreeText: N/A

      CasePreviousTesting: N/A

      PreviouslyPublished: N/A

      SupplementalData: N/A

      Variant: c.340+770T>C

      LegacyVariant:N/A

      CaseProblemVariantFreeText: N/A

      ClinVarID: 816685 https://www.ncbi.nlm.nih.gov/clinvar/variation/816685/

      CAID: N/A

      gnomAD: 0.00003186 https://gnomad.broadinstitute.org/variant/3-10184641-T-C

      VariantEvidence: N/A

      MutationType: intron_variant

      CivicName: c.340+770T>C and R200W (c.598C>T)

      MultipleGeneVariants: Germline, VHL, c.598C>T (p.Arg200Trp)

    7. F10, II.1c.429C>T/c.429C>TVHL p.Asp143Asp/VHL p.Asp143Asp2002/4.5 yF22.564-77.412.6264Erythrocytosis, splenomegalyβ thalassemia

      PatientID: II.1

      KindredID: F10

      Case: M, 4Y6M, Ethnicity Unknown

      DiseaseAssertion: Polycythemia

      FamilyInfo: This patient’s asymptomatic patients were both found to be carriers of the D143= (c.429C>T) germline variant in VHL. Their other child (II.2) also carried the gene. The current patient was the only one who was homozygous for the variant.

      CasePresentingHPOs: HP:0001901; HP:0001744 (Polycythemia, Splenomegaly)

      CaseHPOFreeText: Diagnosed with erythrocytosis (Polycythemia) and splenomegaly at 4.5 years old (DOB: 2002).

      CaseNotHPOs: N/A

      CaseNotHPOFreeText: N/A

      CasePreviousTesting: N/A

      PreviouslyPublished: N/A

      SupplementalData: N/A

      Variant: p.D143= (c.429C>T)

      LegacyVariant: N/A

      CaseProblemVariantFreeText: N/A

      ClinVarID: 416990, https://www.ncbi.nlm.nih.gov/clinvar/variation/416990/

      CAID: N/A

      gnomAD: 0.000007953, https://gnomad.broadinstitute.org/variant/3-10188286-C-T?dataset=gnomad_r2_1

      VariantEvidence: Variant is present in allele 1 and 2 (i.e. homozygous).

      MutationType: missense_variant;transition; synonymous_variant

      CivicName: D143= (c.429C>T)

      MultipleGeneVariants: Germline, Beta Thalassemia

    8. F4, II.1c.598C>T/c.340+694_711dupVHL p.Arg200Trp/X1 p.Trp159X?1990/7 yM20.6648.2549.9Erythrocytosis, deep vein thrombosis, intracerebral hemorrhageFV Leiden

      PatientID: II.1

      KindredID: F4

      Case: M, 7Y0M, Ethnicity Unknown

      DiseaseAssertion: Polycythemia

      FamilyInfo: Variant c.340+694_340+711dup is inherited from mother (genetically confirmed) and variant R200W (c.598C>T) is assumed to be inherited from father.

      CohortInfo: Patients with Chuvash polycythemia for whom VHL R200W had been found in a heterozygous state.

      CasePresentingHPOs: HP:0001901; HP:0002625; HP:0001342 (Polycythemia, Deep venous thrombosis, Cerebral hemorrhage)

      CaseHPOFreeText: Diagnosed with erythrocytosis (Polycythemia), deep vein thrombosis, intracerebral hemorrhage at age 7 (DOB: 1990).

      CaseNotHPOs: N/A

      CaseNotHPOFreeText: N/A

      CasePreviousTesting: N/A

      PreviouslyPublished: N/A

      SupplementalData: N/A

      Variant: p.R200W (c.598C>T)

      LegacyVariant: N/A

      CaseProblemVariantFreeText: N/A

      ClinVarID: 2232, https://www.ncbi.nlm.nih.gov/clinvar/variation/2232/

      CAID: N/A

      gnomAD: 0.0002016, https://gnomad.broadinstitute.org/variant/3-10191605-C-T

      VariantEvidence: Variants are heterozygous.

      MutationType: missense_variant;transition

      CivicName: R200W (c.598C>T) and c.340+694_340+711dup

      MultipleGeneVariants: Germline, VHL, c.340+694_340+711dup

      MultipleGeneVariants: Germline, Factor V Leiden

    9. F8c.340+617C>G + c.340+648T>C†/WTX1 p.Leu128Val+ X1 p.Leu138Pro/WTNNNNVHL disease—

      PatientID: I.2

      KindredID: F8

      Case: M, Age Unknown, Ethnicity Unknown

      DiseaseAssertion: VHL

      FamilyInfo: 6/10 genetically tested family members across two generations were found to harbor the c.340+648T>C and c.340+617C>G germline mutations of the VHL gene. Patient I.2 presented with retinal capillary hemangioma, pheochromocytoma (pheo) and renal cell carcinoma. Patient I.3 presented with CNS hemangioblastoma and pheo. Patient II.1 presented with pheo. Patients II.2, II.6 and II.7 presented with retinal capillary hemangioma.

      CasePresentingHPOs: HP:0005584; HP:0009711; HP:0002666 (Renal cell carcinoma, Retinal capillary hemangioma, Pheochromocytoma)

      CaseHPOFreeText: Presented with renal cell carcinoma, retinal capillary hemangioma and pheochromocytoma. Tumors detected at ages 15, 46 and 52.

      CaseNotHPOs: N/A

      CaseNotHPOFreeText: N/A

      CasePreviousTesting: N/A

      PreviouslyPublished: N/A

      SupplementalData: N/A

      Variant: c.340+617C>G

      LegacyVariant: N/A

      CaseProblemVariantFreeText: N/A

      ClinVarID: 827582, https://www.ncbi.nlm.nih.gov/clinvar/variation/827582/

      CAID: N/A

      gnomAD: N/A

      VariantEvidence: These variants segregated in 6 patients of this family who developed VHL disease and were absent in 4 healthy tested descendants, indicating their presence on a single disease-associated allele. Sequencing of tumor DNA did not display loss of heterozygosity, suggesting that a WT VHL deletion (as observed in classic VHL disease) may not be a prerequisite in cells of patients with this specific VHL genotype.

      MutationType: missense_variant;transversion; splice_site_variant

      CivicName: c.340+617C>G and c.340+648T>C

      MultipleGeneVariants: Germline, VHL, c.340+648T>C

    10. F10, II.1c.429C>T/c.429C>TVHL p.Asp143Asp/VHL p.Asp143Asp2002/4.5 yF22.564-77.412.6264Erythrocytosis, splenomegalyβ thalassemia

      PatientID: II.1

      KindredID: F10

      Case: M, 4Y6M, Ethnicity Unknown

      DiseaseAssertion: Polycythemia

      FamilyInfo: This patient’s asymptomatic patients were both found to be carriers of the D143= (c.429C>T) germline variant in VHL. Their other child (II.2) also carried the gene. The current patient was the only one who was homozygous for the variant.

      CasePresentingHPOs: HP:0001901; HP:0001744 (Polycythemia, Splenomegaly)

      CaseHPOFreeText: Diagnosed with erythrocytosis (Polycythemia) and splenomegaly at 4.5 years old (DOB: 2002).

      CaseNotHPOs: N/A

      CaseNotHPOFreeText: N/A

      CasePreviousTesting: N/A

      PreviouslyPublished: N/A

      SupplementalData: N/A

      Variant: p.D143= (c.429C>T)

      LegacyVariant: N/A

      CaseProblemVariantFreeText: N/A

      ClinVarID: 416990, https://www.ncbi.nlm.nih.gov/clinvar/variation/416990/

      CAID: N/A

      gnomAD: 0.000007953, https://gnomad.broadinstitute.org/variant/3-10188286-C-T?dataset=gnomad_r2_1

      VariantEvidence: Variant is present in allele 1 and 2 (i.e. homozygous).

      MutationType: missense_variant;transition; synonymous_variant

      CivicName: D143= (c.429C>T)

      MultipleGeneVariants: Germline, Beta Thalassemia

    11. F4, II.1c.598C>T/c.340+694_711dupVHL p.Arg200Trp/X1 p.Trp159X?1990/7 yM20.6648.2549.9Erythrocytosis, deep vein thrombosis, intracerebral hemorrhageFV Leiden

      PatientID: II.1

      KindredID: F4

      Case: M, 7Y0M, Ethnicity Unknown

      DiseaseAssertion: Polycythemia

      FamilyInfo: Variant c.340+694_340+711dup is inherited from mother (genetically confirmed) and variant R200W (c.598C>T) is assumed to be inherited from father.

      CohortInfo: Patients with Chuvash polycythemia for whom VHL R200W had been found in a heterozygous state.

      CasePresentingHPOs: HP:0001901; HP:0002625; HP:0001342 (Polycythemia, Deep venous thrombosis, Cerebral hemorrhage)

      CaseHPOFreeText: Diagnosed with erythrocytosis (Polycythemia), deep vein thrombosis, intracerebral hemorrhage at age 7 (DOB: 1990).

      CaseNotHPOs: N/A

      CaseNotHPOFreeText: N/A

      CasePreviousTesting: N/A

      PreviouslyPublished: N/A

      SupplementalData: N/A

      Variant: p.R200W (c.598C>T)

      LegacyVariant: N/A

      CaseProblemVariantFreeText: N/A

      ClinVarID: 2232, https://www.ncbi.nlm.nih.gov/clinvar/variation/2232/

      CAID: N/A

      gnomAD: 0.0002016, https://gnomad.broadinstitute.org/variant/3-10191605-C-T

      VariantEvidence: Variants are heterozygous.

      MutationType: missense_variant;transition

      CivicName: R200W (c.598C>T) and c.340+694_340+711dup

      MultipleGeneVariants: Germline, VHL, c.340+694_340+711dup

      MultipleGeneVariants: Germline, Factor V Leiden

    12. F8c.340+617C>G + c.340+648T>C†/WTX1 p.Leu128Val+ X1 p.Leu138Pro/WTNNNNVHL disease—

      PatientID: I.2

      KindredID: F8

      Case: M, Age Unknown, Ethnicity Unknown

      DiseaseAssertion: VHL

      FamilyInfo: 6/10 genetically tested family members across two generations were found to harbor the c.340+648T>C and c.340+617C>G germline mutations of the VHL gene. Patient I.2 presented with retinal capillary hemangioma, pheochromocytoma (pheo) and renal cell carcinoma. Patient I.3 presented with CNS hemangioblastoma and pheo. Patient II.1 presented with pheo. Patients II.2, II.6 and II.7 presented with retinal capillary hemangioma.

      CasePresentingHPOs: HP:0005584; HP:0009711; HP:0002666 (Renal cell carcinoma, Retinal capillary hemangioma, Pheochromocytoma)

      CaseHPOFreeText: Presented with renal cell carcinoma, retinal capillary hemangioma and pheochromocytoma. Tumors detected at ages 15, 46 and 52.

      CaseNotHPOs: N/A

      CaseNotHPOFreeText: N/A

      CasePreviousTesting: N/A

      PreviouslyPublished: N/A

      SupplementalData: N/A

      Variant: c.340+617C>G

      LegacyVariant: N/A

      CaseProblemVariantFreeText: N/A

      ClinVarID: 827582, https://www.ncbi.nlm.nih.gov/clinvar/variation/827582/

      CAID: N/A

      gnomAD: N/A

      VariantEvidence: These variants segregated in 6 patients of this family who developed VHL disease and were absent in 4 healthy tested descendants, indicating their presence on a single disease-associated allele. Sequencing of tumor DNA did not display loss of heterozygosity, suggesting that a WT VHL deletion (as observed in classic VHL disease) may not be a prerequisite in cells of patients with this specific VHL genotype.

      MutationType: missense_variant;transversion; splice_site_variant

      CivicName: c.340+617C>G and c.340+648T>C

      MultipleGeneVariants: Germline, VHL, c.340+648T>C

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    1. Inhibition of iduronic acid biosynthesis by ebselen reduces glycosaminoglycan accumulation in mucopolysaccharidosis type I fibroblasts

      PMID: 34192316

      Gene: IDUA

      Disease: MPS1

      Inheritance: AR

      InsufficientEvidence: Study used fibroblasts from patients with MPS-1. Protein changes associated with the variants in the fibroblasts are provided, but no other patient details are provided.

    1. R to Q amino acid substitution in the GFFKR sequence of the cytoplasmic domain of the integrin IIb subunit in a patient with a Glanzmann's thrombasthenia-like syndrome.

      Case1: (Patient A.P) Male, 21 years old, Italian)

      DiseaseAssertion: Glanzmann thrombasthenia

      FamilyInfo: N/A

      ParentalGenotype: Biocurator should see Table 1, if any important info to be obtained from here

      CasePresentingHPOs: HP:0000421, HP:0000225, HP:0000967, HP:0002249

      (Epistaxis, gingival bleeding, petechiae, melena)

      CaseHPOFreeText: Hematoma

      CaseNotHPOs: N/A

      ProteinExpression: As detailed earlier, the main features of A.P.’s platelets are a total αIIbβ3 content that is about half that observed with normal platelets yet with a surface expression that is sparse compared with the size of the internal pool --> observed decrease of αIIbβ3 on the surface of his platelets (approximately 15% of normal levels)

      Platelet Aggregation: Aggregation remained defective when ADP was added to PRP anti-coagulated with heparin, and when measured in citrated whole blood by impedance aggregometry in response to ADP, collagen, and arachidonic acid. When ADP was added to washed platelets together with fibrinogen, the aggregation response was somewhat improved. An improved aggregation response was also seen when washed platelets were incubated with collagen (not shown). However, with a-thrombin, a slow and irreversible aggregationwas again observed.

      CasePreviousTesting: PCR SSCP of ITGA2B and ITGB3 "To define the genetic defect responsible for the disease, we performed an extensive analysis of the exons of the αIIb and β3 genes using nonradioactive PCR-SSCP methodology developed in our laboratory."

