2,467 Matching Annotations
  1. Last 7 days
    1. c.496_506del11 (p.Val166Serfs*4) in seven individuals, belonging to two pedigrees.

      PatientID: 82

      KindredID: 82

      Case: Sex Unknown, Age Unknown, Ethnicity Unknown

      DiseaseAssertion: VHL

      FamilyInfo: N/A

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

      CaseHPOFreeText: N/A

      CaseNotHPOs: HP:0006770; HP:0100634; HP:0030405; HP:0030421 (clear cell renal cell carcinoma; Neuroendocrine neoplasm, pancreatic neuroendocrine neoplasm, Epididymal neoplasm)

      CaseNotHPOFreeText: N/A

      CasePreviousTesting: N/A

      PreviouslyPublished: 29437867 (likely family 17 - see here for more info)

      SupplementalData: Yes; see table S1 for VHL subject genetic and manifestation information.

      Variant: p.V166Sfs*4 (c.496_506del)

      LegacyVariant: N/A

      CaseProblemVariantFreeText: N/A

      ClinVarID: 223229 https://www.ncbi.nlm.nih.gov/clinvar/variation/223229/

      CAID: N/A

      gnomAD: N/A

      VariantEvidence: N/A

      MutationType: minus_2_frameshift_variant

      CivicName: V166Sfs*4 (c.496_506del)

      MultipleGeneVariants: N/A

    1. Patient 1 The first patient had no familial history of VHL disease and was 21 years old when he experienced a sudden right hearing loss. The resulting cophosis was irreversible. The radiological work-up revealed an osteolytic mass of the right temporal bone of heterogeneous signal on both T1- and T2-weighted images (Fig. 1), consistent with the diagnosis of endolymphatic sac tumor. The tumor invaded the otic capsule and the petrous apex but did not extend in the cerebellopontine angle. Its mean tumor diameter (MTD) at diagnosis was approximately 2.6 cm (formula—MTD = (length×width×height)1/3MTD = (length×width×height)1/3 {\hbox{MTD = }}{\left( {{\hbox{length}} \times {\hbox{width}} \times {\hbox{height}}} \right)^{{1/3}}} ) [16]. The rest of the neurological exam was normal and a conservative management was decided. During follow-up, the patient suffered from other manifestations of VHL disease: retinal and central nervous system hemangioblastomas, pheochromocytoma, renal tumors, and pancreatic cysts. The germline mutation of the VHL gene was also identified (c.337C>T, p.Arg113X). After 20 years of radiological surveillance, the size of his endolymphatic sac tumor remains stable (Fig. 2). Apart from his deafness, the patient does not suffer from any vestibular symptoms and his facial function is normal (House and Brackmann grade I).

      PatientID: 1

      KindredID: 1

      Case: M, 41Y0M, Ethnicity Unknown

      DiseaseAssertion: assumed VHL

      FamilyInfo: No family history of VHL disease.

      CasePresentingHPOs: HP:0030393; HP:0009711; HP:0010797; HP:0002666; HP:0009726; HP:0001737 (endolymphatic sac tumor, retinal capillary hemangioma, hemangioblastoma, pheochromocytoma, renal neoplasm, pancreatic cysts)

      CaseHPOFreeText: patient was 21 years old when he experienced a sudden right hearing loss (cophosis). During a follow-up, the patient suffered from other manifestations of VHL disease mentioned above.

      CaseNotHPOs: N/A

      CaseNotHPOFreeText: N/A

      CasePreviousTesting: N/A

      PreviouslyPublished: N/A

      SupplementalData: N/A

      Variant: p.R113* (c.337C>T)

      LegacyVariant: N/A

      CaseProblemVariantFreeText: N/A

      ClinVarID: 220414 https://www.ncbi.nlm.nih.gov/clinvar/variation/220414/

      CAID: N/A

      gnomAD: N/A

      VariantEvidence: N/A

      MutationType: stop_gained

      CivicName: R113*(c.337C>T)

      MultipleGeneVariants: N/A

    1. PatientID: 9

      KindredID: 9

      Case: F, 16Y0M, Korean

      DiseaseAssertion: VHL

      FamilyInfo: No family history of VHL.

      CohortInfo: 26 Korean patients with more than one HAB in the CNS or eye, a single HAB in the CNS or retina plus a visceral manifestation (multiple renal, pancreatic or hepatic cysts, pheochromocytoma and RCC) and positive family history plus any one of the above manifestations.

      CasePresentingHPOs: HP:0009711 (Retinal capillary hemangioma)

      CaseHPOFreeText: Diagnosed with VHL Type 1.

      CaseNotHPOs: HP:0002666; HP:0005584; HP:0010797 (Pheochromocytoma, Renal cell carcinoma, Hemangioblastoma)

      CaseNotHPOFreeText: N/A

      CasePreviousTesting: N/A

      PreviouslyPublished: N/A

      SupplementalData: N/A

      Variant: p.E70K (c.208G>A)

      LegacyVariant: N/A

      CaseProblemVariantFreeText: N/A

      ClinVarID: 43598, https://www.ncbi.nlm.nih.gov/clinvar/variation/43598/

      CAID: N/A

      gnomAD: 0.000004365, https://gnomad.broadinstitute.org/variant/3-10183739-G-A

      VariantEvidence: N/A

      MutationType: missense_variant;transition

      CivicName: E70K (c.208G>A)

      MultipleGeneVariants: N/A

    2. PatientID: 12

      KindredID: 12

      Case: F, 41Y0M, Korean

      DiseaseAssertion: VHL

      FamilyInfo: Daughter has the same mutation and presented with CNS hemangioblastoma.

      CohortInfo: 26 Korean patients with more than one HAB in the CNS or eye, a single HAB in the CNS or retina plus a visceral manifestation (multiple renal, pancreatic or hepatic cysts, pheochromocytoma and RCC) and positive family history plus any one of the above manifestations.

      CasePresentingHPOs: HP:0005584 (Renal cell carcinoma)

      CaseHPOFreeText: Other phenotypes presented but not specified (one or more of: pancreatic cyst or tumor, renal or hepatic cyst). Diagnosed with VHL Type 1.

      CaseNotHPOs: HP:0002666; HP:0009711; HP:0010797 (Pheochromocytoma, Retinal capillary hemangioma, Hemangioblastoma)

      CaseNotHPOFreeText: N/A

      CasePreviousTesting: N/A

      PreviouslyPublished: https://doi.org/10.3803/jkes.2006.21.3.239

      SupplementalData: N/A

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

      LegacyVariant: N/A

      CaseProblemVariantFreeText: N/A

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

      CAID: N/A

      gnomAD: N/A

      VariantEvidence: N/A

      MutationType: missense_variant;transition; stop_gained

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

      MultipleGeneVariants: N/A

    1. PatientID: 431

      KindredID: 431

      Case: Sex Unknown, 15Y0M, Ethnicity Unknown

      DiseaseAssertion: VHL

      FamilyInfo: N/A

      CasePresentingHPOs: HP:0010797; HP:0009711 (Hemangioblastoma, Retinal capillary hemangioma)

      CaseHPOFreeText: CNS and retinal hemangioblastoma.