      Gene: ITGA2B

      Variant: NM_000419.3:c.3077G>A (p.Arg1026Gln)

      LegacyVariant: (p.Arg995Gln)

      ClinVar: 50232

      CAiD: CA10575572

      gnomAD MAF in the European (non-Finnish) population is 0.000008801https://gnomad.broadinstitute.org/variant/17-42449775-C-T

      PreviouslyPublished: PMID: 1638023

    1. PatientID: N/A

      KindredID: 2034

      Case: Age unknown, Sex unknown, Ethnicity unknown

      DiseaseAssertion: assumed VHL

      FamilyInfo: Paper states familial VHL; germline mutation

      CasePresentingHPOs: HP:0010797; HP:0009711; HP:0005584 (hemangioblastoma; retinal capillary hemangioma; renal cell carcinoma)

      CaseHPOFreeText: Patient had CNS HB, RA and a Grawitz tumor (RCC)

      CaseNotHPOs: N/A

      CaseNotHPOFreeText: N/A

      CasePreviousTesting: N/A

      PreviouslyPublished: 32179488

      SupplementalData: Yes (Specifically Supp. Table S2)

      Variant: p.F76del (c.227_229delTCT)

      LegacyVariant: N/A

      CaseProblemVariantFreeText: N/A

      ClinVarID: N/A

      CAID: CA357012 http://reg.clinicalgenome.org/redmine/projects/registry/genboree_registry/allele?hgvsOrDescriptor=NM_000551.3%3Ac.227_229delTCT

      gnomAD: N/A

      VariantEvidence: N/A

      MutationType: inframe_deletion

      CivicName: F76del (c.227_229delTCT)

      MultipleGeneVariants: N/A

    2. PatientID: None

      KindredID: 14482

      Case: Age unknown, Sex unknown, Belgian

      DiseaseAssertion: VHL

      FamilyInfo: Paper states: Belgian family; Germline mutation

      CasePresentingHPOs: N/A

      CaseHPOFreeText: N/A

      CaseNotHPOs: N/A

      CaseNotHPOFreeText: N/A

      CasePreviousTesting: N/A

      PreviouslyPublished: N/A

      SupplementalData: Yes

      Variant: p.R167Q (c.500G>A)

      LegacyVariant: N/A

      CaseProblemVariantFreeText: N/A

      ClinVarID: 2216 https://www.ncbi.nlm.nih.gov/clinvar/variation/2216/

      CAID: N/A

      gnomAD: 0.000003977 https://gnomad.broadinstitute.org/variant/3-10191507-G-A

      VariantEvidence: N/A

      MutationType: missense_variant;transition

      CivicName: R167Q (c.500G>A)

      MultipleGeneVariants: N/A

    3. PatientID: N/A

      KindredID: 442

      Case: Age unknown, Sex unknown, Ethnicity unknown

      DiseaseAssertion: assumed VHL

      FamilyInfo: Paper states: Germline, de novo (no clear confirmation)

      CasePresentingHPOs: HP:0005584; HP:0010797 (renal cell carcinoma, hemangioblastoma)

      CaseHPOFreeText: Bilateral RCC and a hemangioblastoma

      CaseNotHPOs: N/A

      CaseNotHPOFreeText: N/A

      CasePreviousTesting: N/A

      PreviouslyPublished: N/A

      SupplementalData: Yes (Specifically Supp. Table S2)

      Variant: p.G144* (c.430G>T)

      LegacyVariant: N/A

      CaseProblemVariantFreeText: N/A

      ClinVarID: 223208 https://www.ncbi.nlm.nih.gov/clinvar/variation/223208/

      CAID: N/A

      gnomAD: N/A

      VariantEvidence: N/A

      MutationType: stop_gained

      CivicName: G144* (c.430G>T)

      MultipleGeneVariants: N/A

    4. PatientID: N/A

      KindredID: 198

      Case: Age unknown, Sex unknown, Ethnicity unknown

      DiseaseAssertion: assumed VHL

      FamilyInfo: Paper states: Germline, de novo

      CasePresentingHPOs: HP:0010797 (hemangioblastoma)

      CaseHPOFreeText: N/A

      CaseNotHPOs: N/A

      CaseNotHPOFreeText: N/A

      CasePreviousTesting: N/A

      PreviouslyPublished: N/A

      SupplementalData: Yes (Specifically Supp. Table S2)

      Variant: p.W117Cfs*42 (c.351del)

      LegacyVariant: N/A

      CaseProblemVariantFreeText: paper states c.350delG which automaps to NM_000551.3:c.351delG

      ClinVarID: 223197 https://www.ncbi.nlm.nih.gov/clinvar/variation/223197/

      CAID: N/A

      gnomAD: N/A

      VariantEvidence: N/A

      MutationType: minus_1_frameshift_variant

      CivicName: W117fs (c.351del)

      MultipleGeneVariants: N/A

    5. PatientID: N/A

      KindredID: 23530

      Case: Age unknown, Sex unknown, Ethnicity unknown

      DiseaseAssertion: assumed VHL

      FamilyInfo: Paper states familial VHL

      CasePresentingHPOs: HP:0010797; HP:0005584; HP:0001737; HP:0000107 (hemangioblastoma; renal cell carcinoma; pacreatic cysts; renal cyst)

      CaseHPOFreeText: N/A

      CaseNotHPOs: N/A

      CaseNotHPOFreeText: N/A

      CasePreviousTesting: N/A

      PreviouslyPublished: N/A

      SupplementalData: Yes (Specifically Supp. Table S2)

      Variant: p.L89P (c.266T>C)

      LegacyVariant: N/A

      CaseProblemVariantFreeText: N/A

      ClinVarID: 182979 https://www.ncbi.nlm.nih.gov/clinvar/variation/182979

      CAID: N/A

      gnomAD: N/A

      VariantEvidence: N/A

      MutationType: missense_variant;transition

      CivicName: L89P (c.266T>C)

      MultipleGeneVariants: N/A

    6. PatientID: N/A

      KindredID: 23530

      Case: Age unknown, Sex unknown, Ethnicity unknown

      DiseaseAssertion: assumed VHL

      FamilyInfo: Paper states familial VHL

      CasePresentingHPOs: HP:0010797; HP:0005584; HP:0001737; HP:0000107 (hemangioblastoma; renal cell carcinoma; pacreatic cysts; renal cyst)

      CaseHPOFreeText: N/A

      CaseNotHPOs: N/A

      CaseNotHPOFreeText: N/A

      CasePreviousTesting: N/A

      PreviouslyPublished: N/A

      SupplementalData: Yes (Specifically Supp. Table S2)

      Variant: p.L89P (c.266T>C)

      LegacyVariant: N/A

      CaseProblemVariantFreeText: N/A

      ClinVarID: 182979 https://www.ncbi.nlm.nih.gov/clinvar/variation/182979

      CAID: N/A

      gnomAD: N/A

      VariantEvidence: N/A

      MutationType: missense_variant;transition

      CivicName: L89P (c.266T>C)

      MultipleGeneVariants: N/A

    1. Eighteen VHL patients who underwent pancreatectomy for one or several endocrine tumors at Beaujon hospital from 1997 to 2008 were retrieved from the file of VHL patients (Table 1).

      PatientID: 2

      KindredID: 2

      Case: F, 28Y0M, Ethnicity unknown

      DiseaseAssertion: pancreatic endocrine tumor

      FamilyInfo: None

      CasePresentingHPOs: HP:0030405 (pancreatic endocrine tumor)

      CaseHPOFreeText: See Table 1 for more information

      CaseNotHPOs: N/A

      CaseNotHPOFreeText: N/A

      CasePreviousTesting: N/A

      PreviouslyPublished: N/A

      SupplementalData: N/A

      Variant: p.R167W (c.499C>T)

      CaseProblemVariantFreeText: N/A

      LegacyVariant: N/A

      ClinVarID: 2218 https://www.ncbi.nlm.nih.gov/clinvar/variation/2218/

      CAID: CA020450 http://reg.clinicalgenome.org/redmine/projects/registry/genboree_registry/allele?hgvsOrDescriptor=NM_000551.3%3Ac.499C%3ET

      gnomAD: 0.000007954 https://gnomad.broadinstitute.org/variant/3-10191506-C-T?dataset=gnomad_r2_1

      VariantEvidence: N/A

      MutationType: missense_variant; transition

      CivicName: R167W (c.499C>T)

      MultipleGeneVariants: N/A

    2. Eighteen VHL patients who underwent pancreatectomy for one or several endocrine tumors at Beaujon hospital from 1997 to 2008 were retrieved from the file of VHL patients (Table 1).

      PatientID: 7

      KindredID: 7

      Case: M, 26Y0M, Ethnicity unknown

      DiseaseAssertion: pancreatic endocrine tumor

      FamilyInfo: None

      CasePresentingHPOs: HP:0030405 (pancreatic endocrine tumor)

      CaseHPOFreeText: See Table 1 for more information

      CaseNotHPOs: N/A

      CaseNotHPOFreeText: N/A

      CasePreviousTesting: N/A

      PreviouslyPublished: N/A

      SupplementalData: N/A

      Variant: N/A; Null (large rearrangement)

      CaseProblemVariantFreeText: N/A

      LegacyVariant: N/A

      ClinVarID: N/A

      CAID: N/A

      gnomAD: N/A

      VariantEvidence: N/A

      MutationType: rearrangement_region

      CivicName: Rearrangement

      MultipleGeneVariants: N/A

    3. Eighteen VHL patients who underwent pancreatectomy for one or several endocrine tumors at Beaujon hospital from 1997 to 2008 were retrieved from the file of VHL patients (Table 1).

      PatientID: 6

      KindredID: 6

      Case: F, 49Y0M, Ethnicity unknown

      DiseaseAssertion: VHL

      FamilyInfo: None

      CasePresentingHPOs: HP:0030405 (pancreatic endocrine tumor)

      CaseHPOFreeText: See Table 1 for more information

      CaseNotHPOs: N/A

      CaseNotHPOFreeText: N/A

      CasePreviousTesting: N/A

      PreviouslyPublished: N/A

      SupplementalData: N/A

      Variant: p.L89P (c.266T>C)

      CaseProblemVariantFreeText: N/A

      LegacyVariant: N/A

      ClinVarID: 182979 https://www.ncbi.nlm.nih.gov/clinvar/variation/182979/

      CAID: CA020207 http://reg.clinicalgenome.org/redmine/projects/registry/genboree_registry/allele?hgvsOrDescriptor=NM_000551.3%3Ac.266T%3EC

      gnomAD: N/A

      VariantEvidence: N/A

      MutationType: missense_variant; transition

      CivicName: L89P (c.266T>C)

      MultipleGeneVariants: N/A

    4. Eighteen VHL patients who underwent pancreatectomy for one or several endocrine tumors at Beaujon hospital from 1997 to 2008 were retrieved from the file of VHL patients (Table 1).

      PatientID: 15

      KindredID: 15

      Case: M, 48Y0M, Ethnicity unknown

      DiseaseAssertion: pancreatic endocrine tumor

      FamilyInfo: None

      CasePresentingHPOs: HP:0030405 (pancreatic endocrine tumor)

      CaseHPOFreeText: See Table 1 for more information

      CaseNotHPOs: N/A

      CaseNotHPOFreeText: N/A

      CasePreviousTesting: N/A

      PreviouslyPublished: N/A

      SupplementalData: N/A

      Variant: p.R82P (c.245G>C)

      CaseProblemVariantFreeText: N/A

      LegacyVariant: N/A

      ClinVarID: 193118 https://www.ncbi.nlm.nih.gov/clinvar/variation/193118/

      CAID: CA020159 http://reg.clinicalgenome.org/redmine/projects/registry/genboree_registry/allele?hgvsOrDescriptor=NM_000551.3%3Ac.245G%3EC

      gnomAD: N/A

      VariantEvidence: N/A

      MutationType: missense_variant; transversion

      CivicName: R82P (c.245G>C)

      MultipleGeneVariants: N/A

    5. Eighteen VHL patients who underwent pancreatectomy for one or several endocrine tumors at Beaujon hospital from 1997 to 2008 were retrieved from the file of VHL patients (Table 1).

      PatientID: 14

      KindredID: 14

      Case: F, 56Y0M, Ethnicity unknown

      DiseaseAssertion: pancreatic endocrine tumor

      FamilyInfo: None

      CasePresentingHPOs: HP:0030405 (pancreatic endocrine tumor)

      CaseHPOFreeText: See Table 1 for more information

      CaseNotHPOs: N/A

      CaseNotHPOFreeText: N/A

      CasePreviousTesting: N/A

      PreviouslyPublished: N/A

      SupplementalData: N/A

      Variant: p.Y112H (c.334T>C)

      CaseProblemVariantFreeText: N/A

      LegacyVariant: N/A

      ClinVarID: 2222 https://www.ncbi.nlm.nih.gov/clinvar/variation/2222/

      CAID: CA020277 http://reg.clinicalgenome.org/redmine/projects/registry/genboree_registry/allele?hgvsOrDescriptor=NM_000551.3%3Ac.334T%3EC

      gnomAD: N/A

      VariantEvidence: N/A

      MutationType: missense_variant; transition

      CivicName: Y112H (c.334T>C)

      MultipleGeneVariants: N/A

    6. Eighteen VHL patients who underwent pancreatectomy for one or several endocrine tumors at Beaujon hospital from 1997 to 2008 were retrieved from the file of VHL patients (Table 1).

      PatientID: 9

      KindredID: 9

      Case: M, 51Y0M, Ethnicity unknown

      DiseaseAssertion: pancreatic endocrine tumor

      FamilyInfo: None

      CasePresentingHPOs: HP:0030405 (pancreatic endocrine tumor)

      CaseHPOFreeText: See Table 1 for more information

      CaseNotHPOs: N/A

      CaseNotHPOFreeText: N/A

      CasePreviousTesting: N/A

      PreviouslyPublished: N/A

      SupplementalData: N/A

      Variant: p.H191Tfs*11 (c.571delC)

      CaseProblemVariantFreeText: N/A

      LegacyVariant: N/A

      ClinVarID: N/A

      CAID: CA658795182 http://reg.clinicalgenome.org/redmine/projects/registry/genboree_registry/allele?hgvsOrDescriptor=NM_000551.3%3Ac.571delC

      gnomAD: N/A

      VariantEvidence: N/A

      MutationType: minus_1_frameshift_variant

      CivicName: H191Tfs*11 (c.571delC)

      MultipleGeneVariants: N/A

    1. WM03 VHL VHL 0.74 

      PatientID: WM03

      KindredID: 9

      Case: Sex Unknown, 3Y0M, Ethnicity Unknown

      DiseaseAssertion: pheochromocytoma

      FamilyInfo: N/A

      CasePresentingHPOs: HP:0002666 (pheochromocytoma)

      CaseHPOFreeText: N/A

      CaseNotHPOs: N/A

      CaseNotHPOFreeText: N/A

      CasePreviousTesting: MAX, RET, SDHA, SDHB, SDHC, SDHD, TMEM127

      PreviouslyPublished: N/A

      SupplementalData: Yes

      Variant: Unspecified Exon 1 mutation

      LegacyVariant: Unspecified Exon 1 mutation - no other information given

      CaseProblemVariantFreeText: N/A

      ClinVarID: N/A

      CAID: N/A

      gnomAD: N/A

      VariantEvidence: N/A

      MutationType: N/A

      CivicName: N/A

      MultipleGeneVariants: N/A

    2. WM06 VHL VHL 0.84 

      PatientID: WM06

      KindredID: 12

      Case: Sex Unknown, 10Y0M, Ethnicity Unknown

      DiseaseAssertion: pheochromocytoma

      FamilyInfo: N/A

      CasePresentingHPOs: HP:0002666 (pheochromocytoma)

      CaseHPOFreeText: N/A

      CaseNotHPOs: N/A

      CaseNotHPOFreeText: N/A

      CasePreviousTesting: MAX, RET, SDHA, SDHB, SDHC, SDHD, TMEM127

      PreviouslyPublished: N/A

      SupplementalData: Yes

      Variant: N/A - Unspecified

      LegacyVariant: Given as an unspecified germline mutation

      CaseProblemVariantFreeText: N/A

      ClinVarID: N/A

      CAID: N/A

      gnomAD: N/A

      VariantEvidence: N/A

      MutationType: N/A

      CivicName: N/A

      MultipleGeneVariants: N/A

    3. We have described the development and validation of a new gene-expression diagnostic test called Pheo-type for classification of PPGL tumors based on the underlying genetic driver of the disease. Our assay confirms that the predominant gene-expression subtypes of PPGL are closely linked to tumor genotype and for the first time show that classification can be achieved using a relatively small gene set. Pheo-type is similar to other clinical assays developed on the Nanostring platform for subtyping of solid tumors (50–52). As with these other studies, we have shown that robust gene-expression analysis can be achieved from small amounts of FFPE tissue material generating data that are comparable to other gene-expression platforms. The assay is rapid, largely automated, and cost effective, enabling the generation of results in 2 days from RNA extraction to data analysis, facilitating its implementation in a routine diagnostic laboratory.
    4. VCB.14T VHL VHL 0.63 

      PatientID: VCB.14T

      KindredID: 6

      Case: Sex Unknown, 34Y0M, Ethnicity Unknown

      DiseaseAssertion: pheochromocytoma

      FamilyInfo: N/A

      CasePresentingHPOs: HP:0002668; HP:0002666 (paraganglioma, pheochromocytoma)

      CaseHPOFreeText: Presented with bilateral pheochromocytoma

      CaseNotHPOs: N/A

      CaseNotHPOFreeText: N/A

      CasePreviousTesting: MAX, RET, SDHA, SDHB, SDHC, SDHD, TMEM127

      PreviouslyPublished: 25545346 (see table S1 and S10)

      SupplementalData: Yes

      Variant: p.R167W (c.499C>T)

      LegacyVariant: N/A

      CaseProblemVariantFreeText: N/A

      ClinVarID: 2218, https://www.ncbi.nlm.nih.gov/clinvar/variation/2218/

      CAID: N/A

      gnomAD: 0.000007954, https://gnomad.broadinstitute.org/variant/3-10191506-C-T?dataset=gnomad_r2_1

      VariantEvidence: N/A

      MutationType: missense_variant;transition

      CivicName: R167W (c.499C>T)

      MultipleGeneVariants: SDHA, Germline, c.619A>C (p.Arg207=); SDHA, Germline, c.1969G>A (p.Val657Ile); KIF1B, Germline, c.2192A>G (p.Asn777Ser); MDH2, Somatic, c.26C>T (p.Ala9Val)

    1. Ninety-eight individuals were tested for VHL mutations--23 symptomatic and 75 asymptomatic individuals belonging to 16 families. Seven of the families had definite clinical criteria of VHL disease, five had sporadic hemangioblastoma, and four had CNS hemangioblastoma combined with minor visceral signs. Molecular genetic testing identified five germline mutations in six of the definite VHL families (sensitivity 85%), but none in the possible VHL and sporadic hemangioblastoma cases; four of these mutations had been previously described and one is a novel mutation present in two unrelated families. After patients carrying the mutation were identified, they underwent clinical screening and asymptomatic VHL-related lesions were identified in 43%.

      PatientID: 19

      KindredID: C

      Case: Sex Unknown, 30Y0M, Mexican (Latino/Admixed American)

      DiseaseAssertion: assumed VHL

      FamilyInfo: At least 13 members in this family presented with the mutation. 5 were asymptomatic (ages 9, 12, 13, 17, and 29Y). Other family manifestations include: cerebellar, spinal, retinal HBs, pancreatic, hepatic, suprarenal and kidney cysts, epididymal cystadenoma, and RCC. Fig 1 displays family pedigree.

      CasePresentingHPOs: HP:0009713 (spinal hemangioblastoma)

      CaseHPOFreeText: Patient had 2 spinal HBs. They however appeared absent of clinical manifestations of VHL disease prior to clinical and imaging scrutiny.

      CaseNotHPOs: N/A

      CaseNotHPOFreeText: N/A

      CasePreviousTesting: N/A

      PreviouslyPublished: 20064270 (Here, the family cohort is given with a reportedly different variant of: p.G34Rfs*98 (c.99_100insA). Unclear of why this is or which most correctly corresponds to the family).

      SupplementalData: N/A

      Variant: p.T100Nfs*32 (c.298dupA)

      LegacyVariant: c.1012_1013insA

      CaseProblemVariantFreeText: The ‘1012_1013insA’ mutation is out-of-frame, leading to a modification of 31 amino acids downstream and a premature stop codon at nucleotides 5441-5443 (amino acid residue 131).

      ClinVarID: N/A

      CAID: CA2573129737 https://reg.clinicalgenome.org/redmine/projects/registry/genboree_registry/allele?hgvsOrDescriptor=NM_000551.3%3Ac.298dupA

      gnomAD: N/A

      VariantEvidence: The modified amino acids are located in a domain common to all pVHL isoforms, the highly conserved cctbinding domain of the protein, involved in the formation of the pVHL elongin complex that is crucial for tumor suppression. Furthermore, the mutant protein is prematurely truncated and lacks the C-terminal half of exon 2 and exon 3 completely, which includes the nuclear export signal and the elongin C binding site of pVHL. Thus, this truncated protein would affect the two functional isoforms of pVHL: the major isoform pVHL30 and pVHL19, but not isoform 2, which lacks exon 2 but is not functional

      MutationType: plus_1_frameshift_variant; duplication

      CivicName: T100Nfs*32 (c.298dupA)

      MultipleGeneVariants: N/A

    2. Ninety-eight individuals were tested for VHL mutations--23 symptomatic and 75 asymptomatic individuals belonging to 16 families. Seven of the families had definite clinical criteria of VHL disease, five had sporadic hemangioblastoma, and four had CNS hemangioblastoma combined with minor visceral signs. Molecular genetic testing identified five germline mutations in six of the definite VHL families (sensitivity 85%), but none in the possible VHL and sporadic hemangioblastoma cases; four of these mutations had been previously described and one is a novel mutation present in two unrelated families. After patients carrying the mutation were identified, they underwent clinical screening and asymptomatic VHL-related lesions were identified in 43%.

      PatientID: 13

      KindredID: C

      Case: Sex Unknown, 17Y0M, Mexican (Latino/Admixed American)

      DiseaseAssertion: asymptomatic

      FamilyInfo: At least 13 members in this family presented with the mutation. 5 were asymptomatic (ages 9, 12, 13, 17, and 29Y). Other family manifestations include: cerebellar, spinal, retinal HBs, pancreatic, hepatic, suprarenal and kidney cysts, epididymal cystadenoma, and RCC. Fig 1 displays family pedigree.

      CasePresentingHPOs: N/A

      CaseHPOFreeText: Patient was asymptomatic at the time, likely due to young age

      CaseNotHPOs: N/A

      CaseNotHPOFreeText: N/A

      CasePreviousTesting: N/A

      PreviouslyPublished: 20064270 (Here, the family cohort is given with a reportedly different variant of: p.G34Rfs*98 (c.99_100insA). Unclear of why this is or which most correctly corresponds to the family).

      SupplementalData: N/A

      Variant: p.G34Rfs*98 (c.99_100insA)

      LegacyVariant: c.1012_1013insA

      CaseProblemVariantFreeText: The ‘1012_1013insA’ mutation is out-of-frame, leading to a modification of 31 amino acids downstream and a premature stop codon at nucleotides 5441-5443 (amino acid residue 131).

      ClinVarID: N/A

      CAID: CA2018007671 http://reg.clinicalgenome.org/redmine/projects/registry/genboree_registry/by_caid?caid=CA2018007671

      gnomAD: N/A

      VariantEvidence: The modified amino acids are located in a domain common to all pVHL isoforms, the highly conserved cctbinding domain of the protein, involved in the formation of the pVHL elongin complex that is crucial for tumor suppression. Furthermore, the mutant protein is prematurely truncated and lacks the C-terminal half of exon 2 and exon 3 completely, which includes the nuclear export signal and the elongin C binding site of pVHL. Thus, this truncated protein would affect the two functional isoforms of pVHL: the major isoform pVHL30 and pVHL19, but not isoform 2, which lacks exon 2 but is not functional

      MutationType: plus_1_frameshift_variant

      CivicName: G34Rfs (c.99_100insA)

      MultipleGeneVariants: N/A

    3. Ninety-eight individuals were tested for VHL mutations--23 symptomatic and 75 asymptomatic individuals belonging to 16 families. Seven of the families had definite clinical criteria of VHL disease, five had sporadic hemangioblastoma, and four had CNS hemangioblastoma combined with minor visceral signs. Molecular genetic testing identified five germline mutations in six of the definite VHL families (sensitivity 85%), but none in the possible VHL and sporadic hemangioblastoma cases; four of these mutations had been previously described and one is a novel mutation present in two unrelated families. After patients carrying the mutation were identified, they underwent clinical screening and asymptomatic VHL-related lesions were identified in 43%.

      PatientID: 22

      KindredID: C

      Case: Sex unknown, 30Y0M, Mexican (Latino/Admixed American)

      DiseaseAssertion: assumed VHL

      FamilyInfo: At least 13 members in this family presented with the mutation. 5 were asymptomatic (ages 9, 12, 13, 17, and 29Y). Other family manifestations include: cerebellar, spinal, retinal HBs, pancreatic, hepatic, suprarenal and kidney cysts, epididymal cystadenoma, and RCC. Fig 1 displays family pedigree.

      CasePresentingHPOs: HP:0006880; HP:0001737; HP:0000107 (cerebellar hemangioblastoma, pancreatic cysts, renal cyst)

      CaseHPOFreeText: Patient had 1 cerebellar HB, pancreatic and kidney cysts.

      CaseNotHPOs: N/A

      CaseNotHPOFreeText: N/A

      CasePreviousTesting: N/A

      PreviouslyPublished: 20064270 (Here, the family cohort is given with a reportedly different variant of: p.G34Rfs*98 (c.99_100insA). Unclear of why this is or which most correctly corresponds to the family).

      SupplementalData: N/A

      Variant: p.T100Nfs*32 (c.298dupA)

      LegacyVariant: c.1012_1013insA

      CaseProblemVariantFreeText: The ‘1012_1013insA’ mutation is out-of-frame, leading to a modification of 31 amino acids downstream and a premature stop codon at nucleotides 5441-5443 (amino acid residue 131).

      ClinVarID: N/A

      CAID: CA2573129737 https://reg.clinicalgenome.org/redmine/projects/registry/genboree_registry/allele?hgvsOrDescriptor=NM_000551.3%3Ac.298dupA

      gnomAD: N/A

      VariantEvidence: The modified amino acids are located in a domain common to all pVHL isoforms, the highly conserved cctbinding domain of the protein, involved in the formation of the pVHL elongin complex that is crucial for tumor suppression. Furthermore, the mutant protein is prematurely truncated and lacks the C-terminal half of exon 2 and exon 3 completely, which includes the nuclear export signal and the elongin C binding site of pVHL. Thus, this truncated protein would affect the two functional isoforms of pVHL: the major isoform pVHL30 and pVHL19, but not isoform 2, which lacks exon 2 but is not functional

      MutationType: plus_1_frameshift_variant; duplication

      CivicName: T100Nfs*32 (c.298dupA)

      MultipleGeneVariants: N/A

    4. Ninety-eight individuals were tested for VHL mutations--23 symptomatic and 75 asymptomatic individuals belonging to 16 families. Seven of the families had definite clinical criteria of VHL disease, five had sporadic hemangioblastoma, and four had CNS hemangioblastoma combined with minor visceral signs. Molecular genetic testing identified five germline mutations in six of the definite VHL families (sensitivity 85%), but none in the possible VHL and sporadic hemangioblastoma cases; four of these mutations had been previously described and one is a novel mutation present in two unrelated families. After patients carrying the mutation were identified, they underwent clinical screening and asymptomatic VHL-related lesions were identified in 43%.

      PatientID: 11

      KindredID: C

      Case: Sex Unknown, 45Y0M, Mexican (Latino/Admixed American)

      DiseaseAssertion: assumed VHL

      FamilyInfo: At least 13 members in this family presented with the mutation. 5 were asymptomatic (ages 9, 12, 13, 17, and 29Y). Other family manifestations include: cerebellar, spinal, retinal HBs, pancreatic, hepatic, suprarenal and kidney cysts, epididymal cystadenoma, and RCC. Fig 1 displays family pedigree.

      CasePresentingHPOs: HP:0006880; HP:0001737; HP:0000107; HP:0005584 (cerebellar hemangioblastoma, pancreatic cysts, renal cyst, renal cell carcinoma)

      CaseHPOFreeText: Patient had 1 cerebellar HB, pancreatic & kidney cysts, RCC

      CaseNotHPOs: N/A

      CaseNotHPOFreeText: N/A

      CasePreviousTesting: N/A

      PreviouslyPublished: 20064270 (Here, the family cohort is given with a reportedly different variant of: p.G34Rfs*98 (c.99_100insA). Unclear of why this is or which most correctly corresponds to the family).

      SupplementalData: N/A

      Variant: p.T100Nfs*32 (c.298dupA)

      LegacyVariant: c.1012_1013insA

      CaseProblemVariantFreeText: The ‘1012_1013insA’ mutation is out-of-frame, leading to a modification of 31 amino acids downstream and a premature stop codon at nucleotides 5441-5443 (amino acid residue 131).

      ClinVarID: N/A

      CAID: CA2573129737 https://reg.clinicalgenome.org/redmine/projects/registry/genboree_registry/allele?hgvsOrDescriptor=NM_000551.3%3Ac.298dupA

      gnomAD: N/A

      VariantEvidence: The modified amino acids are located in a domain common to all pVHL isoforms, the highly conserved cctbinding domain of the protein, involved in the formation of the pVHL elongin complex that is crucial for tumor suppression. Furthermore, the mutant protein is prematurely truncated and lacks the C-terminal half of exon 2 and exon 3 completely, which includes the nuclear export signal and the elongin C binding site of pVHL. Thus, this truncated protein would affect the two functional isoforms of pVHL: the major isoform pVHL30 and pVHL19, but not isoform 2, which lacks exon 2 but is not functional

      MutationType: plus_1_frameshift_variant; duplication

      CivicName: T100Nfs*32 (c.298dupA)

      MultipleGeneVariants: N/A

    5. Ninety-eight individuals were tested for VHL mutations--23 symptomatic and 75 asymptomatic individuals belonging to 16 families. Seven of the families had definite clinical criteria of VHL disease, five had sporadic hemangioblastoma, and four had CNS hemangioblastoma combined with minor visceral signs. Molecular genetic testing identified five germline mutations in six of the definite VHL families (sensitivity 85%), but none in the possible VHL and sporadic hemangioblastoma cases; four of these mutations had been previously described and one is a novel mutation present in two unrelated families. After patients carrying the mutation were identified, they underwent clinical screening and asymptomatic VHL-related lesions were identified in 43%.

      PatientID: 16

      KindredID: C

      Case: Sex Unknown, 54Y0M, Mexican (Latino/Admixed American)

      DiseaseAssertion: assumed VHL

      FamilyInfo: At least 13 members in this family presented with the mutation. 5 were asymptomatic (ages 9, 12, 13, 17, and 29Y). Other family manifestations include: cerebellar, spinal, retinal HBs, pancreatic, hepatic, suprarenal and kidney cysts, epididymal cystadenoma, and RCC. Fig 1 displays family pedigree.

      CasePresentingHPOs: HP:0000107 (renal cyst)

      CaseHPOFreeText: Patient had renal cysts. They however appeared absent of clinical manifestations of VHL disease prior to clinical and imaging scrutiny.

      CaseNotHPOs: N/A

      CaseNotHPOFreeText: N/A

      CasePreviousTesting: N/A

      PreviouslyPublished: 20064270 (Here, the family cohort is given with a reportedly different variant of: p.G34Rfs*98 (c.99_100insA). Unclear of why this is or which most correctly corresponds to the family).

      SupplementalData: N/A

      Variant: p.T100Nfs*32 (c.298dupA)

      LegacyVariant: c.1012_1013insA

      CaseProblemVariantFreeText: The ‘1012_1013insA’ mutation is out-of-frame, leading to a modification of 31 amino acids downstream and a premature stop codon at nucleotides 5441-5443 (amino acid residue 131).