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

      CaseNotHPOFreeText: N/A

      CasePreviousTesting: N/A

      PreviouslyPublished:N/A

      SupplementalData: Table S1, S2 and S3

      Variant: Exon 3 Deletion (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; deletion

      CivicName: Exon 3 Deletion

      MultipleGeneVariants: N/A

    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. The L153P (c.458T>C) germline missense mutation of the VHL gene was found in a 36 yr old VHL patient with renal cysts as well as central nervous system and retinal hemangioblastoma (index case 191).

    3. PatientID: 83

      KindredID: 83

      Case: Sex Unknown, 11Y0M, Ethnicity Unknown

      DiseaseAssertion: VHL

      FamilyInfo: N/A

      CasePresentingHPOs: HP:0010797 (Hemangioblastoma)

      CaseHPOFreeText: CNS hemangioblastoma.

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

      CaseNotHPOFreeText: N/A

      CasePreviousTesting: N/A

      PreviouslyPublished:N/A

      SupplementalData: Table S1, S2 and S3

      Variant: Partial Deletion (4.6kb)

      LegacyVariant: N/A

      CaseProblemVariantFreeText: N/A

      ClinVarID: N/A

      CAID: N/A

      gnomAD: N/A

      VariantEvidence: N/A

      MutationType: deletion

      CivicName: Null (Partial deletion of 4.6kb)

      MultipleGeneVariants: N/A

    4. 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

    5. PatientID: 246

      KindredID: 246

      Case: Sex Unknown, 26Y0M, Ethnicity Unknown

      DiseaseAssertion: VHL

      FamilyInfo: N/A

      CasePresentingHPOs: HP:0010797; HP:0009711; HP:0006770 (Hemangioblastoma, Retinal capillary hemangioma, Clear cell renal cell carcinoma)

      CaseHPOFreeText: CNS and retinal hemangioblastoma and clear cell renal cell carcinoma.

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

      CaseNotHPOFreeText: N/A

      CasePreviousTesting: N/A

      PreviouslyPublished:N/A

      SupplementalData: Table S1, S2 and S3

      Variant: Partial Deletion (0.7kb)

      LegacyVariant: N/A

      CaseProblemVariantFreeText: N/A

      ClinVarID: N/A

      CAID: N/A

      gnomAD: N/A

      VariantEvidence: N/A

      MutationType: deletion

      CivicName: Partial deletion of 0.7kb

      MultipleGeneVariants: N/A

    6. 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

    7. 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

    1. IV 10 21 2 pheo (12 years) 1 retinal hb (10 years) M c.278G > A (p.Gly93Asp)

      PatientID: IV

      KindredID: 3

      Case: Sex Unknown, 21Y0M, Danish

      DiseaseAssertion: VHL

      FamilyInfo: 3 other family members presented with his VHL mutation. Patient 3-I was asymptomatic. Patients 3-II and 3-III both presented with pheochromocytoma at 15Y.

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

      CaseHPOFreeText: Diagnosed with VHL at age 10Y. Presented with pheochromocytoma at 12Y and retinal hemangioblastoma at 10Y. Age at the end of study: 21Y.

      CaseNotHPOs: N/A

      CaseNotHPOFreeText: N/A

      CasePreviousTesting: N/A

      PreviouslyPublished: N/A

      SupplementalData: N/A

      Variant: p.G93D (c.278G>A)

      LegacyVariant: N/A

      CaseProblemVariantFreeText: N/A

      ClinVarID: 496054, https://www.ncbi.nlm.nih.gov/clinvar/variation/496054/

      CAID: N/A

      gnomAD: N/A

      VariantEvidence: N/A

      MutationType: missense_variant;transition

      CivicName: G93D (c.278G>A)

      MultipleGeneVariants: N/A

    2. 4 I 7 Dead at age 53 years 2 retinal hb (7 + 14 years) M c.407 T > C (p.Phe136Ser)

      PatientID: I

      KindredID: 4

      Case: Sex Unknown, 53Y0M, Danish

      DiseaseAssertion: VHL

      FamilyInfo: N/A

      CasePresentingHPOs: HP:0009711 (Retinal capillary hemangioma)

      CaseHPOFreeText: Diagnosed with VHL at age 7Y. Presented with retinal hemangioblastoma at 7Y and 14Y. Age of death: 53Y.

      CaseNotHPOs: N/A

      CaseNotHPOFreeText: N/A

      CasePreviousTesting: N/A

      PreviouslyPublished: N/A

      SupplementalData: N/A

      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: N/A

      VariantEvidence: N/A

      MutationType: missense_variant;transition

      CivicName: F136S (c.407T>C)

      MultipleGeneVariants: N/A

    1. 18 c.509T>A p.Val170Asp p.V170D Familial VHL

      GroupID/ KindredID: 18

      DiseaseAssertion: VHL

      GroupSize: 14

      GroupNumberMales: N/A

      GroupNumberFemales: N/A

      GroupEthnicity: N/A

      GroupAgeRange: N/A

      GroupInfo: 14 registrants belonging to the same family (18) have the germline VHL mutation.

      GroupPresentingHPOs:HP:0009711; HP:0010797; HP:0001737; HP:0005584; HP:0000107; HP:0002666; HP:0030393; HP:0001407 (retinal capillary hemangioma, hemangioblastoma, pancreatic cysts, renal cell carcinoma, renal cyst, pheochromocytoma, endolymphatic sac tumor, hepatic cysts)

      GroupHPOFreeText: 6 had retinal hemangioblastoma, 9 had CNS hemangioblastoma, 7 had renal cell carcinoma, 8 had renal cysts, 4 had pheochromocytoma, 5 had pancreatic cysts, 2 had endolymphatic sac tumors, 1 with adnexal papillary tumor of probably mesonephric origin, and 5 had hepatic cysts.

      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.V170D (c.509T>A)

      CaseProblemVariantFreeText: N/A

      LegacyVariant: N/A

      ClinVarID: 625256 https://www.ncbi.nlm.nih.gov/clinvar/variation/625256/

      CAID: N/A

      gnomAD: N/A

      VariantEvidence: N/A

      MutationType: missense_variant;transversion

      CivicName: V170D (c.509T>A)

      MultipleGeneVariants: N/A

    2. 11 c.452T>C p.Ile151Thr p.I151T Familial VHL

      Between 1994 and 2001, the Dutch VHL working group conducted DNA analysis on 146 probands with VHL-associated manifestations. DNA of probands was extracted from peripheral blood samples. Exons 1, 2 and 3 of the VHL gene and their flanking untranslated and intronic coding sequences were amplified by PCR and subjected to semi-automated sequence analysis. Screening for structural rearrangements, including deletions, involving the VHL gene was performed by Southern blot analysis and the multiplex ligation-dependent probe amplification (MLPA) assay. Deletions encompassing the entire VHL gene were confirmed by FISH analysis on lymphocytes from affected individuals. VHL mutations were identified in 43 families. This mutation (c.452T>C) was detected in a VHL patient with CNS hemangioblastomas and renal cell carcinoma (family no. 11). This was published in a future publication: PMID: 32179488.