      ClinVarID: N/A

      CAID: CA2573129737 https://reg.clinicalgenome.org/redmine/projects/registry/genboree_registry/allele?hgvsOrDescriptor=NM_000551.3%3Ac.298dupA

      gnomAD: N/A

      VariantEvidence: The modified amino acids are located in a domain common to all pVHL isoforms, the highly conserved cctbinding domain of the protein, involved in the formation of the pVHL elongin complex that is crucial for tumor suppression. Furthermore, the mutant protein is prematurely truncated and lacks the C-terminal half of exon 2 and exon 3 completely, which includes the nuclear export signal and the elongin C binding site of pVHL. Thus, this truncated protein would affect the two functional isoforms of pVHL: the major isoform pVHL30 and pVHL19, but not isoform 2, which lacks exon 2 but is not functional

      MutationType: plus_1_frameshift_variant; duplication

      CivicName: T100Nfs*32 (c.298dupA)

      MultipleGeneVariants: N/A

    1. 2,3Deletion

      PatientID: I:1

      KindredID: 1

      Case: M, 50Y0M, Chinese

      DiseaseAssertion: VHL

      FamilyInfo: the patient’s son was observed to be affected with CNS hemangioblastoma diagnosed at 37Y, retinal capillary hemangioma at 31Y, and epididymal/ovarian cystadenoma at 16Y

      CasePresentingHPOs: HP:0010797 (hemangioblastoma)

      CaseHPOFreeText: patient had hemangioblastomas at 50Y

      CaseNotHPOs: N/A

      CaseNotHPOFreeText: N/A

      CasePreviousTesting: N/A

      PreviouslyPublished: N/A

      SupplementalData: N/A

      Variant: exon 2,3 deletion

      CaseProblemVariantFreeText: N/A

      LegacyVariant: N/A

      ClinVarID: N/A

      CAID: N/A

      gnomAD: N/A

      VariantEvidence: N/A

      MutationType: exon_loss_variant

      CivicName: exon 2-3 deletion

      MultipleGeneVariants: N/A

    2. c.269A>T p.Asn90Ile

      PatientID: II:3 (proband 4)

      KindredID: 4

      Case: M, 38Y0M, Chinese

      DiseaseAssertion: VHL

      FamilyInfo: Patient’s mother (I:1) was found with the same mutation and RCC at 63Y. The proband’s brother (II:1) died before diagnosis; thus no DNA sample available. He presented with hemangioblastoma at 19Y

      CasePresentingHPOs: HP:0010797; HP:0009711 (hemangioblastoma, retinal capillary hemangioma)

      CaseHPOFreeText: patient had hemangioblastoma at 22Y and retinal capillary hemangioma at 32Y

      CaseNotHPOs: N/A

      CaseNotHPOFreeText: N/A

      CasePreviousTesting: N/A

      PreviouslyPublished: N/A

      SupplementalData: N/A

      Variant: p.N90I (c.269A>T)

      CaseProblemVariantFreeText: N/A

      LegacyVariant: N/A

      ClinVarID: 223172 https://www.ncbi.nlm.nih.gov/clinvar/variation/223172/

      CAID: N/A

      gnomAD: N/A

      VariantEvidence: N/A

      MutationType: missense_variant; transversion

      CivicName: N90I (c.269A>T)

      MultipleGeneVariants: N/A

    3. c.499C>T p.Arg167Trp

      PatientID: II:4 (proband 5’s sister 2)

      KindredID: 5

      Case: F, 34Y0M, Chinese

      DiseaseAssertion: VHL

      FamilyInfo: Her father and two sisters presented with this same mutation. The father had RCC diagnosed at 54Y. The one sister (II:3) had had pancreatic tumors at 36Y and hemangioblastomas at 38Y. The brother (II:1) appeared to be non-affected, while the other sister (II:2) had hemangioblastoma, renal cell carcinoma, pancreatic cysts, and Papillary cystadenoma of the epididymis diagnosed at 37Y; and pheochromocytoma at 39Y

      CasePresentingHPOs: HP:0009711 (retinal capillary angiomas)

      CaseHPOFreeText: had retinal angiomas at 34Y

      CaseNotHPOs: N/A

      CaseNotHPOFreeText: N/A

      CasePreviousTesting: N/A

      PreviouslyPublished: N/A

      SupplementalData: N/A

      Variant: p.R167W (c.499C>T)

      CaseProblemVariantFreeText: N/A

      LegacyVariant: N/A

      ClinVarID: 2218 (https://www.ncbi.nlm.nih.gov/clinvar/variation/2218/)

      CAID: N/A

      gnomAD: 0.000007954 https://gnomad.broadinstitute.org/variant/3-10191506-C-T

      VariantEvidence: N/A

      MutationType: missense_variant; transition

      CivicName: R167W (c.499C>T)

      MultipleGeneVariants: N/A

    4. 1Deletion

      PatientID: II:2

      KindredID: 8

      Case: F, 43Y0M, Chinese

      DiseaseAssertion: VHL

      FamilyInfo: a 3 generational family found with 5 phenotypically affected members, two of which were confirmed with the exon 1 deletion. This patient and her son were tested to be found with the deletion of exon 1. Her son was found with retinal angiomas at 17Y, pancreatic cysts and epididymal/ovarian cystadenoma at 19Y, and hemangioblastomas at 23Y. Her two sisters and father all had hemangioblastomas; and father also had RCC, however the father and one sister were deceased; and the other sister was not available to provide a DNA sample.

      CasePresentingHPOs: HP:0009711; HP:0010797 (retinal capillary hemangioma, hemangioblastoma)

      CaseHPOFreeText: patient was found with retinal hemangioblastomas at 35Y and hemangioblastomas at 43Y

      CaseNotHPOs: N/A

      CaseNotHPOFreeText: N/A

      CasePreviousTesting: N/A

      PreviouslyPublished: N/A

      SupplementalData: N/A

      Variant: exon 1 deletion

      CaseProblemVariantFreeText: N/A

      LegacyVariant: N/A

      ClinVarID: N/A

      CAID: N/A

      gnomAD: N/A

      VariantEvidence: N/A

      MutationType: exon_loss_variant

      CivicName: exon 1 deletion

      MultipleGeneVariants: N/A

    5. 3Deletion

      PatientID: unknown (sister)

      KindredID: 13

      Case: F, 30Y0M, Chinese

      DiseaseAssertion: VHL

      FamilyInfo: the patient’s brother was found with hemangioblastomas, RCC, and multiple pancreatic cysts or tumors at 23Y, and retinal angiomas at 24Y. Their mother was found at 43Y with CNS hemangioblastomas, however she died before diagnosis; no DNA sample was available.

      CasePresentingHPOs: HP:0010797; HP:0005584; HP:0001737 (hemangioblastoma; renal cell carcinoma; pancreatic cysts)

      CaseHPOFreeText: patient had hemangioblastomas, RCC, and multiple pancreatic cysts or tumors diagnosed at 30Y

      CaseNotHPOs: N/A

      CaseNotHPOFreeText: N/A

      CasePreviousTesting: N/A

      PreviouslyPublished: N/A

      SupplementalData: N/A

      Variant: exon 3 deletion

      CaseProblemVariantFreeText: N/A

      LegacyVariant: N/A

      ClinVarID: N/A

      CAID: N/A

      gnomAD: N/A

      VariantEvidence: N/A

      MutationType: exon_loss_variant

      CivicName: exon 3 deletion

      MultipleGeneVariants: N/A

    6. c.263G>A p.Trp88Stop

      PatientID: None (proband 11)

      KindredID: 11

      Case: M, 38Y0M, Chinese

      DiseaseAssertion: VHL

      FamilyInfo: Patient’s mother (last known age 36Y) had a CNS hemangioblastoma diagnosed at 36Y.

      CasePresentingHPOs: HP:0005584; HP:0001737 (renal cell carcinoma, pancreatic cysts)

      CaseHPOFreeText: RCC and multiple pancreatic cysts or tumors diagnosed at age 34 and 38Y.

      CaseNotHPOs: N/A

      CaseNotHPOFreeText: N/A

      CasePreviousTesting: N/A

      PreviouslyPublished: 22357542

      SupplementalData: N/A

      Variant: p.W88* (c.263G>A)

      CaseProblemVariantFreeText: N/A

      LegacyVariant: N/A

      ClinVarID: 182978 https://www.ncbi.nlm.nih.gov/clinvar/variation/182978/

      CAID: N/A

      gnomAD: N/A

      VariantEvidence: N/A

      MutationType: stop_gained

      CivicName: W88* (c.263G>A)

      MultipleGeneVariants: N/A

    7. c.269A>T p.Asn90Ile

      PatientID: I:1

      KindredID: 4

      Case: F, 63Y0M, Chinese

      DiseaseAssertion: VHL

      FamilyInfo: Patient’s one son (II:3) was found with the same mutation and hemangioblastoma at 22Y and retinal capillary hemangioma at 32Y. Her other son (II:1) died before diagnosis; thus no DNA sample available. He presented with hemangioblastoma at 19Y

      CasePresentingHPOs: HP:0005584 (renal cell carcinoma)

      CaseHPOFreeText: patient had RCC at 63Y

      CaseNotHPOs: N/A

      CaseNotHPOFreeText: N/A

      CasePreviousTesting: N/A

      PreviouslyPublished: N/A

      SupplementalData: N/A

      Variant: p.N90I (c.269A>T)

      CaseProblemVariantFreeText: N/A

      LegacyVariant: N/A

      ClinVarID: 223172 https://www.ncbi.nlm.nih.gov/clinvar/variation/223172/

      CAID: N/A

      gnomAD: N/A

      VariantEvidence: N/A

      MutationType: missense_variant; transversion

      CivicName: N90I (c.269A>T)

      MultipleGeneVariants: N/A

    Tags

    Annotators

    URL

    1. PMID: 29813026

      PatientID: 3

      KindredID: 3

      Case: Sex Unknown, Age Unknown, Ethnicity Unknown

      DiseaseAssertion: hemangioblastoma

      FamilyInfo: N/A - Not specified

      CasePresentingHPOs: HP:0010797 (hemangioblastoma)

      CaseHPOFreeText: VHL syndromic HB

      CaseNotHPOs: N/A

      CaseNotHPOFreeText: N/A

      CasePreviousTesting: N/A

      PreviouslyPublished: N/A

      SupplementalData: N/A

      Variant: p.E94K (c.280G>A)

      LegacyVariant: N/A

      CaseProblemVariantFreeText: N/A

      ClinVarID: 135955 https://www.ncbi.nlm.nih.gov/clinvar/variation/135955/

      CAID: N/A

      gnomAD: 0.000004460 https://gnomad.broadinstitute.org/variant/3-10183811-G-A?dataset=gnomad_r2_1

      VariantEvidence: N/A

      MutationType: missense_variant; transition

      CivicName: E94K (c.280G>A)

      MultipleGeneVariants: N/A

    2. PMID: 29813026

      PatientID: 2

      KindredID: 2

      Case: Sex Unknown, Age Unknown, Ethnicity Unknown

      DiseaseAssertion: hemangioblastoma

      FamilyInfo: N/A - Not specified

      CasePresentingHPOs: HP:0010797 (hemangioblastoma)

      CaseHPOFreeText: VHL syndromic HB

      CaseNotHPOs: N/A

      CaseNotHPOFreeText: N/A

      CasePreviousTesting: N/A

      PreviouslyPublished: N/A

      SupplementalData: N/A

      Variant: Null (Complete deletion)

      LegacyVariant: N/A

      CaseProblemVariantFreeText: N/A

      ClinVarID: N/A

      CAID: N/A

      gnomAD: N/A

      VariantEvidence: A VHL subject in our patient population had a full length deletion (FLD) in the germline VHL gene, but a VHL gene tumor second hit mutation (c.360-362 del AGA) causing an amino acid change of p.RD120-121S detected in the HB tumor

      MutationType: deletion

      CivicName: Deletion AND R120_121S (c.360_362delAGA)

      MultipleGeneVariants: Somatic, VHL, c.360_362delAGA, p.Arg120_121Ser

    3. PMID: 29813026

      PatientID: 1

      KindredID: 1

      Case: Sex Unknown, Age Unknown, Ethnicity Unknown

      DiseaseAssertion: hemangioblastoma

      FamilyInfo: N/A - Not specified

      CasePresentingHPOs: HP:0010797 (hemangioblastoma)

      CaseHPOFreeText: VHL syndromic HB

      CaseNotHPOs: N/A

      CaseNotHPOFreeText: N/A

      CasePreviousTesting: N/A

      PreviouslyPublished: N/A

      SupplementalData: N/A

      Variant: p.Q96_P102del (c.287_307del)

      LegacyVariant: N/A

      CaseProblemVariantFreeText: N/A

      ClinVarID: N/A

      CAID: CA2573106190 https://reg.clinicalgenome.org/redmine/projects/registry/genboree_registry/by_caid?caid=CA2573106190

      gnomAD: N/A

      VariantEvidence: N/A

      MutationType: inframe_deletion

      CivicName: Q96_P102del (c.287_307del)

      MultipleGeneVariants: N/A

    1. his two brothers (32 and 36 years),

      PatientID: None

      KindredID: 1

      Case: M, 36Y0M, Danish

      DiseaseAssertion: Asymptomatic

      FamilyInfo: The patient's half brothers both carried the mutation, one was asymptomatic and one had renal cell carcinoma. The patient's mother was found to carry the mutation and had breast cancer. The maternal grandmother also harboured the mutation but was asymptomatic. See Figure 1 for family pedigree.

      CasePresentingHPOs: N/A

      CaseHPOFreeText: N/A

      CaseNotHPOs: N/A

      CaseNotHPOFreeText: N/A

      CasePreviousTesting: N/A

      PreviouslyPublished: N/A

      SupplementalData: N/A

      Variant: p.P81S (c.241C>T)

      LegacyVariant: N/A

      CaseProblemVariantFreeText: N/A

      ClinVarID: 2233 https://www.ncbi.nlm.nih.gov/clinvar/variation/2233/

      CAID: N/A

      gnomAD: 0.0002179 https://gnomad.broadinstitute.org/variant/3-10183772-C-T

      VariantEvidence: N/A

      MutationType: missense_variant;transition

      CivicName:P81S (c.241C>T)

      MultipleGeneVariants: N/A

    2. proband’s mother (52 years)

      PatientID: None

      KindredID: 1

      Case: F, 52Y0M, Danish

      DiseaseAssertion: Breast carcinoma

      FamilyInfo: The patient had three sons all of whom carried the VHL mutation. Two of the sons were asymptomatic and one had renal cell carcinoma. The affected son also had a P2P mutation and he had a child who was found to have the VHL mutation (P2P). The patient's mother had the mutation but was also asymptomatic. See Figure 1 for family pedigree.

      CasePresentingHPOs: HP:0003002 (Breast carcinoma)

      CaseHPOFreeText: The patient had breast cancer at age 34.