    1. c.99_100InsA*

      PatientID: None (XIII)

      KindredID: 7

      Case: Sex and Ethnicity unknown; Age >18Y0M

      DiseaseAssertion: asymptomatic

      FamilyInfo: Total of 13 family members belonging to Family 7 (see Table 2; or follow KindredID 7)

      CasePresentingHPOs: None

      CaseHPOFreeText: N/A

      CaseNotHPOs: N/A

      CaseNotHPOFreeText: N/A

      CasePreviousTesting: N/A

      PreviouslyPublished: 16572651

      SupplementalData: N/A

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

      CaseProblemVariantFreeText: N/A

      LegacyVariant: N/A

      ClinVarID: N/A

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

      gnomAD: N/A

      VariantEvidence: N/A

      MutationType: plus_1_frameshift_variant

      CivicName: G34Rfs (c.99_100insA)

      MultipleGeneVariants: N/A

    1. NephewExon 1 DeletionAsy––––––

      PatientID: None

      KindredID: 16

      Case: M, Age Unknown, Chinese

      DiseaseAssertion:Asymptomatic

      FamilyInfo: Positive. The patient's uncle was the proband and presented with hemangioblastoma, renal cell carcinoma, and abnormality of the pancreas. The patient's mother and cousin also had the mutation but were asymptomatic.

      CasePresentingHPOs: N/A

      CaseHPOFreeText: N/A

      CaseNotHPOs: HP:0010797, HP:0009711, HP:0002666, HP:0005584, HP:0001732 (hemangioblastoma, retinal capillary hemangioma, pheochromocytoma, renal cell carcinoma, abnormality of the pancreas)

      CaseNotHPOFreeText: The patient did not present with epididymal or ovarian cystadenomas.

      CasePreviousTesting: N/A

      PreviouslyPublished:29330336

      Variant: Exon 1 deletion

      LegacyVariant: N/A

      CaseProblemVariantFreeText: N/A

      ClinVar: N/A

      CAID: N/A

      gnomAD: N/A

      VariantEvidence: N/A

      MutationType: exon_loss_variant

      CivicName: Exon 1 Deletion

      MultipleGeneVariants: N/A

    2. C.292T > A, p.Tyr98Asn

      Using polymerase chain reaction (PCR)-direct sequencing and universal primer quantitative fluorescent multiplex–PCR, mutations in VHL gene in 19 VHL disease families recruited from the Department of Urology, Peking University First Hospital in the period from 2009 to 2012 were examined. One proband and their sister (family 1) were found to carry the mutation c.292T>A in exon 1 of the VHL gene. The proband presented with hemangioblastoma at age 35, retinal angioma and pancreatic cysts or tumours at age 37, and renal cell carcinoma at age 39. The patient had positive VHL family history and their first sister also carried this germline mutation but was asympromatic. Patient's mother did not undergo genetic testing but had a hemangioblastoma at age 50 and a pancreatic cyst or tumour at age 62. Another one of the patient's sisters presented with hemangioblastoma (age 40), renal cell carcinoma (age 43), and pancreatic cysts or tumours (age 43). This patient died before diagnosis. The proband's brother also died before diagnosis and presented with hemangioblastoma and retinal angioma at age 27.This family was previously published in 29330336.

    1. c.461C > T p.Pro154Leu

      216 patients with clinically expected VHL disease due to family history or presence of VHL typical tumours were routinely examined in an eye centre in Germany between January 2019 and January 2020, majority of which were of European descent (~95%). Since data on the genotype–phenotype correlation of the onset of Retinal Hemangioblastoma (RH) is scarce in relation to VHL disease, this study wanted to inversitage the relationship between VHL gene variants (truncating vs single amino acid substitutions) and the ocular phenotype of the disease. 42 different rare VHL gene variants in 148 patients were detected - some of whom had RH and some who did not. Although date of onset of RH, as well as data on central nervous system haemangioblastomas (CNSH), pheochromocytoma/paraganglioma (PPGL), clear cell renalcell carcinoma (ccRCC) and pancreatic neuroendocrine neoplasm (PNEN) were collected, it was not reported on a per patient basis and therefore could not be discussed per variant. There was 1 patient reported with the c.461C>T (p.P154L) mutation. This member presented with retinal hemangiomas. No family information was provided.

    2. 2 (100)

      GroupID: 37

      DiseaseAssertion: VHL

      GroupSize: 2

      GroupNumberMales: N/A

      GroupNumberFemales: N/A

      GroupEthnicity: N/A

      GroupAgeRange: N/A

      GroupInfo: a retrospective cohort study from an eye centre in Germany involved 148 VHL patients and their genetic data involved in retinal capillary hemangiomas.

      GroupPresentingHPOs: HP:0009711 (retinal capillary hemangioma)

      GroupHPOFreeText: These 2 patients with a c.463G>C mutation had retinal capillary hemangiomas. Other VHL manifestations were discussed but not per- variant.

      GroupNotHPOs: N/A

      GroupNotHPOFreeText: N/A

      GroupPreviousTesting: N/A

      PreviouslyPublished: N/A

      SupplementalData: N/A

      Variant: p.V155L (c.463G>C)

      LegacyVariant: N/A

      GroupProblemVariantFreeText: N/A

      ClinVarID: 1023631 https://www.ncbi.nlm.nih.gov/clinvar/variation/1023631

      CAID: N/A

      gnomAD: N/A

      VariantEvidence: N/A

      MutationType: missense_variant; transversion

      CivicName: V155L (c.463G>C)

      MultipleGeneVariants: N/A

    3. 2 (66.7)

      GroupID: 14a

      DiseaseAssertion: VHL

      GroupSize: 2

      GroupNumberMales: N/A

      GroupNumberFemales: N/A

      GroupEthnicity: N/A

      GroupAgeRange: N/A

      GroupInfo: a retrospective cohort study from an eye centre in Germany involved 148 VHL patients and their genetic data involved in retinal capillary hemangiomas.

      GroupPresentingHPOs: HP:0009711 (retinal capillary hemangioma)

      GroupHPOFreeText: These 2/3 patients with a Q164* (c.490C>T) mutation had retinal capillary hemangiomas. Other VHL manifestations were discussed but not per- variant.

      GroupNotHPOs: N/A

      GroupNotHPOFreeText: N/A

      GroupPreviousTesting: N/A

      PreviouslyPublished: N/A

      SupplementalData: N/A

      Variant: p.Q164* (c.490C>T)

      LegacyVariant: N/A

      GroupProblemVariantFreeText: N/A

      ClinVarID: 223228 https://www.ncbi.nlm.nih.gov/clinvar/variation/223228/

      CAID: N/A

      gnomAD: N/A

      VariantEvidence: N/A

      MutationType: stop_gained

      CivicName: Q164* (c.490C>T)

      MultipleGeneVariants: N/A

    1. PatientID: 9

      KindredID: 2

      Case: F, 29Y0M, African/African American

      DiseaseAssertion: VHL

      FamilyInfo: She was 23 weeks pregnant at the time of a pheochromocytoma resection. Her 6-year-old daughter screened positive for the mutation; her 8-year-old son was negative. Both mother (although no testing conducted) and daughter were said to be investigated further and monitored long-term.