      CaseNotHPOs: N/A

      CaseNotHPOFreeText: N/A

      CasePreviousTesting: N/A

      PreviouslyPublished: N/A

      SupplementalData: N/A

      Variant: p.P81S (c.241C>T)

      LegacyVariant: N/A

      CaseProblemVariantFreeText: N/A

      ClinVarID: 2233 https://www.ncbi.nlm.nih.gov/clinvar/variation/2233/

      CAID: N/A

      gnomAD: 0.0002179 https://gnomad.broadinstitute.org/variant/3-10183772-C-T

      VariantEvidence: N/A

      MutationType: missense_variant;transition

      CivicName:P81S (c.241C>T)

      MultipleGeneVariants: N/A

    1. V#3exon 3c.525C > Ap.Y175XPancreatic cysts and renal carcinoma

      PatientID: 3

      KindredID: 3

      Case: Sex Unknown, Age Unknown, Ethnicity Unknown

      DiseaseAssertion: VHL

      FamilyInfo: N/A

      CasePresentingHPOs HP:0001737; HP:0005584 (Pancreatic cysts; Renal cell carcinoma)

      CaseHPOFreeText: N/A

      CaseNotHPOs: N/A

      CaseNotHPOFreeText: N/A

      CasePreviousTesting: N/A

      PreviouslyPublished: N/A

      SupplementalData: Yes

      Variant: p.Y175* (c.525C>A)

      LegacyVariant: N/A

      CaseProblemVariantFreeText: N/A

      ClinVarID: 1298905, https://www.ncbi.nlm.nih.gov/clinvar/variation/1298905/

      CAID: N/A

      gnomAD: N/A

      VariantEvidence: N/A

      MutationType: stop_gained

      CivicName: Y175* (c.525C>A)

      MultipleGeneVariants: N/A

    2. V#2exon 3c.485G > Ap.C162YCNS-HB

      PatientID: 2

      KindredID: 2

      Case: Sex Unknown, Age Unknown, Ethnicity Unknown

      DiseaseAssertion: VHL

      FamilyInfo: N/A

      CasePresentingHPOs: HP:0010797 (hemangioblastoma)

      CaseHPOFreeText: N/A

      CaseNotHPOs: N/A

      CaseNotHPOFreeText: N/A

      CasePreviousTesting: N/A

      PreviouslyPublished: N/A

      SupplementalData: Yes

      Variant: p.C162Y (c.485G>A)

      LegacyVariant: N/A

      CaseProblemVariantFreeText: N/A

      ClinVarID: 223225, https://www.ncbi.nlm.nih.gov/clinvar/variation/223225/

      CAID: N/A

      gnomAD: N/A

      VariantEvidence: N/A

      MutationType: missense_variant;transition

      CivicName: C162Y (c.485G>A)

      MultipleGeneVariants: N/A

    3. V#1exon 3c.500G > Ap.R167QCNS-HB, renal carcinoma

      PatientID: 1

      KindredID: 1

      Case: Sex Unknown, Age Unknown, Ethnicity Unknown

      DiseaseAssertion: VHL

      FamilyInfo: N/A

      CasePresentingHPOs: HP:0010797; HP:0005584 (Hemangioblastoma; Renal cell carcinoma)

      CaseHPOFreeText: N/A

      CaseNotHPOs: N/A

      CaseNotHPOFreeText: N/A

      CasePreviousTesting: N/A

      PreviouslyPublished: N/A

      SupplementalData: Yes

      Variant: p.R167Q (c.500G>A)

      LegacyVariant: N/A

      CaseProblemVariantFreeText: N/A

      ClinVarID: 2216, https://www.ncbi.nlm.nih.gov/clinvar/variation/2216/

      CAID: N/A

      gnomAD: 0.000003977, https://gnomad.broadinstitute.org/variant/3-10191507-G-A

      VariantEvidence: Confocal staining shows the distribution of pVHL in the cell cytoplasm.

      MutationType: missense_variant; transition

      CivicName: R167Q (c.500G>A)

      MultipleGeneVariants: N/A

    4. V#1exon 3c.500G > Ap.R167QCNS-HB, renal carcinoma

      PatientID: 1

      KindredID: 1

      Case: Sex Unknown, Age Unknown, Ethnicity Unknown

      DiseaseAssertion: VHL

      FamilyInfo: N/A

      CasePresentingHPOs: HP:0010797; HP:0005584 (Hemangioblastoma; Renal cell carcinoma)

      CaseHPOFreeText: N/A

      CaseNotHPOs: N/A

      CaseNotHPOFreeText: N/A

      CasePreviousTesting: N/A

      PreviouslyPublished: N/A

      SupplementalData: Yes

      Variant: p.R167Q (c.500G>A)

      LegacyVariant: N/A

      CaseProblemVariantFreeText: N/A

      ClinVarID: 2216, https://www.ncbi.nlm.nih.gov/clinvar/variation/2216/

      CAID: N/A

      gnomAD: 0.000003977, https://gnomad.broadinstitute.org/variant/3-10191507-G-A

      VariantEvidence: Confocal staining shows the distribution of pVHL in the cell cytoplasm.

      MutationType: missense_variant; transition

      CivicName: R167Q (c.500G>A)

      MultipleGeneVariants: N/A

    1. The VHL mutation pattern includes point mutations, small deletions and large deletions.

      PatientID: VH3

      KindredID: F2

      Case: F, 18Y0M, Ethnicity Unknown

      DiseaseAssertion: VHL

      FamilyInfo: Family history of pheo (type 2 VHL) - Her asymptomatic sibling however was tested and did not carry the mutation nor had large deletion.

      CasePresentingHPOs: HP:0002666; HP:0030405 (pheochromocytoma; pancreatic endocrine tumor)

      CaseHPOFreeText: N/A

      CaseNotHPOs: N/A

      CaseNotHPOFreeText: N/A

      CasePreviousTesting: N/A

      PreviouslyPublished: 24735130

      SupplementalData: N/A

      Variant: c.463+3A>G

      LegacyVariant: IVS2+3A>G

      CaseProblemVariantFreeText: N/A

      ClinVarID: 428796 https://www.ncbi.nlm.nih.gov/clinvar/variation/428796/

      CAID: N/A

      gnomAD: N/A

      VariantEvidence: N/A

      MutationType: splice_site_variant

      CivicName: Splice Region (c.463+3A>G)

      MultipleGeneVariants: N/A

    1. A deletion of exon 3 in the VHL gene was found in this family.

      PatientID: III-5

      KindredID: Family A

      Case: F, 32Y0M, Ethnicity unknown

      DiseaseAssertion: VHL

      FamilyInfo: Patient’s grandfather (I-1), now deceased, and aunt (II-1) had CNS/spinal hemangioblastoma and the confirmed VHL gene mutation. Her mom II-2 had confirmed VHL and CNS hemangioblastoma; and her cousin (III-6) has renal cell carcinoma and CNS/spinal hemangioblastoma and also the confirmed VHL gene mutation. Her uncle (II-3) has confirmed VHL gene and pancreatic and renal cysts. Her brother and sister (III-3; III-4) both were found with the confirmed VHL gene mutation; III-3 with retinal hemangioblastoma and CNS/spinal hemangioblastomas and III-4 with pancreatic and ovarian cysts. IV-1 and IV-3, were confirmed with the VHL gene mutation although no other manifestations.

      CasePresentingHPOs: HP:0010797; HP:0009711 (CNS hemangioblastoma, retinal capillary hemangioblastoma)

      CaseHPOFreeText: developed hemangioblastoma at the optic nerve in her left eye at the age of 16. At the age of 30, patient A III-5 underwent surgery for a CNS hemangioblastoma.

      CaseNotHPOs: HP:0005584; HP:0002666 (renal cell carcinoma, pheochromocytoma)

      CaseNotHPOFreeText: N/A

      CasePreviousTesting: N/A

      PreviouslyPublished: N/A

      SupplementalData: N/A

      Variant: Deletion of exon 3 (c.464-?_642+?del)

      LegacyVariant: N/A

      CaseProblemVariantFreeText: N/A

      ClinVarID: N/A

      CAID: N/A

      gnomAD: N/A

      VariantEvidence: N/A

      MutationType: exon_loss_variant

      CivicName: Exon 3 Deletion

      MultipleGeneVariants: N/A

    2. c.236G>C, p.R79P

      PatientID: II-1

      KindredID: Family B

      Case: M, 23Y0M, Ethnicity unknown

      DiseaseAssertion: VHL

      FamilyInfo: Family positive pedigree showing patient’s father with RCC and CNS hemangioblastoma; as well as 2 sisters with CNS/spinal and retinal hemangioblastomas

      CasePresentingHPOs: HP:0010797; HP:0009711 (hemangioblastoma; retinal capillary hemangioblastoma)

      CaseHPOFreeText: underwent surgery for multiple CNS hemangioblastomas at the age of 15, and at the same age multiple peripheral retinal hemangioblastomas were found in his right eye, which were treated successfully with laser photocoagulation and cryotherapy. At the age of 20, he developed a large peripheral retinal hemangioblastoma in his left eye, which was treated successfully with cryotherapy.

      CaseNotHPOs: HP:0005584; HP:0002666 (renal cell carcinoma, pheochromocytoma)

      CaseNotHPOFreeText: N/A

      CasePreviousTesting: N/A

      PreviouslyPublished: N/A

      SupplementalData: N/A

      Variant: p.R79P (c.236G>C)

      LegacyVariant: N/A

      CaseProblemVariantFreeText: N/A

      ClinVarID: N/A

      CAID: CA351749311 http://reg.clinicalgenome.org/redmine/projects/registry/genboree_registry/allele?hgvsOrDescriptor=NM_000551.3%3Ac.236G%3EC

      gnomAD: N/A

      VariantEvidence: N/A

      MutationType: missense_variant; transversion

      CivicName: R79P (c.236G>C)

      MultipleGeneVariants: N/A

    3. c.236G>C, p.R79P

      PatientID: II-1

      KindredID: Family B

      Case: M, 23Y0M, Ethnicity unknown

      DiseaseAssertion: VHL

      FamilyInfo: Family positive pedigree showing patient’s father with RCC and CNS hemangioblastoma; as well as 2 sisters with CNS/spinal and retinal hemangioblastomas

      CasePresentingHPOs: HP:0010797; HP:0009711 (hemangioblastoma; retinal capillary hemangioblastoma)

      CaseHPOFreeText: underwent surgery for multiple CNS hemangioblastomas at the age of 15, and at the same age multiple peripheral retinal hemangioblastomas were found in his right eye, which were treated successfully with laser photocoagulation and cryotherapy. At the age of 20, he developed a large peripheral retinal hemangioblastoma in his left eye, which was treated successfully with cryotherapy.

      CaseNotHPOs: HP:0005584; HP:0002666 (renal cell carcinoma, pheochromocytoma)

      CaseNotHPOFreeText: N/A

      CasePreviousTesting: N/A

      PreviouslyPublished: N/A

      SupplementalData: N/A

      Variant: p.R79P (c.236G>C)

      LegacyVariant: N/A

      CaseProblemVariantFreeText: N/A

      ClinVarID: N/A

      CAID: CA351749311 http://reg.clinicalgenome.org/redmine/projects/registry/genboree_registry/allele?hgvsOrDescriptor=NM_000551.3%3Ac.236G%3EC

      gnomAD: N/A

      VariantEvidence: N/A

      MutationType: missense_variant; transversion

      CivicName: R79P (c.236G>C)

      MultipleGeneVariants: N/A

    1. c.341-6C > T (intron 1)

      PatientID: None

      KindredID: 5

      Case: Sex, Age, Ethnicity unknown

      DiseaseAssertion: dilatation of the cerebral artery

      FamilyInfo: None

      CasePresentingHPOs: HP:0004944 (dilatation of the cerebral artery)

      CaseHPOFreeText: Patient had an intracranial aneurysm

      CaseNotHPOs: N/A

      CaseNotHPOFreeText: N/A

      CasePreviousTesting: N/A

      PreviouslyPublished: N/A

      SupplementalData: N/A

      Variant: c.341-6C>T

      CaseProblemVariantFreeText: N/A

      LegacyVariant: N/A

      ClinVarID: 371898 https://www.ncbi.nlm.nih.gov/clinvar/variation/371898/

      CAID: N/A

      gnomAD: 0.00008132 https://gnomad.broadinstitute.org/variant/3-10188192-C-T

      VariantEvidence: N/A

      MutationType: splice_site_variant

      CivicName: Splice Site (341-6C>T)

      MultipleGeneVariants: N/A

    2. c.463 + 43A > G (intron 2)

      GroupID/ KindredID: None

      DiseaseAssertion: dilatation of the cerebral artery

      GroupSize: 8

      GroupNumberMales: N/A

      GroupNumberFemales: N/A

      GroupEthnicity: N/A

      GroupAgeRange: N/A

      GroupInfo: 8 patients are listed with this SNP mutation; any relation is unknown.

      GroupPresentingHPOs: HP:0004944 (dilatation of the cerebral artery)

      GroupHPOFreeText: All members are stated to have intracranial aneurysms. Other manifestations are possible but not clear.

      GroupNotHPOs: N/A

      GroupNotHPOFreeText: N/A

      GroupPreviousTesting: N/A

      PreviouslyPublished: N/A

      SupplementalData: N/A

      Variant: c.463+43A>G

      CaseProblemVariantFreeText: N/A

      LegacyVariant: N/A

      ClinVarID: 1244574 https://www.ncbi.nlm.nih.gov/clinvar/variation/1244574/

      CAID: N/A

      gnomAD: 0.01186 https://gnomad.broadinstitute.org/variant/3-10188363-A-G

      VariantEvidence: This variant’s large allele frequency means this is likely non disease causing (not deleterious; polymorphism).

      MutationType: splice_site_variant; intron_variant

      CivicName: Splice Region (463+43A>G)

      MultipleGeneVariants: N/A

    3. c.463 + 8C > T (intron 2)

      PatientID: None

      KindredID: 6

      Case: Sex, Age, Ethnicity unknown

      DiseaseAssertion: dilatation of the cerebral artery

      FamilyInfo: None

      CasePresentingHPOs: HP:0004944 (dilatation of the cerebral artery)

      CaseHPOFreeText: Patient had an intracranial aneurysm

      CaseNotHPOs: N/A

      CaseNotHPOFreeText: N/A

      CasePreviousTesting: N/A

      PreviouslyPublished: N/A

      SupplementalData: N/A

      Variant: c.463+8C>T

      CaseProblemVariantFreeText: N/A

      LegacyVariant: N/A

      ClinVarID: 127830 https://www.ncbi.nlm.nih.gov/clinvar/variation/127830/

      CAID: N/A

      gnomAD: 0.0005055 https://gnomad.broadinstitute.org/variant/3-10188328-C-T

      VariantEvidence: N/A

      MutationType: splice_site_variant

      CivicName: Splice Region (c.463+8C>T)

      MultipleGeneVariants: N/A

    1. not only showed loss of the open-reading frame, but more extended deletions by using c11 and P1 demonstrating complete loss of the VHL gene sequence (>35 kb, but <90 kb)

      PatientID: 2

      KindredID: 2

      Case: Sex Unknown, Age Unknown, Ethnicity Unknown

      DiseaseAssertion: Hemangioblastoma

      FamilyInfo: None

      CasePresentingHPOs: HP:0010797 (Hemangioblastoma)

      CaseHPOFreeText: N/A

      CaseNotHPOs: N/A

      CaseNotHPOFreeText: N/A

      CasePreviousTesting: N/A

      PreviouslyPublished: N/A

      SupplementalData: N/A

      Variant: deletion (deletion on chromosome 3 (>35kb, <90kb) resulting in complete loss of VHL gene)

      LegacyVariant: N/A

      CaseProblemVariantFreeText: N/A

      ClinVarID: N/A

      CAID: N/A

      gnomAD: N/A

      VariantEvidence: germline deletion on chromosome 3 (>35kb, <90kb) resulting in complete loss of VHL gene. Hemangioblastoma from this patient shows a missense mutation R200W(c.598C>T) in the second copy of VHL gene.