      CasePresentingHPOs: HP:0006748; HP:0009713 (adrenal pheochromocytoma; spinal hemangioblastoma)

      CaseHPOFreeText: At the time, the patient was 23 weeks pregnant and had bilateral adrenal phaeochromocytomas removed. There were no clinical features of VHL syndrome; however, MRI showed a haemangioblastoma in the cervical spine.

      CaseNotHPOs: N/A

      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

    1. 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

    2. 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

    3. 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

    1. DNA extraction, PCR, single strand conformation polymorphism and/or denaturing high-performance liquid chromatography, heteroduplex analysis and sequencing Screening for mutations in the SDHD, SDHB and SDHC genes was performed in all patients. RET and VHL were analysed in all patients with abdominal pheochromocytoma/paraganglioma and a subset of patients with head and neck paraganglioma (27/36). Venous blood samples were drawn for all participants and DNA was extracted from whole blood (DNA purification kit, Gentra Systems Inc, Minneapolis, Minnesota, USA). The different exons and intron–exon boundaries of the three SDH and the RET and VHL genes were amplified by PCR. Screening for mutations was performed by single strand conformation polymorphism (SSCP), and heteroduplex analysis, as described [15] or by denaturing high performance liquid chromatography (dHPLC) analysis, using the WAVE 3500 HT system (Transgenomic, Inc., Omaha, Nebraska, USA). Fragments showing abnormal migration were reamplified and sequenced on a CEQ2000 capillary sequencer (Beckman Coulter, High Wycombe, UK).

      ArticleReferenceSequence: Not specified- Assumption: Nucleotide change is not specified in the paper, only protein coding change is. cDNA variant was inferred based on protein coding change, and reported based on VHL reference sequence NM_000551.3

      GenotypingMethod: Screening for mutations was performed by single strand conformation polymorphism (SSCP), and heteroduplex analysis, as described or by denaturing high performance liquid chromatography (dHPLC) analysis, using the WAVE 3500 HT system (Transgenomic, Inc., Omaha, Nebraska, USA). Fragments showing abnormal migration were reamplified and sequenced on a CEQ2000 capillary sequencer (Beckman Coulter, High Wycombe, UK).

      SamplingMethod: whole blood

    2. D126N

      Patients with either sporadic or familial pheochromocytoma or paraganglioma diagnosed at or referred to the Cliniques Universitaires Saint Luc (Universite´ catholique de Louvain) from May 2003 to May 2006 had DNA from peripheral blood screened for the coding parts of SDH, VHL and RET genes, performed by SSCP. A VHL germline mutation (D126N) was found in a Belgian patient with sporadic right jugulotympanic paraganglioma, diagnosed at 53, without any other VHL phenotypes. This patient was previously published in 12393546.

    1. 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. MSL128F1 (5.6)1 (3.8)

      GroupID: 8

      Case: Age, Sex, Ethnicity Unknown

      DiseaseAssertion: VHL

      FamilyInfo: 1 individual belonging to 1 family was mentioned with this VHL mutation. No other family info was provided.

      CasePresentingHPOs: HP:0002666 (pheochromocytoma)

      CaseHPOFreeText: Other manifestations aside from pheochromocytoma are possible; but not specified.

      CaseNotHPOs: N/A

      CaseNotHPOFreeText: N/A

      CasePreviousTesting: N/A

      PreviouslyPublished: N/A

      SupplementalData: N/A

      Variant: p.L128F (c.381_382delinsTT)

      CaseProblemVariantFreeText: Paper called "L" Lysine but it matches to Leucine in all 3 cases. Likely an error in word choice by authors.

      LegacyVariant: N/A

      ClinVarID: 223203 https://www.ncbi.nlm.nih.gov/clinvar/variation/223203

      CAID: CA357088 http://reg.clinicalgenome.org/redmine/projects/registry/genboree_registry/allele?hgvsOrDescriptor=NM_000551.3%3Ac.381_382delinsTT

      gnomAD: N/A

      VariantEvidence: N/A

      MutationType: delins

      CivicName: L128F (c.381_382delinsTT)

      MultipleGeneVariants: N/A

    1. PatientID: 162

      KindredID: 62

      Case: F, 14Y0M, Chinese

      DiseaseAssertion: VHL

      FamilyInfo: The patient's mother presented with a CNS hemangioblastoma at age 28, and a renal cell carcinoma, multiple pancreatic cysts/tumors, and a pheochromocytoma at age 41.

      CasePresentingHPOs: HP:0010797; HP:0001737; HP:0001732 (Hemangioblastoma, Pancreatic cysts, Abnormality of the pancreas)

      CaseHPOFreeText: The proband presented with a CNS hemangioblastoma and multiple pancreatic cysts/tumors at age 14.

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

      CaseNotHPOFreeText: N/A

      CasePreviousTesting: N/A

      PreviouslyPublished: This cohort was also published in a later paper by Wang et al., 2018 (PMID: 29330336).

      SupplementalData: Patient and family genotype-phenotype information is listed in Supplementary Table 1.

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

      LegacyVariant: N/A

      CaseProblemVariantFreeText: N/A

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

      CAID: N/A

      gnomAD: N/A

      VariantEvidence: N/A

      MutationType: missense_variant;transition

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

      MultipleGeneVariants: N/A

    2. PatientID: 271

      KindredID: 105

      Case: F, 42Y0M, Chinese

      DiseaseAssertion: VHL

      FamilyInfo: N/A

      CasePresentingHPOs: HP:0001737; HP:0001732; HP:0010797 (Pancreatic cysts, Abnormality of the pancreas, Hemangioblastoma)

      CaseHPOFreeText: The proband presented at age 48 with renal cell carcinoma, multiple pancreatic cysts/tumors, and pheochromocytoma.

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

      CaseNotHPOFreeText: N/A

      CasePreviousTesting: N/A

      PreviouslyPublished: This cohort was also published in a later paper by Wang et al., 2018 (PMID: 29330336).

      SupplementalData: Patient and family genotype-phenotype information is listed in Supplementary Table 1.

      Variant: Exon 2 Deletion (c.341-?_463+?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 2 Deletion

      MultipleGeneVariants: N/A

    3. PatientID: 124

      KindredID: 44

      Case: M, Age 24Y0M, Chinese

      DiseaseAssertion: VHL

      FamilyInfo: N/A

      CasePresentingHPOs: HP:0010797; HP:0001737; HP:0001732; HP:0005584 (Hemangioblastoma, Pancreatic cysts, Abnormality of the pancreas, Renal cell carcinoma)

      CaseHPOFreeText: The proband presented with a CNS hemangioblastoma at 18, renal cell carcinoma and multiple pancreatic cysts/tumors at 24.

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

      CaseNotHPOFreeText: N/A

      CasePreviousTesting: N/A

      PreviouslyPublished: This patient was also published in an earlier paper by Wang et al., 2014 (PMID: 24581539) and a later paper by Wang et al., 2018 (PMID: 29330336).

      SupplementalData: Patient and family genotype-phenotype information is listed in Supplementary Table 1.

      Variant: p.W117S (c.350G>C)

      LegacyVariant: N/A

      CaseProblemVariantFreeText: N/A

      ClinVarID: N/A

      CAID: CA351753671; https://reg.clinicalgenome.org/redmine/projects/registry/genboree_registry/allele?hgvsOrDescriptor=NM_000551.3%3Ac.350G%3EC

      gnomAD: N/A

      VariantEvidence: N/A

      MutationType: missense_variant;transversion

      CivicName: W117S (c.350G>C)

      MultipleGeneVariants: N/A

    4. PatientID: 194

      KindredID: 74

      Case: F, 36Y0M, Chinese

      DiseaseAssertion: VHL

      FamilyInfo: The proband, patient 193, has a mother (patient 194) who was also found to have the same germline mutation. The proband had a CNS hemangioblastoma at age 16.

      CasePresentingHPOs: HP:0002666 (Pheochromocytoma)

      CaseHPOFreeText: The patient presented with a pheochromocytoma at age 36.

      CaseNotHPOs: HP:0005584; HP:0009711; HP:0001737; HP:0001732; HP:0010797 (Renal cell carcinoma, Retinal capillary hemangioma, Pancreatic cysts, Abnormality of the pancreas, CNS hemangioblastoma)

      CaseNotHPOFreeText: N/A

      CasePreviousTesting: N/A

      PreviouslyPublished: This patient was also published in a later paper by Wang et al., 2018 (PMID: 29330336).

      SupplementalData: Patient and family genotype-phenotype information is listed in Supplementary Table 1.

      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: N/A

    5. PatientID: 146

      KindredID: 52

      Case: M, Age Unknown, Chinese

      DiseaseAssertion: Asymptomatic

      FamilyInfo: The proband (patient 138) had multiple family members affected with the mutation. Their daughter (pt 139) was asymptomatic at the time of assessment; their son (pt 140) was also asymptomatic at the time of assessment; their mother (pt 141) presented with a CNS hemangioblastoma at 66, renal cell carcinoma at 69, and multiple pancreatic cysts/tumors at 66; their sister 1 (pt 142) presented with a CNS hemangioblastoma at 32, renal cell carcinoma at 36, and multiple pancreatic cysts/tumors at 36; the son of sister 1 was asymptomatic at the time of analysis; the daughter of sister 1 was asymptomatic at the time of analysis; the proband's sister 2 presented at age 39 with CNS hemangioblastoma, renal cell carcinoma, and multiple pancreatic cysts/tumors; and the son of sister 2 was asymptomatic at the time of analysis. All members of this family were genetically confirmed to have this mutation.

      CasePresentingHPOs: N/A

      CaseHPOFreeText: The proband's nephew (son of sister 2) was asymptomatic at the time of assessment.

      CaseNotHPOs: HP:0010797; HP:0005584; HP:0001737; HP:0001732; HP:0002666; HP:0009711 (Hemangioblastoma, Renal cell carcinoma, Pancreatic cysts, Abnormality of the pancreas, Pheochromocytoma, Retinal capillary hemangioma)

      CaseNotHPOFreeText: N/A

      CasePreviousTesting: N/A

      PreviouslyPublished: This patient was also published in a later paper by Wang et al., 2018 (PMID: 29330336).

      SupplementalData: Patient and family genotype-phenotype information is listed in Supplementary Table 1.

      Variant: c.464-1G>C

      LegacyVariant: N/A

      CaseProblemVariantFreeText: N/A

      ClinVarID: 223220; https://www.ncbi.nlm.nih.gov/clinvar/variation/223220/

      CAID: N/A

      gnomAD: N/A

      VariantEvidence: N/A

      MutationType: splice_site_variant

      CivicName: Splice Site (c.464-1G>C)

      MultipleGeneVariants: N/A

    6. PatientID: 184

      KindredID: 71

      Case: M, Age 27Y0M, Chinese

      DiseaseAssertion: VHL

      FamilyInfo: The proband's mother (patient 185) was confirmed with the mutation but was asymptomatic at the time of testing. The proband (patient 184) presented with renal cell carcinoma at 27, and multiple pancreatic cysts/tumors and a pheochromocytoma at age 24.

      CasePresentingHPOs: HP:0005584, HP:0002666, HP:0001737, HP:0001732 (Renal cell carcinoma, Pheochromocytoma, Pancreatic cysts, Abnormality of the pancreas)

      CaseHPOFreeText: The proband presented with renal cell carcinoma at 27, and multiple pancreatic cysts/tumors and a pheochromocytoma at age 24.

      CaseNotHPOs: HP:0010797; HP:0009711 (Hemangioblastoma, Retinal capillary hemangioma)

      CaseNotHPOFreeText: N/A

      CasePreviousTesting: N/A

      PreviouslyPublished: This patient was also published in an earlier paper by Wang et al., 2014 (PMID 24581539) as well as a later paper by Wang et al., 2018 (PMID: 29330336).

      SupplementalData: Patient and family genotype-phenotype information is listed in Supplementary Table 1.

      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: N/A

    7. PatientID: 265

      KindredID: 104

      Case: M, 48Y0M, Chinese

      DiseaseAssertion: VHL

      FamilyInfo: The proband (patient 265) has multiple family members who presented with VHL symptoms but were unconfirmed with the mutation, due to no DNA sample being available or due to death before diagnosis. The proband's son (patient 266) presented with a CNS hemangioblastoma at 19 and retinal angioma at 27. Their first brother (brother 1, patient 267) presented with a CNS hemangioblastoma at 36 and a retinal angioma at 46. Their nephew (son of brother 1, patient 267) presented with a retinal angioma at 16. Their second brother (brother 2, patient 268) had a CNS hemangioblastoma at 30, retinal angioma at 20, and renal cell carcinoma at 41. The proband's second nephew (son of brother 2, patient 269) had a retinal angioma at age 16.

      CasePresentingHPOs: HP:0001737; HP:0001732; HP:0005584; HP:0002666 (Pancreatic cysts, Abnormality of the pancreas, Renal cell carcinoma, Pheochromocytoma)

      CaseHPOFreeText: The proband presented at age 48 with renal cell carcinoma, multiple pancreatic cysts/tumors, and pheochromocytoma.

      CaseNotHPOs: HP:0009711; HP:0010797 (Retinal capillary hemangioma, Hemangioblastoma)

      CaseNotHPOFreeText: N/A

      CasePreviousTesting: N/A

      PreviouslyPublished: This cohort was also published in a later paper by Wang et al., 2018 (PMID: 29330336).