      MutationType: deletion

      CivicName: Deletion AND R200W (c.598C>T)

      MultipleGeneVariants: Somatic, VHL, c.598C>T (p.Arg200Trp)

    1. IPType 1 VWDc.7464C>T11A1>3009635Normal multimer size distribution*

      Case: Female, Caucasian, 11 years at diagnosis

      DiseaseAssertion: VWD1

      FamilyInfo: Non-consanguineous family, parents carry no bleeding history but have risk factors (prolonged closure time and modestly decreased VWF:Ag level)

      ParentalGenotype(s): Mother has c.7464C>T, Father carries no mutation.

      CasePresentingHPOs: HP:0000421, HP:0000978, HP:0001934, HP:0030140, HP:0004846, HP:0006298

      CaseHPOFreeText: Cumulative bleeding score of 17, Reduced VWF:Ag of 9IU/dL, VWF:GPIb of 6 I/dL, and factor VIII coagulant activity of 35 IU/dL, prolonged PFA closure time of >300 and reduced concentration of all multimers.

      CaseNOTHPOs: None reported

      CaseNOTHPOFreeText: Normal multimer size distribution (tested in Agarose gel)

      CasePreviousTesting: NA

      GenotypingMethod: Direct sequencing of genomic DNA exons 1 to 52, exon/intron boundaries, 5' and 3' UTR, promoter region, and whole intron 44 of VWF. RT-PCR followed by sequencing of cDNA to detect splicing defect due to c.7464C>T.

      PreviouslyPublished: PMID:22871923

      Gene: VWF

      Variant: c.7464C>T

      HGVS: NM_000552.5:c.7464C>T (p.Gly2488=)

      ClinVarID: 619755

      CAID: CA232284628

      gnomAD: 0.000008799 MAF in European (non-Finnish) and 0.000008664 MAF in XX. https://gnomad.broadinstitute.org/variant/12-6080849-G-A

    1. 3 patients with Glanzmann thrombasthenia

      Case#: patient 1

      DiseaseAssertion: Glanzmann thrombasthenia

      **FamilyInfo: **

      ParentalGenotype: If noted by authors, annotate with the carrier status of each parent in regards to the variant(s) identified in the proband.

      CasePresentingHPOs:

      PlateletAggregation: absent platelet integrin αIIbβ3. Monolayer of spread platelets essentially devoid of fibrinogen binding but with high CD62P expression and phosphatidylserine exposure (Figure S1). Figure 5.

      CaseHPOFreeText:

      CaseNotHPOs:

      **CaseNotHPOFreeText: **

      ProteinExpression:

      CasePreviousTesting:

      **PreviouslyPublished: **

      Gene: ITGA2B

      **HGVS: ** NM_000419.4:c.2943G>A

      **ClinVar: **

      CAID: CA500262444

      **gnomAD: **

    1. c.463+

      PatientID: VHL 11

      KindredID: VHL 11

      Case: Sex, Age, Ethnicity unknown

      DiseaseAssertion: hemangioblastoma

      FamilyInfo: N/A

      CasePresentingHPOs: HP:0010797 (hemangioblastoma)

      CaseHPOFreeText: Three samples of VHL hemangioblastomas were represented here (.1, .2, .3). They are recorded as both germline and somatic, involving the VHL- and C3ORF10-gene.

      CaseNotHPOs: N/A

      CaseNotHPOFreeText: N/A

      CasePreviousTesting: N/A

      PreviouslyPublished: N/A - This sample was likely duplicated in 24132471

      SupplementalData: Yes - See Supplementary Table 1

      Variant: c.463+3A>C

      LegacyVariant: N/A

      CaseProblemVariantFreeText: Supplemental data records this as a c.463+3A>C (p.(?)) mutation. The only time the text mentions a splice site mutation however is at: c.463+2T>C p.(?). Will go by supplemental data but be cautious of this discrepancy.

      ClinVarID: N/A

      CAID: CA645525016 http://reg.clinicalgenome.org/redmine/projects/registry/genboree_registry/allele?hgvsOrDescriptor=NM_000551.3%3Ac.463%2B3A%3EC

      gnomAD: N/A

      VariantEvidence: N/A

      MutationType: splice_site_variant

      CivicName: Splice Region (c.463+3A>C) 

      MultipleGeneVariants: N/A

    1. A 20-year-old Caucasian woman presented to our institution with decreased vision in the right eye (RE) with a 4-month evolution. The patient’s vital signs were within normal limits, and no abnormalities were noticed upon physical and neurological examination. Similarly, her past medical history was unremarkable. Her best corrected visual acuity (BCVA) was 50 ETDRS (Early Treatment Diabetic Retinopathy Study) letters in the RE and 84 ETDRS letters in the left eye. Her intraocular pressure (IOP) was normal in both eyes, and the result of her anterior segment examination was unremarkable. Upon ophthalmoscopic examination, a red-colored globular lesion of 3 disk diameters (DDs) with prominent feeder vessels was noticed in the superior temporal region of the retina in the RE (Fig. 1). The fellow eye was normal on fundus examination, and no other lesions were found in the posterior pole or periphery. Optical coherence tomography (OCT) was carried out using the DRI OCT Triton™ SS-OCT device (Topcon Medical, Tokyo, Japan).

      PatientID: None

      KindredID: 1

      Case: F, 20Y0M, Caucasian

      DiseaseAssertion: VHL

      FamilyInfo: The patient’s mother had died of pulmonary edema during pregnancy at the age of 40.

      CasePresentingHPOs: HP:0009711 (Retinal capillary hemangioma)

      CaseHPOFreeText: The patient presented with decreased vision in the right eye with a 4-month evolution. The patient’s vital signs were within normal limits, and no abnormalities were noticed upon physical and neurological examination. Similarly, her past medical history was unremarkable. Upon ophthalmoscopic examination, a red-colored globular lesion of 3 disk diameters with prominent feeder vessels was noticed in the superior temporal region of the retina. A structural OCT B-scan showed a diffuse cystoid macular edema, which involved the posterior pole and expanded outside the vascular arcades. The other eye was normal.

      CaseNotHPOs: HP:0012443; HP:0011732 (Abnormality of brain morphology, abnormality of renal morphology)

      CaseNotHPOFreeText: Results of renal ultrasonography and magnetic resonance imaging of the brain were both negative for visceral lesions.

      CasePreviousTesting: N/A

      PreviouslyPublished: N/A

      SupplementalData: N/A

      Variant: p.Y112C (c.335A>G)

      LegacyVariant: N/A

      ClinVarID: 223189, https://www.ncbi.nlm.nih.gov/clinvar/variation/223189/

      gnomAD: N/A

      VariantEvidence: N/A

      MutationType: missense_variant;transition

      CivicName: Y112C(c.335A>G)

      MultipleGeneVariants: N/A

    1. M22redMale22Pro86Arg1st R (2 subs R, no L)Former- <10 pack years33.46 (5*)No

      PatientID: None

      KindredID: 3

      Case: M, 22Y0M, Ethnicity Unknown

      DiseaseAssertion: Clear Cell Renal Cell Carcinoma

      FamilyInfo: N/A

      CohortInfo: The National Cancer Institute has a frozen tumour bank of ccRCC tumours that have been removed from VHL patients. We selected six patients, three males and three females, with at least five tumours from a single surgery from one kidney.

      CasePresentingHPOs: HP:0006770 (clear cell renal cell carcinoma)

      CaseHPOFreeText: One of the samples from this patient had few variants and clustered with the normal samples. Further inspection showed these samples were cyst-like rather than tumours, so they were excluded from further analysis. This suggests that the patient had renal cysts alongside ccRCC at age 22.

      CaseNotHPOs: N/A

      CaseNotHPOFreeText: N/A

      CasePreviousTesting: N/A

      PreviouslyPublished: N/A

      SupplementalData: N/A

      Variant: p.P86R(c.257C>G)

      LegacyVariant:N/A

      CaseProblemVariantFreeText: N/A

      ClinVarID: 223170 https://www.ncbi.nlm.nih.gov/clinvar/variation/223170/

      CAID: N/A

      gnomAD: N/A

      VariantEvidence: N/A

      MutationType: missense_variant;transversion

      CivicName: P86R(c.257C>G)

      MultipleGeneVariants: N/A

    1. Von Hippel-Lindau (VHL) is a tumor suppressor that negatively regulates the production of angiogenic factors. Mutations in the VHL gene cause VHL syndrome, which is characterized by highly vascularized tumors. Here we report a c.464T>A mutation of the VHL gene in three patients with hemangioblastoma from a Chinese family. This mutation was not reported previously and was absent in the unaffected family members. The mutation is predicted to cause Val to Glu substitution at VHL protein residue 155 in a conserved region. Previous biochemical studies demonstrated that residue Val-155 was critical for VHL protein binding to chaperonin TRiC/CCT, an essential step for proper VHL protein folding. Our finding of naturally occurring VHL V155E mutation in patients with VHL syndrome supports the functional importance of Val-155 residue in VHL protein and illustrates the diversity of VHL gene defects underlying VHL syndrome.

      PatientID: III-1

      KindredID: 1

      Case: F, 26Y0M, Chinese

      DiseaseAssertion: assumed VHL

      FamilyInfo: 10 members of this Chinese family were tested, and 3 were found with the same genetic mutation (c.464T>A). The proband’s grandmother (I-1, 79Y), and father (II-1, 53Y) had hemangioblastomas, and tested positive for the mutation. This mutation was not found in the other unaffected members in the family.

      CasePresentingHPOs: HP:0006880; HP:0030405; HP:0002666 (cerebellar hemangioblastoma, endolyphmatic sac tumor, pheochromocytoma)

      CaseHPOFreeText: patient suffered with dizziness and headache and frequent vomiting since 25Y (CT and MRI identified occupying lesions and obstructive hydrocephalus in the cerebellar vermis). The cerebellar tumor nodes were removed surgically. Abdominal CT showed multiple lesions in the liver, pancreas and posterior peritoneum. The tumors in the proband’s pancreatic tail and retroperitoneal space also were removed subsequently. Histological analysis indicated the tumors to be pancreatic isletcell tumor and phaeochromocytoma, respectively.

      CaseNotHPOs: N/A

      CaseNotHPOFreeText: patient was negative in the bilateral Babinski’s sign test

      CasePreviousTesting: N/A

      PreviouslyPublished: N/A

      SupplementalData: N/A

      Variant: p.V155E (c.464T>A)

      LegacyVariant: N/A

      CaseProblemVariantFreeText: N/A

      ClinVarID: N/A

      CAID: CA351756032 https://reg.clinicalgenome.org/redmine/projects/registry/genboree_registry/allele?hgvsOrDescriptor=NM_000551.3%3Ac.464T%3EA

      gnomAD: N/A

      VariantEvidence: N/A

      MutationType: missense_variant;transversion

      CivicName: V155E (c.464T>A)

      MultipleGeneVariants: N/A

    1. Patient 2 A 17-year-old girl with a history of primitive headache, intense nocturnal sweating and 2-month-long amenorrhoea and elevated blood pressure presented a 7-cm-diameter right adrenal mass at abdominal sonography, confirmed by MRI. The mass showed inhomogeneous density: hypodensity in T1 and hyperdensity in T2 and after Gadolinium contrast. Immunometric assays indicated very high levels of chromogranin A (242 UI/L; NR 2–18) and catecholamines: noradrenaline levels were 14·460 nmol/day (NR: 90–470), and adrenaline and dopamine levels were in the normal range. A 123I-MIBG scintigraphy showed a high tracer uptake in right adrenal gland, as expected. The patient underwent surgical removal of the mass, which was 8 × 6 × 5 cm in size. Immunohistochemical assays indicated that the tumour was positive for chromogranin A and synaptophysin, compatible with a diagnosis of PHEO. Follow-up blood test after 2 years was within normal limits, except for a still moderate elevated CgA (67 UI/L, NR 2–18). The family history was negative for PHEO or other neuroendocrine tumours.

      PatientID: 2

      KindredID: 2

      Case: F, 17Y0M, Ethnicity Unknown

      DiseaseAssertion: adrenal pheochromocytoma

      FamilyInfo: None - The family history was negative for PHEO or other neuroendocrine tumours. Their parents however, decided not to be tested neither to extend the test to other family members

      CasePresentingHPOs: HP:0006748 (adrenal pheochromocytoma)

      CaseHPOFreeText: Apparently sporadic pheo. She had a history of primitive headache, intense nocturnal sweating and 2-month-long amenorrhoea and elevated blood pressure presented a 7-cm-diameter right adrenal mass at abdominal sonography, confirmed by MRI.

      CaseNotHPOs: N/A

      CaseNotHPOFreeText: N/A

      CasePreviousTesting: RET, SDHB, SDHD

      PreviouslyPublished: N/A

      SupplementalData: N/A

      Variant: p.D197N (c.589G>A)

      LegacyVariant: p.D197N (g.13,278)

      CaseProblemVariantFreeText: N/A

      ClinVarID: N/A

      CAID: CA351756524 https://reg.clinicalgenome.org/redmine/projects/registry/genboree_registry/allele?hgvsOrDescriptor=NM_000551.3%3Ac.589G%3EA

      gnomAD: N/A

      VariantEvidence: N/A

      MutationType: missense_variant;transition

      CivicName: D197N (c.589G>A)

      MultipleGeneVariants: N/A

    1. Poorer survival has been associated with loss of function events (frameshift or nonsense mutations) compared with wild-type, missense mutations, and mutations of unknown biological consequence (25, 32) although numbers of cases in the LOF group were very small. We found no prognostic effect of VHL mutation but a trend (although not quite statistically significant) was seen for increased frequency of microvascular invasion in tumors where the presumed deletion would occur essentially from the elongin binding region onwards, possibly indicating a role for either HIF-regulated factors or other VHL substrates in this aspect of tumorigenesis. The largest previous study also found no relationship between clinicopathologic factors and VHL mutation/LOH in cRCC (26, 35). In marked contrast, however, is that 0 of 11 cRCC cases with methylation had an intragenic mutation whereas we found 14 of 19 methylated cases to have a confirmed mutation, although their mutation and methylation frequencies overall were much lower (51% and 5.4%, respectively). However, a significantly better cancer-free and overall survival was seen in patients with stage I to III cancer with VHL alteration (mutation or methylation) but wasn't seen in stage IV disease (35). Our data fails to confirm this although when stage IV patients were included a similar trend was seen. Differences between studies might reflect samples sizes, length of follow-up, and postoperative treatment.
    1. PatientID: III-9

      KindredID: 1

      Case: F, Age Unknown, Middle Eastern

      DiseaseAssertion: VHL

      FamilyInfo: Multigenerational Kuwaiti family with Arabian and Persian genetic admixture. Thirteen members of the family had been clinically diagnosed as having VHL. Patient 1-I had 6 children, 5 of which were found with VHL and the p.W117C mutation. 7/20 of her grandchildren also found to have VHL and the same mutation.