      SupplementalData: Patient and family genotype-phenotype information is listed in Supplementary Table 1.

      Variant: Exon 2 Deletion (c.341-?_463+?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 2 Deletion

      MultipleGeneVariants: N/A

    8. PatientID: 26

      KindredID: 8

      Case: M, 66Y0M, Chinese

      DiseaseAssertion: VHL

      FamilyInfo: N/A

      CasePresentingHPOs: HP:0001737; HP:0001732; HP:0005584; HP:0009711; HP:0010797 (Pancreatic cysts, Abnormality of the pancreas, Renal cell carcinoma, Retinal capillary hemangioma, Hemangioblastoma)

      CaseHPOFreeText: The proband, patient 26, presented with CNS hemangioblastoma at age 66, retinal angioma at age 66, renal cell carcinoma at age 37, and pancreatic cysts/ tumors at age 54.

      CaseNotHPOs: HP:0002666 (Pheochromocytoma)

      CaseNotHPOFreeText: N/A

      CasePreviousTesting: N/A

      PreviouslyPublished: This patient was also published in a later paper by Wang et al., 2018 (PMID: 29330336), and was likely previously published in Wang et al 2014 (24581539).

      SupplementalData: Patient and family genotype-phenotype information is listed in Supplementary Table 1.

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

      LegacyVariant: N/A

      CaseProblemVariantFreeText: N/A

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

      CAID: N/A

      gnomAD: N/A

      VariantEvidence: N/A

      MutationType: missense_variant;transition

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

      MultipleGeneVariants: N/A

    Tags

    Annotators

    URL

    1. Table 1

      PatientID: N/A

      KindredID: 13

      Case: F, Age Unknown, Indian

      DiseaseAssertion: VHL

      FamilyInfo: Family history not mentioned. Patient’s variant reported as germline.

      CasePresentingHPOs: HP:0002666 (Pheochromocytoma)

      CaseHPOFreeText: Patient had Unilateral PH (see table 1). Previously published 2018 paper (PMID:29124493) reports patient as an Indian 45Y female.

      CaseNotHPOs: N/A

      CaseNotHPOFreeText: N/A

      CasePreviousTesting: N/A

      PreviouslyPublished: 29124493

      SupplementalData:  N/A

      Variant: p.F76del (c.227_229del)

      LegacyVariant: N/A

      CaseProblemVariantFreeText: N/A

      ClinVarID: N/A

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

      gnomAD: N/A

      VariantEvidence: Variant reported as c.224_226del and was mapped to c.227_229del.

      MutationType: inframe_deletion

      CivicName: F76del (c.227_229del)

      MultipleGeneVariants: N/A

    2. Table 1

      PatientID: N/A

      KindredID: 9

      Case: Sex Unknown, Age Unknown, Ethnicity Unknown

      DiseaseAssertion: VHL

      FamilyInfo: Family history not mentioned. Patient’s variant reported as germline.

      CasePresentingHPOs: N/A

      CaseHPOFreeText: Patient had VHL disease.

      CaseNotHPOs: N/A

      CaseNotHPOFreeText: N/A

      CasePreviousTesting: N/A

      PreviouslyPublished: 28388566

      SupplementalData:  N/A

      Variant: p.F76del (c.227_229del)

      LegacyVariant: N/A

      CaseProblemVariantFreeText: N/A

      ClinVarID: N/A

      CAID: CA357012, https://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_229del)

      MultipleGeneVariants: N/A

    1. DNA analysisBoston University School of Medicine's laboratory performed CLIA-approved DNA full sequence analysis of the VHL gene for the proband and site-specific DNA analysis for the proband's mother. Genomic DNA was extracted from peripheral blood lymphocytes using standard procedures. Sequence analysis consisted of polymerase chain reaction (PCR) amplification and automated fluorescence sequencing of all three VHL exons. Multiple ligation probe amplification (MLPA), using the VHL kit from MRC-Holland was also performed. The VHL kit from MRC-Holland detects approximately 97% of all deletion mutations in the VHL gene.

      ArticleReferenceSequence: Not specified - Assumption: variants assumed to have been documented by the author under reference sequence NM_000551.3.

      GenotypingMethod: Analysis consisted of polymerase chain reaction (PCR) amplification and automated fluorescence sequencing. Additionally, multiple ligation probe amplification (MLPA). Western blot analysis was also performed using horseradish peroxidase (HRP)-conjugated secondary antibodies and an enhanced chemiluminescence kit.

      SamplingMethod: Peripheral blood

    2. Proband's mother – 12

      PatientID: None

      KindredID: 1

      Case: F, 48Y0M, Ethnicity Unknown

      DiseaseAssertion: Assumed VHL

      FamilyInfo: The patient’s aunt presented with Hodgkin’s lymphoma at 38Y and was deceased at 40Y. The patient’s father presented with liver cancer at 72Y and was deceased at 74Y. Additionally, the patient’s deceased grandfather had an unspecified cancer. The patient’s son presented with unilateral pheochromocytoma at 13Y. The patient’s daughter presented with pheochromocytoma at 12Y, and bilateral retinal hemangioblastoma, right adrenal pheochromocytoma, and islet cell neuroendocrine carcinoma of the pancreas with nodal metastasis at 20Y, and was found to carry the mutation the patient carried.

      CasePresentingHPOs: HP:0002666; HP:0009711 (Pheochromocytoma, retinal hemangioblastoma)

      CaseHPOFreeText: The patient presented with bilateral pheochromocytoma at 12Y and retinal hemangioblastoma at 13Y.

      CaseNotHPOs: N/A

      CaseNotHPOFreeText: N/A

      CasePreviousTesting: N/A

      PreviouslyPublished: N/A

      SupplementalData: N/A

      Variant: p.*214Lext*14(c.641G>T)

      LegacyVariant: N/A

      ClinVarID: 223236, http://www.ncbi.nlm.nih.gov/clinvar/variation/223236

      gnomAD: N/A

      VariantEvidence: N/A

      MutationType: stop_loss

      CivicName: *214Lext*14(c.641G>T)

      MultipleGeneVariants: N/A

    1. 1 Italy c.358A>G p.Arg120Gly

      GroupID: 15

      Case: Sex unknown, Age unknown, Italian

      DiseaseAssertion: VHL

      FamilyInfo: Unknown. 1 registrant was found with this variant; no family info was mentioned

      CasePresentingHPOs: HP:0030393 (Endolymphatic sac tumor)

      CaseHPOFreeText: N/A

      CaseNotHPOs: N/A

      CaseNotHPOFreeText: N/A

      CasePreviousTesting: N/A

      PreviouslyPublished: N/A

      SupplementalData: N/A

      Variant: p.R120G (c.358A>G)

      CaseProblemVariantFreeText: N/A

      LegacyVariant: N/A

      ClinVarID: 223199 https://www.ncbi.nlm.nih.gov/clinvar/variation/223199/

      CAID: N/A

      gnomAD: N/A

      VariantEvidence: N/A

      MutationType: missense_variant; transition

      CivicName: R120G (c.358A>G)

      MultipleGeneVariants: N/A

    2. 2 France c.486C>G p.Cys162Trp

      GroupID: 26

      DiseaseAssertion: VHL

      GroupSize: 2

      GroupNumberMales: N/A

      GroupNumberFemales: N/A

      GroupEthnicity: French

      GroupAgeRange: N/A

      GroupInfo: 2 registrants from France were grouped in this study via the mutation of c.486C>G

      GroupPresentingHPOs: HP:0030393 (Endolymphatic sac tumor)

      GroupHPOFreeText: N/A

      GroupNotHPOs: N/A

      GroupNotHPOFreeText: N/A

      GroupPreviousTesting: N/A

      PreviouslyPublished: N/A

      SupplementalData: N/A

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

      CaseProblemVariantFreeText: N/A

      LegacyVariant: 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

    3. 2 France c.583C>T p.Gln195*

      GroupID: 35

      DiseaseAssertion: VHL

      GroupSize: 2

      GroupNumberMales: N/A

      GroupNumberFemales: N/A

      GroupEthnicity: N/A

      GroupAgeRange: N/A

      GroupInfo: Two registrants from France both have the same mutation of c.583C>T.

      GroupPresentingHPOs: HP:0030393 (Endolymphatic sac tumor)

      GroupHPOFreeText: N/A

      GroupNotHPOs: N/A

      GroupNotHPOFreeText: N/A

      GroupPreviousTesting: N/A

      PreviouslyPublished: N/A

      SupplementalData: N/A

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

      CaseProblemVariantFreeText: N/A

      LegacyVariant: N/A

      ClinVarID: 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. 3 France c.481C>T p.Arg161* Argentina

      GroupID: 24

      DiseaseAssertion: VHL

      GroupSize: 3

      GroupNumberMales: N/A

      GroupNumberFemales: N/A

      GroupEthnicity: N/A

      GroupAgeRange: N/A

      GroupInfo: Three registrants from either France or Argentina have the same mutation of c.481C>T.

      GroupPresentingHPOs: HP:0030393 (Endolymphatic sac tumor)

      GroupHPOFreeText: N/A

      GroupNotHPOs: N/A

      GroupNotHPOFreeText: N/A

      GroupPreviousTesting: 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

    1. PMID: 7977367

      KindredID: 17

      DiseaseAssertion: VHL

      GroupSize: Unknown

      GroupNumberMales: N/A

      GroupNumberFemales: N/A

      GroupEthnicity: N/A

      GroupAgeRange: N/A

      GroupInfo: This is a family belonging to prefigure No. 17. They are described as ‘VHL-affected’.

      GroupPresentingHPOs: HP:0005584 (renal cell carcinoma)

      GroupHPOFreeText: RCC-affected; other manifestations are possible but not clear.

      GroupNotHPOs: N/A

      GroupNotHPOFreeText: N/A

      GroupPreviousTesting: N/A

      PreviouslyPublished: N/A

      SupplementalData: N/A

      Variant: p.76delF (c.227_229delTTC)

      LegacyVariant: p.147delF (c.437_439del3)

      CaseProblemVariantFreeText: c.224_226 automaps to NM_000551.3:c.227_229delTCT (updated; verified)

      ClinVarID: N/A

      CAID: CA357012 https://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_229delTCT)

      MultipleGeneVariants: N/A

    1. c.565delG1 (1%)130HBc, Cr

      PatientID: None

      KindredID: 16

      Case: Sex Unknown, 30Y0M, Ethnicity Unknown

      DiseaseAssertion: VHL

      FamilyInfo: N/A

      CohortInfo: All VHL mutation carriers of 18 years or older who underwent surveillance according to Dutch VHL guidelines between 1972 and 2012 in the VHL expertise centers University Medical Center Groningen (UMCG) and University Medical Center Utrecht (UMCU) were included. Patients with VHL-disease subtype 2C (pheochromocytoma only) were excluded.

      CasePresentingHPOs: HP:0006880; HP:0000107 (Cerebellar hemangioblastoma, Renal cyst)

      CaseHPOFreeText: VHL Type 1.

      CaseNotHPOs: N/A

      CaseNotHPOFreeText: N/A

      CasePreviousTesting: N/A

      PreviouslyPublished: 24132471

      SupplementalData: Table 1

      Variant: p.E189Kfs*13 (c.565del)

      LegacyVariant: N/A

      CaseProblemVariantFreeText: N/A

      ClinVarID: 625267, https://www.ncbi.nlm.nih.gov/clinvar/variation/625267/

      CAID: N/A

      gnomAD: N/A

      VariantEvidence: N/A

      MutationType: minus_1_frameshift_variant; deletion

      CivicName: E189fs (c.565del)

      MultipleGeneVariants: N/A

    2. c.509T > A15 (20%)2a/b45 (16–71)HBr, HBc,HBsc, RCC, pNET, Pheo, Cr, Cp

      atientID: None

      KindredID: 15

      Case: Sex Unknown, 71Y0M, Ethnicity Unknown

      DiseaseAssertion: VHL

      FamilyInfo: N/A

      CohortInfo: All VHL mutation carriers of 18 years or older who underwent surveillance according to Dutch VHL guidelines between 1972 and 2012 in the VHL expertise centers University Medical Center Groningen (UMCG) and University Medical Center Utrecht (UMCU) were included. Patients with VHL-disease subtype 2C (pheochromocytoma only) were excluded.

      CasePresentingHPOs: HP:0009711; HP:0006880; HP:0009713; HP:0005584; HP:0030405; HP:0000107; HP:0001737; HP:0002666 (Retinal capillary hemangioma, Cerebellar hemangioblastoma, Spinal hemangioblastoma, Renal cell carcinoma, Pancreatic endocrine tumor, Renal cyst, Pancreatic cysts, Pheochromocytoma)

      CaseHPOFreeText: VHL Type 2a/b.

      CaseNotHPOs: N/A

      CaseNotHPOFreeText: N/A

      CasePreviousTesting: N/A

      PreviouslyPublished: 24132471

      SupplementalData: Table 1

      Variant: p.V170D (c.509T>A)

      LegacyVariant: N/A

      CaseProblemVariantFreeText: N/A

      ClinVarID: 625256, https://www.ncbi.nlm.nih.gov/clinvar/variation/625256/

      CAID: N/A

      gnomAD: N/A

      VariantEvidence: N/A

      MutationType: missense_variant;transversion

      CivicName: V170D (c.509T>A)

      MultipleGeneVariants: N/A

    1. R167Q aminoacidic change (the somatic c.500 G > A substitution is marked by a black arrow).

      PatientID: 1

      KindredID: 1

      Case: F, 40Y0M, Caucasian

      DiseaseAssertion: VHL

      FamilyInfo: N/A

      CasePresentingHPOs: HP:0006880, HP:0006770, HP:0006748, HP:0001737, HP:0000107, HP:0009713 (Cerebellar hemangioblastoma, Clear cell renal cell carcinoma, Adrenal pheochromocytoma, Pancreatic cysts, Renal cyst, Spinal hemangioblastoma)

      CaseHPOFreeText: The patient was found to have two extraneuraxial hemangioblastomas, the locations of these tumors included intra/paraspinal (extradural) and the nerve roots. Her past medical history included  cerebellar hemangioblastomas, clear cell renal cell carcinoma, an adrenal pheochromocytoma, and cysts in both the   kidney and  pancreas. Clinical symptoms and imaging features include Radicular lumbarpain, lowerlimb paresthesia &weakness/CT, MRI: contrastenhancing masses &erosion of lumbarspine & sacrum.