      CasePresentingHPOs: HP:0010797; HP:0006770; HP:0009713; HP:0009711; HP:0006880 (hemangioblastoma; clear cell renal cell carcinoma; spinal hemangioblastoma; retinal capillary hemangioma; cerebellar hemangioblastoma)

      CaseHPOFreeText: Member had clear cell renal carcinomas in addition to hemangioblastomas. She had undergone multiple surgeries because of tumors involving the cerebellum, cervical spine, lumbar spine, multiple abdominal and pelvic organs and the retina. The tumor had been demonstrated on angiography as very extensive and vascular. The patient had had a partial nephrectomy, adrenalectomy, distal pancreatomy for involvement of the tail of the pancreas with a hemangioblastoma and a left salpingoophorectomy.

      CaseNotHPOs: HP:0002666 (pheochromocytoma)

      CaseNotHPOFreeText: Lacked evidence of any pheos.

      CasePreviousTesting: N/A

      PreviouslyPublished: N/A

      SupplementalData: N/A

      Variant: p.W117C (c.351G>T)

      LegacyVariant: p.Trp117Cys (c.564G>T)

      CaseProblemVariantFreeText: N/A

      ClinVarID: 167827 https://www.ncbi.nlm.nih.gov/clinvar/variation/167827/

      CAID: N/A

      gnomAD: N/A

      VariantEvidence: N/A

      MutationType: missense_variant;transversion

      CivicName: W117C (c.351G>T)

      MultipleGeneVariants: N/A

    2. PatientID: III-8

      KindredID: 1

      Case: F, Age Unknown, Middle Eastern

      DiseaseAssertion: VHL

      FamilyInfo: Multigenerational Kuwaiti family with Arabian and Persian genetic admixture. Thirteen members of the family had been clinically diagnosed as having VHL. Patient 1-I had 6 children, 5 of which were found with VHL and the p.W117C mutation. 7/20 of her grandchildren also found to have VHL and the same mutation.

      CasePresentingHPOs: HP:0010797; HP:0006770; HP:0009725; HP:0030692 (hemangioblastoma; clear cell renal cell carcinoma; bladder tumour; brain tumour)

      CaseHPOFreeText: Member had clear cell renal carcinomas in addition to hemangioblastomas. She was also the only member of the family to be diagnosed as having a bladder tumor, considered rare in VHL cases, and a brain tumor.

      CaseNotHPOs: HP:0002666 (pheochromocytoma)

      CaseNotHPOFreeText: Lacked evidence of any pheos.

      CasePreviousTesting: N/A

      PreviouslyPublished: N/A

      SupplementalData: N/A

      Variant: p.W117C (c.351G>T)

      LegacyVariant: p.Trp117Cys (c.564G>T)

      CaseProblemVariantFreeText: N/A

      ClinVarID: 167827 https://www.ncbi.nlm.nih.gov/clinvar/variation/167827/

      CAID: N/A

      gnomAD: N/A

      VariantEvidence: N/A

      MutationType: missense_variant;transversion

      CivicName: W117C (c.351G>T)

      MultipleGeneVariants: N/A

    3. PatientID: III-7

      KindredID: 1

      Case: M, Age Unknown (deceased), Middle Eastern

      DiseaseAssertion: VHL

      FamilyInfo: Multigenerational Kuwaiti family with Arabian and Persian genetic admixture. Thirteen members of the family had been clinically diagnosed as having VHL. Patient 1-I had 6 children, 5 of which were found with VHL and the p.W117C mutation. 7/20 of her grandchildren also found to have VHL and the same mutation.

      CasePresentingHPOs: HP:0010797; HP:0006770 (hemangioblastoma; clear cell renal cell carcinoma)

      CaseHPOFreeText: Member had clear cell renal carcinomas that were the main cause of mortality, in addition to hemangioblastomas

      CaseNotHPOs: HP:0002666 (pheochromocytoma)

      CaseNotHPOFreeText: Lacked evidence of any pheos.

      CasePreviousTesting: N/A

      PreviouslyPublished: N/A

      SupplementalData: N/A

      Variant: p.W117C (c.351G>T)

      LegacyVariant: p.Trp117Cys (c.564G>T)

      CaseProblemVariantFreeText: N/A

      ClinVarID: 167827 https://www.ncbi.nlm.nih.gov/clinvar/variation/167827/

      CAID: N/A

      gnomAD: N/A

      VariantEvidence: N/A

      MutationType: missense_variant;transversion

      CivicName: W117C (c.351G>T)

      MultipleGeneVariants: N/A

    1. p.Pro81Ser has been inherited from his healthy father (I.1)

      PatientID: I.1

      KindredID: 3

      Case: M, Age Unknown, Ethnicity Unknown

      DiseaseAssertion:Asymptomatic

      FamilyInfo: The patient had a son who he passed this mutation to. The son (II.1) presented with hemangioblastoma and pancreatic cysts and had an additional de novo exon 1-3 deletion. Refer to figure 1, pedigree C for family information.

      CohortInfo: Patients were registrants from the European-American Pheochromocytoma-Paraganglioma and German von Hippel-Lindau Disease Registries.

      CasePresentingHPOs: N/A

      CaseHPOFreeText: N/A

      CaseNotHPOs: N/A

      CaseNotHPOFreeText: N/A

      CasePreviousTesting: RET/SDHB/SDHD/SDHC

      PreviouslyPublished: May have been previously published in 11106358 and/or 7563486.

      SupplementalData: Yes, File 1 for methods.

      Variant: p.P81S(c.241C>T)

      LegacyVariant: N/A

      CaseProblemVariantFreeText: N/A

      ClinVarID: 2233 https://www.ncbi.nlm.nih.gov/clinvar/variation/2233/

      CAID: N/A

      gnomAD: 0.0002179 https://gnomad.broadinstitute.org/variant/3-10183772-C-T

      VariantEvidence: N/A

      MutationType: missense_variant;transition

      CivicName: P81S(c.241C>T)

      MultipleGeneVariants: N/A

    1. Germline de novo mutations and linkage markers vs. DNA sequencing for carrier detection in von Willebrand disease F. Ahmad,  Corresponding Author F. Ahmad Department of Haematology, All India Institute of Medical Sciences (AIIMS), New Delhi, India Center for Translational Medicine, School of Medicine Temple University, Philadelphia, PA, USA Correspondence: Firdos Ahmad, PhD, Center for Translational Medicine, School of Medicine Temple University, 3500 N Broad Street, Philadelphia, PA 19140, USA. Tel.: +1 215 707 6518; fax: +1 215 707 9820; e-mail: firdos.ahmad@temple.edu Renu Saxena, MD, Professor and Head, Department of Hematology, All India Institute of Medical Sciences, New Delhi, India 110029. Tel: +91-11-2659 4670 Fax: +91-11-2658 8663 e-mail: renusaxena@outlook.comSearch for more papers by this authorF. Oyen,  F. Oyen Department of Pediatric Haematology Oncology, University Medical Centre Hamburg Eppendorf, Hamburg, GermanySearch for more papers by this authorR. Jan,  R. Jan Department of Haematology, All India Institute of Medical Sciences (AIIMS), New Delhi, IndiaSearch for more papers by this authorU. Budde,  U. Budde Hämostaseology, Medilys Laborgesellschaft mbH, Hamburg, GermanySearch for more papers by this authorR. Schneppenheim,  R. Schneppenheim Department of Pediatric Haematology Oncology, University Medical Centre Hamburg Eppendorf, Hamburg, GermanySearch for more papers by this authorR. Saxena,  Corresponding Author R. Saxena Department of Haematology, All India Institute of Medical Sciences (AIIMS), New Delhi, India Correspondence: Firdos Ahmad, PhD, Center for Translational Medicine, School of Medicine Temple University, 3500 N Broad Street, Philadelphia, PA 19140, USA. Tel.: +1 215 707 6518; fax: +1 215 707 9820; e-mail: firdos.ahmad@temple.edu Renu Saxena, MD, Professor and Head, Department of Hematology, All India Institute of Medical Sciences, New Delhi, India 110029. Tel: +91-11-2659 4670 Fax: +91-11-2658 8663 e-mail: renusaxena@outlook.comSearch for more papers by this author

      PMID: 24712919

      Gene: VWF

      HGNCID: 12726

      Note: abnormal multimers found in patient with p.I1628T variant

    1. 3'

      PatientID: 4

      KindredID: 4

      Case: F, 16Y0M, Ethnicity Unknown

      DiseaseAssertion: retinal capillary hemangioma

      FamilyInfo: N/A - family history was unremarkable. The paper states however that this patient inherited the duplication from a nonsymptomatic parent.

      CasePresentingHPOs: HP:0009711 (retinal capillary hemangioma)

      CaseHPOFreeText: a 16- year-old girl referred to this center for VHL testing due to an isolated retinal angioma

      CaseNotHPOs: N/A

      CaseNotHPOFreeText: N/A

      CasePreviousTesting: N/A

      PreviouslyPublished: N/A

      SupplementalData: N/A

      Variant: c.*1149A>G

      LegacyVariant: N/A

      CaseProblemVariantFreeText: N/A

      ClinVarID: N/A

      CAID: CA2573130264 https://reg.clinicalgenome.org/redmine/projects/registry/genboree_registry/by_caid?caid=CA2573130264

      gnomAD: N/A

      VariantEvidence: Quantitative Southern blot/real-time quantitative PCR analyses was normal in this patient. Known polymorphic variant on the 3’UTR of the VHL gene, as well as the 5’UTR. PCR–RFLP assay approach showed that both alleles were expressed in apparently equimolar amounts (Fig. 2d) suggesting that the 11 bp duplication has no effect on expression of the affected allele.

      MutationType: 3_prime_UTR_variant

      CivicName: c.–65_–55dup11 AND 3' UTR alteration (c.*1149A>G)

      MultipleGeneVariants: Germline, VHL, c.–65_–55dup11

    1. nonsense mutation

      PatientID: 96

      KindredID: None

      Case: Age and Sex unknown, Chinese

      DiseaseAssertion: VHL

      FamilyInfo: None

      CasePresentingHPOs: HP:0010797; HP:0001737; HP:0000107 (hemangioblastoma, pancreatic cysts, renal cyst)

      CaseHPOFreeText: N/A

      CaseNotHPOs: HP:0005584; HP:0009711; HP:0002666; HP:0030405; HP:0030393 (Renal cell carcinoma, Retinal capillary haemangioblastoma, Pheochromocytoma, Pancreatic endocrine tumour, Endolymphatic sac tumour)

      CaseNotHPOFreeText: N/A

      CasePreviousTesting: N/A

      PreviouslyPublished: N/A

      SupplementalData: Yes; See Suppl 1 (Supporting table)

      Variant: p.Y175* (c.525C>G)

      CaseProblemVariantFreeText: N/A

      LegacyVariant: N/A

      ClinVarID: 182974 https://www.ncbi.nlm.nih.gov/clinvar/variation/182974/

      CAID: CA020466 http://reg.clinicalgenome.org/redmine/projects/registry/genboree_registry/allele?hgvsOrDescriptor=NM_000551.3%3Ac.525C%3EG

      gnomAD: N/A

      VariantEvidence: N/A

      MutationType: stop_gained

      CivicName: Y175* (c.525C>G)

      MultipleGeneVariants: N/A

    1. In a family with VHL, we identified a novel missense mutation (N78D), which affects a fully conserved residue in the VHL protein. Interestingly, several other missense mutations reported at same codon in the VHL protein that might be associated with a low risk of renal cell carcinoma (RCC) but not pheochromocytoma appear to be associated with a VHL type 1 phenotype. At the moment, RCC is present in none of the affected mutation carriers in the family described here. In contrast to other missense changes at codon 78, the change in our VHL family is predicted to have a mild effect on VHL function, which apparently is insufficient to cause predisposition to RCC.

      PatientID: II-3

      KindredID: 1

      Case: F, 35Y0M, Ethnicity Unknown

      DiseaseAssertion: VHL

      FamilyInfo: Reported 3 siblings (II:3, II:6, II:7) of a family clinically diagnosed as having VHL type 1 was identified with the c.232A>G mutation. Two female siblings (II:1, II:2) died from CHB. Three (II:3, II:6, II:7) of the ten siblings had multiple CNS haemangioblastomas, and all tested positive for the mutation. The age of onset for all patients varied from 20 to 25 years, and it was likely inherited from the mother who had died at the age of 40 years due to haemangioblastoma (in the medulla oblongata), and hydrocephalus after having multiple operations.

      CasePresentingHPOs: HP:0009713; HP:0006880; HP:0030393; HP:0001737; HP:0000107 (spinal hemangioblastoma, cerebellar hemangioblastoma; endolymphatic sac tumor; pancreatic cysts; renal cyst)

      CaseHPOFreeText: Patient presented with headache, tinnitus and abdominal pain. She had a history of endolymphatic sac tumors (ELSTs) treated by surgery. She had cerebellar/spinal haemangioblastomas, pancreas and kidney cystic masses.

      CaseNotHPOs: HP:0005584 (renal cell carcinoma)

      CaseNotHPOFreeText: N/A

      CasePreviousTesting: N/A

      PreviouslyPublished: N/A

      SupplementalData: N/A

      Variant: p.N78D (c.232A>G)

      LegacyVariant: N/A

      CaseProblemVariantFreeText: N/A

      ClinVarID: 625226 https://www.ncbi.nlm.nih.gov/clinvar/variation/625226/

      CAID: N/A

      gnomAD: N/A

      VariantEvidence: N/A

      MutationType: missense_variant;transition

      CivicName: N78D (c.232A>G)

      MultipleGeneVariants: N/A

    1. PMID: 24112165 Item in Clipboard

      PatientID: 2 (II:2)

      KindredID: 1

      Case: F, 40Y0M, Chinese

      DiseaseAssertion: VHL

      FamilyInfo: large family history of VHL was tested - 3 members found. The patient's brother and her daughter had the same mutation - Her brother (patient 1) was diagnosed with spinal hemangioblastoma, and at 43Y he was diagnosed with ccRCC in his right kidney

      CasePresentingHPOs: HP:0010797; HP:0006770; HP:0000107; HP:0001737 (hemangioblastoma, clear cell renal cell carcinoma; renal cysts; pancreatic cysts)

      CaseHPOFreeText: had cerebellum hemangioblastoma at 38Y and a neoplasm of both kidneys at 40Y, as well as ccRCC, renal and pancreatic cysts.

      CaseNotHPOs: N/A

      CaseNotHPOFreeText: N/A

      CasePreviousTesting: N/A

      PreviouslyPublished: 22398592

      SupplementalData: N/A

      Variant: p.L101R (c.302T>G)

      LegacyVariant: L101R (c.515T>G)

      CaseProblemVariantFreeText: N/A

      ClinVarID: N/A

      CAID: CA351751004 https://reg.clinicalgenome.org/redmine/projects/registry/genboree_registry/allele?hgvsOrDescriptor=NM_000551.3%3Ac.302T%3EG

      gnomAD: N/A

      VariantEvidence: N/A

      MutationType: missense_variant;transversion

      CivicName: L101R (c.302T>G)

      MultipleGeneVariants: N/A

    1. Case 1: Clinical historyA 25-year-old woman presented with a 1-year history of slowly progressive and gradual decrease in hearing. Two years previously, the patient had undergone brain surgery because of hemangioblastoma of the cerebellum. Gene analysis performed at that time showed mutation in VHL gene in exon 1 TCG(Ser65)→TTG(Leu). On physical examination, she was found to have a middle ear mass that protruded into the external auditory canal. Bone destruction was found radiographically. At surgery, vascular tumor tissue and cysts were seen permeating and destroying the adjacent petrous portion of the temporal bone with invasion of the mastoid and the semicircular canal. The patient underwent a complete removal of the tumor from the middle ear, mastoid, and petrous bone. However, recurrent destructive tumor of the middle ear appeared after 26 months.Family historyThe family medical history disclosed the presence of symptoms of VHLD in the patient's grandfather, uncle, and father. In particular, the patient's father presented with multi-tumor syndrome and evidence of genetic VHLD due to causal mutation in VHL gene in exon 1 TCG(Ser65)→TTG(Leu). At the age of 30, he was operated on for cerebellar hemangioblastoma, and died of disseminated bilateral renal cell carcinoma of kidneys with multi-organ distant metastases 13 years later at the age of 43.

      PatientID: 1

      KindredID: 1

      Case: F, 25Y0M, Ethnicity Unknown

      DiseaseAssertion: assumed VHL

      FamilyInfo: The family medical history disclosed the presence of symptoms of VHLD in the patient’s grandfather, uncle, and father. In particular, the patient’s father presented with multi-tumor syndrome and a confirmed genetic mutation of c.194C>T. The father died of disseminated bilateral renal cell carcinoma of kidneys with multi-organ distant metastases at the age of 43.

      CasePresentingHPOs: HP:0006880;HP:0030393 (cerebellar hemangioblastoma, endolymphatic sac tumour)

      CaseHPOFreeText: Woman presented with slowly progressive and gradual decrease in hearing (beginning at 24Y). At 23Y the patient had undergone brain surgery because of hemangioblastoma of the cerebellum. Physical examination revealed a middle ear mass that protruded into the external auditory canal (recurrent restrictive tumor)

      CaseNotHPOs: N/A

      CaseNotHPOFreeText: N/A

      CasePreviousTesting: N/A

      PreviouslyPublished: N/A

      SupplementalData: N/A

      Variant: p.S65L (c.194C>T)

      LegacyVariant: N/A

      CaseProblemVariantFreeText: N/A

      ClinVarID: 182975, https://www.ncbi.nlm.nih.gov/clinvar/variation/182975/

      CAID: N/A

      gnomAD: https://gnomad.broadinstitute.org/variant/3-10183725-C-T

      VariantEvidence: genetic tests on tissue but suspected germline because father had same mutation, and 2 different tissue samples had same mutation; grandfather and uncle had VHL symptoms but not specified and no genetic confirmation

      MutationType: missense_variant;transition

      CivicName: S65L (c.194C>T)

      MultipleGeneVariants: N/A

    2. Most commonly, the tumors associated with VHLD include retinal, cerebellar, medullary, and spinal cord hemangioblastomas, renal cell carcinomas, and pheochromocytomas. The cell phenotype of these tumors varies according to the site; some tumors are epithelial, the others show an endocrine phenotype. Although most likely mesenchymal, the phenotype of hemangioblastomas has not been clearly defined yet. Histologically, most VHLD linked tumors share a number of features, including clear cell change, papillary cystic structures, and highly vascularized stroma. A possible explanation for the histological similarity between VHLD-associated tumors may lie in the abnormal function of the VHL gene. It is thought that the rich blood vessel supply in VHLD-related tumors may result from an abnormal or absent VHL-protein function, which may cause hypoxia-inducible factor (HIF) stimulation of angiogenesis. The VHL gene normally regulates vascular endothelial growth factor (VEGF), and there is evidence that inactivation of the VHL gene promotes VEGF overexpression and angiogenesis in VHL-associated tumors [12]. This link may explain the highly vascularized nature of all tumors associated with VHLD [1].The histopathological differential diagnosis of ELST includes middle ear adenoma, paraganglioma, chorioid plexus papilloma, and metastatic carcinoma of the thyroid, kidney, prostate, lung, and breast. Middle ear adenoma is a rare tumor displaying mucinous and neuroendocrine differentiation without formation of papillae. Adenomas form an avascular mass limited to the middle ear without bone destruction. Paragangliomas of the middle ear are cytologically benign and may demonstrate papillary structures and cuboidal cells with eosinophilic cytoplasm. However, paraganglioma cells are positive for chromogranin and synaptophysin, and at least focally they are arranged in characteristic nests. Chorioid plexus papilloma may be histologically similar to ELST, but it originates in the ventricle and does not invade bone. Currently, considerations of metastases from thyroid, breast, and prostate can be eliminated by immunohistochemistry. Positive staining for thyroglobulin, GCDFP-15 protein, estrogen and progesterone receptors, and prostatic-specific antigen, respectively, can help in this differential diagnosis. Differentiation of ELST from metastatic renal carcinoma can be more difficult, both tumors may occur in patients with VHLD, and immunohistochemistry does not help. Renal cell carcinoma, however, shows nuclear polymorphism and mitoses.ELST is a primary low-grade adenocarcinoma of the temporal bone that is presumed to originate from the vestibular endolymphatic system [5], [8]. An association of ELST and VHL disease was first published in a large study showing an increased prevalence of ELST among the patients with VHLD [18]. Subsequently, germline mutation of the VHL gene and somatic loss of the wild-type allele were demonstrated in ELST from VHL patients [13], [20]. Genetic analysis of the tumors in patients with VHLD supports the theory that an inherited mutation in one allele, followed by somatic loss of the other allele, is essential for development of the tumors. Tibbs et al. demonstrated a genetic mutation in the VHL gene within the ELST that was similar to mutations previously reported in other VHLD-associated tumors [19]. Somatic VHL gene mutations have been shown in sporadic cases of ELST [10], [21]. Hamazaki et al. [10] showed a mutation of the VHL tumor suppressor gene in a sporadic ELST in a patient without symptoms of VHL disease. Sequencing studies of tumor DNA disclosed a nucleotide substitution of G to T at position 546 of the VHL gene, resulting in an amino acid substitution (Tr to Cys, codon 117) [10]. In a previous analysis of four sporadic ELSTs, two of the cases showed a point mutation in the VHL gene [21]. In one case, Gly to Asp transversion was shown in exon 2, codon 114, whereas in the other case, a deletion in exon 1, codon 4 was identified. Two other sporadic cases of ELST did not show any mutation in the VHL gene [21]. Thus, the findings in this and previous studies warrant that the VHL gene is associated with ELST tumorigenesis when arising in the context of VHL disease. The role of VHL gene mutation in sporadic cases of ELST is still to be elucidated in future studies of additional cases.In conclusion, we have studied two cases of Heffner tumor of identical histomorphology and immunophenotype. One of the patients presented with a medical and family history of VHLD and proven inherited germline mutation of the VHL tumor suppressor gene. The latter was a sporadic case, in a patient with no symptoms of VHLD. While in the patient with VHLD, the ELST and cerebellar hemangioblastoma carry a mutation of VHL gene, resulting in C to T exchange at position 194, the consequence of which is an amino acid exchange S65L. No mutation of the VHL gene was found in all three exons analyzed and in exon–intron junctions in the sporadic case.
    1. The discovery in 1990 that a point mutation at residue 403 (R403Q) in the β-myosin heavy chain (MHC) caused a severe form of FHC was the first of many demonstrations linking FHC to mutations in muscle proteins. A mouse model for FHC has been widely used to study the mechanochemical properties of mutated cardiac myosin, but mouse hearts express α-MHC, whereas the ventricles of larger mammals express predominantly β-MHC. To address the role of the isoform backbone on function, we generated a transgenic mouse in which the endogenous α-MHC was partially replaced with transgenically encoded β-MHC or α-MHC. A His6 tag was cloned at the N terminus, along with R403Q, to facilitate isolation of myosin subfragment 1 (S1).

      We find in agreement with earlier studies that the R403Q mutation in a mouse α-MHC backbone results in a gain of function, a model that has been widely accepted as the primary cause leading to hypertrophic cardiomyopathy. However, we find that this enhancement does not extend to the R403Q mutation in a mouse β-MHC backbone. Our results do not necessarily imply a universal mechanism for FHC mutations in the β-myosin heavy chain.

      NM_000257.4:c.1208G>A (p.Arg403Gln)

    1. Nonsense-mediated mRNA decay efficiency influencesbleeding severity inITGA2Bc.2659C > T (p.Q887X)knock-in mice

      PMID: 33928629

      Previously annotated and reported Probands: PMID: 29675921. New Functional Evidence.

      CAID: CA8602626

      Gene: ITGA2B

      Variant: NM_000419.3:c.2671C>T (p.Gln891Ter)

      FunctionalEvidence: For Q887X mutation: Knock-in mice generated using CRISPR/Cas9 displaed no spontaneous bleeding phenotypes. Platelet morphology cofirmed to be normal and comparable platelet numbers to WT mice. Mean bleeding time increased and platelet aggregation impaired compared to WT. ITGA2B mRNA levels low in KI mice.

    1. 16-year-old girl with VHL consisting of retinal and CNS HBs and pancreatic cysts

      PatientID: II-a

      KindredID: 1

      Case: F, 16Y0M, Greek

      DiseaseAssertion: Assumed VHL

      FamilyInfo: The patient’s 50-year-old father has VHL consisting of retinal HBs diagnosed at the age of 20 years. He also has spinal cord HBs located in the neck. He was also found to carry the mutation NM_000551.3:c.433C>T that the patient carried. The patient’s 18-year-old brother and her 20-year-old sister are phenotypically healthy and repeated biochemical evaluation and imaging studies are negative. Her paternal uncle, aunt and cousins are also phenotypically healthy with no indications from either biochemical or imaging studies as they denied further evaluation. In addition, her paternal grandfather of unknown genotype died at the age of 85 years while her paternal grandmother is alive and has no problems, being 86 years old at time of writing.

      CasePresentingHPOs: HP:0009713; HP:0006880; HP:0009711; HP:0001737 (Spinal hemangioblastoma, cerebellar hemangioblastoma, retinal hemangioblastoma, pancreatic cyst)

      CaseHPOFreeText: The 16Y female patient first presented with back pain, headaches, numbness, dizziness, weakness and pain in the arms and the legs at 12Y. A hemangioblastoma in the thoracic spine and a hemangioblastoma in the neck were found. A year later, at the age of 13, multiple HBs in the right and smaller lesions in the left eye were found. Two asymptomatic cysts (2 cm and 0.8 cm) in the body of the pancreas were also found. During her recent evaluation, at the age of 16 years, MRI imaging revealed a large HB extending from the cerebellum to the Th8 vertebrae, with extensive solid and cystic nodules inside the mass and increased dimensions of the spinal cord.

      CaseNotHPOs: N/A

      CaseNotHPOFreeText: N/A

      CasePreviousTesting: N/A

      PreviouslyPublished: N/A

      SupplementalData: N/A

      Variant: p.Q145*(c.433C>T)

      LegacyVariant: N/A

      ClinVarID: 625249, https://www.ncbi.nlm.nih.gov/clinvar/variation/625249/

      gnomAD: N/A

      VariantEvidence: It has been documented that dynamic organisation of pVHL–HIF1α recognition is focally centred on Gln145 within the L7 loop, and its tumourigenic mutant Q145H abolishes almost all of the correlated dynamic motions. In this report, Q145 is substituted by a stop codon, p.Q145X. This is a nonsense mutation resulting to a truncated VHL protein that lacks the last 68 amino acids and thus its function is abolished.

      MutationType: stop_gained

      CivicName: Q145*(c.433C>T)

      MultipleGeneVariants: N/A

    1. At 21 h post-transfection, the EGFP-tagged MyHC-slow was distributed throughout the cytoplasm, aggregating into discrete structures. The wild-type aggregates formed long, filamentous structures (Fig. 6A, B). The Arg1712Trp mutant MyHC-slow instead formed many small, round inclusions (Fig. 6C).

      ExperimentalAssay

      Variant: NM_000257.4(MYH7):c.5134C>T (p.Arg1712Trp), homozygous

      ClinVar: 14118, https://www.ncbi.nlm.nih.gov/clinvar/variation/14118/

    1. German Landrace pigs

      ExperimentalAssay: The authors used TALEN genome editing to introduce the orthologous mutation in MYH7 into pigs. Sanger sequencing verified successful knock-in. Most of the pigs using embryos with this mutation died prematurely, with the surviving cohort showing phenotypes of HCM similar to those in human patients. Whole genome sequencing was also performed to test for off-target mutations, but none were found.


      Human Variant

      Variant: NM_000257.3:c.2167C>G (p.Arg723Gly)

      ClinVar: 42885 https://www.ncbi.nlm.nih.gov/clinvar/variation/42885/

      gnomAD: Not in gnomAD


      Pig Variant

      Variant: NM_213855:c.2223C>G

      This variant is orthologous to the above mutation in humans.

    1. codon 120, exon 3 (R120*)

      Clinical case report of a 32-year-old male presenting with hematuria. Blood and tissue samples were isolated and samples were paired-end multiplex sequenced on the Illumina HiSeq platform to a median target depth of >100×.A germline de novo nonsense mutation, c.358A>T leading to an early stop codon, was confirmed on exon 3 of the VHL gene. The man also presented with multiple renal cysts; renal cell carcinoma; capillary retinal angiomas; brain hemangioma; and spinal hemangioma. Confirmation of paternity and maternity was not described, therefore assumed de novo.

    1. The mother, aged 49, had a history of well-controlled hypertension. Supine plasma normetanephrine was elevated (1382 pmol/l, RR <900 pmol/l) whilst plasma metanephrine was normal (117 pmol/l, RR <500 pmol/l). MRI of the brain, spine and abdomen revealed multiple, asymptomatic VHL-associated lesions. These included a spinal haemangioblastoma, bilateral T2-hyperintense adrenal lesions (18 mm and 12 mm), subsequently confirmed to be PCCs, and two pancreatic lesions (11 mm and 16 mm), subsequently confirmed to be grade 1 neuroendocrine tumours.

      PatientID: N/A (mother)

      KindredID: 1

      Case: F, 49Y0M, Ethnicity Unknown

      DiseaseAssertion: VHL

      FamilyInfo: Prior to her daughter being tested, there was no family history of PCC/paraganglioma (PGL), multiple endocrine neoplasia type 2 (MEN2), neurofibromatosis type 1 (NF1) or VHL. Genetic testing and observation found the mutation (c.361G>C) in her daughter, who also presented with extraadrenal and adrenal pheochromocytoma.

      CasePresentingHPOs: HP:0009713; HP:0006748; HP:0030405 (spinal hemangioblastoma, adrenal pheochromocytoma, pancreatic endocrine tumor)

      CaseHPOFreeText: MRI of the brain, spine and abdomen revealed multiple, asymptomatic VHL-associated lesions. These included a spinal haemangioblastoma, bilateral T2-hyperintense adrenal lesions (18 mm and 12 mm), subsequently confirmed to be PCCs, and two pancreatic lesions (11 mm and 16 mm), subsequently confirmed to be grade 1 neuroendocrine tumours.

      CaseNotHPOs: N/A

      CaseNotHPOFreeText: N/A

      CasePreviousTesting: N/A

      PreviouslyPublished: SDHA, SDHB

      SupplementalData: N/A

      Variant: p.D121H (c.361G>C)

      LegacyVariant: N/A

      CaseProblemVariantFreeText: N/A

      ClinVarID: N/A

      CAID: CA351753752 https://reg.clinicalgenome.org/redmine/projects/registry/genboree_registry/allele?hgvsOrDescriptor=NM_000551.3%3Ac.361G%3EC

      gnomAD: N/A

      VariantEvidence: N/A

      MutationType: missense_variant;transversion

      CivicName: D121H (c.361G>C)

      MultipleGeneVariants: N/A