      CaseNotHPOs: N/A

      CaseNotHPOFreeText: Normal kidney.

      CasePreviousTesting: N/A

      PreviouslyPublished: N/A

      SupplementalData: Supplemental Digital Content 1. Primer Sequences for VHL gene amplification, LOH and methylation analysis.

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

      LegacyVariant: N/A

      CaseProblemVariantFreeText: N/A

      ClinVar: 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) and I151N (c.452T>A)

      MultipleGeneVariants: Germline, VHL, c. 452T>A (p.Ile151Asn)

    1. 10Cerebellum479 T/CL89PMissenseNINegative

      PatientID: 10

      KindredID: 4

      Case: Sex Unknown, Age Unknown, Ethnicity Unknown

      DiseaseAssertion: VHL

      FamilyInfo: Patient 10 and 4 are related with the same p.L89P mutation and cerebellar hemangioblastomas. Their exact relation was not clear.

      CohortInfo: A total of 42 CNS haemangioblastoma samples were obtained from 31 patients, who were consecutively treated between 1993 and 1997 at the Department of Neurosurgery of the Freiburg University Medical Centre.

      CasePresentingHPOs: HP:0006880 (cerebellar hemangioblastoma)

      CaseHPOFreeText: Patient presented with a VHL-related tumor in the cerebellum.

      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: p.L89P (c.479T>C)

      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. GroupID: 16

      DiseaseAssertion: VHL

      GroupSize: N/A

      GroupNumberMales: N/A

      GroupNumberFemales: N/A

      GroupEthnicity: N/A

      GroupAgeRange: N/A

      GroupInfo: VHL family found to have a germline rearrangement of the VHL gene. The number of family members included in this study is not specified.

      GroupPresentingHPOs: N/A

      GroupHPOFreeText: Patients within this family were found to have a clinical diagnosis of VHL disease, however, the presenting phenotypes were not specified.

      GroupNotHPOs: HP:0002666 (Pheochromocytoma)

      GroupNotHPOFreeText: N/A

      GroupPreviousTesting: N/A

      PreviouslyPublished: N/A

      SupplementalData: N/A

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

      LegacyVariant: c.688delA

      CaseProblemVariantFreeText: N/A

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

      CAID: N/A

      gnomAD: N/A

      VariantEvidence: Variant reported as c.688delA which was mapped to c.477del.

      MutationType: deletion; minus_1_frameshift_variant

      CivicName: E160fs (c.477del)

      MultipleGeneVariants: N/A

    1. 4335Fnt 454 C to T, Pro to SerP, 45959nt 775 C to G, Leu to Val

      PatientID: 43

      KindredID: 5959

      Case: F, 35Y0M, Ethnicity Unknown

      DiseaseAssertion: VHL

      FamilyInfo: N/A

      CasePresentingHPOs: HP:0030405 (pancreatic endocrine tumour)

      CaseHPOFreeText: She presented with four pathologic pancreatic neuroendocrine tumors.

      CaseNotHPOs: N/A

      CaseNotHPOFreeText: N/A

      CasePreviousTesting: N/A

      PreviouslyPublished: N/A

      SupplementalData: N/A

      Variant: p.L188V (c.562C>G)

      LegacyVariant: p.L188V (c.775C>G)

      CaseProblemVariantFreeText: N/A

      ClinVar: 2225 https://www.ncbi.nlm.nih.gov/clinvar/variation/2225/

      CAID: CA020488 http://reg.clinicalgenome.org/redmine/projects/registry/genboree_registry/allele?hgvsOrDescriptor=NM_000551.3%3Ac.562C%3EG

      gnomAD: 0.00002121 https://gnomad.broadinstitute.org/variant/3-10191569-C-G

      VariantEvidence: N/A

      MutationType: missense_variant;transversion

      CivicName: L188V (c.562C>G)

      MultipleGeneVariants: Germline, VHL, c.241C>T (p.Prp81Ser)

    2. nt 695 G to A, Arg to Gln

      PatientID: 28

      KindredID: 6014

      Case: F, 43Y0M, Ethnicity Unknown

      DiseaseAssertion: VHL

      FamilyInfo: N/A

      CasePresentingHPOs: HP:0030405 (pancreatic endocrine tumour)

      CaseHPOFreeText: She presented with one radiologic pancreatic endocrine tumour.

      CaseNotHPOs: N/A

      CaseNotHPOFreeText: N/A

      CasePreviousTesting: N/A

      PreviouslyPublished: N/A

      SupplementalData: N/A

      Variant: p.R161Q (c.482G>A)

      LegacyVariant: p.R161Q (c.695G>A)

      CaseProblemVariantFreeText: N/A

      ClinVar:182983 https://www.ncbi.nlm.nih.gov/clinvar/variation/182983/

      CAID: CA020413 http://reg.clinicalgenome.org/redmine/projects/registry/genboree_registry/allele?hgvsOrDescriptor=NM_000551.3%3Ac.482G%3EA

      gnomAD: N/A

      VariantEvidence: N/A

      MutationType: missense_variant;transition

      CivicName: R161Q (c.482G>A)

      MultipleGeneVariants: N/A

    1. c.748G → A, D179N 

      188 individuals presenting with a single hemangioblastoma, no family history of VHL disease, and no evidence of retinal or abdonimal manigestations of the disease at the time of diagnosis, were investigated for mutations in the VHL gene. Patient B7, male, presented with a cerebellar hemangioblastoma at age 30. Genetic testing via direct sequencing on a DNA blood sample found a c.535G>A (p.Asp179Asn) mutation in their VHL gene (noted as c.748G>A in the paper due to an older VHL transcript build having been used for mapping). One first degree relative tested positive for this mutation, but showed no clinical features of VHL disease at 63 years of age.

    2. B1 Spinal 28 c.582_589delGACACAC N/A 5 y 10 m 

      PatientID: B1

      KindredID: 1

      Case: Sex Unknown, 28Y0M, Ethnicity Unknown

      DiseaseAssertion: Assumed VHL

      FamilyInfo: No testing

      CasePresentingHPOs: HP:0009713, HP:0000107, HP:0001737 (spinal hemangioblastoma, renal cyst, pancreatic cyst)

      CaseHPOFreeText: N/A

      CaseNotHPOs: N/A

      CaseNotHPOFreeText: no other clinical features were found after the cerebellar hemangioblastoma during 5 years 10 months of follow-up

      CasePreviousTesting: N/A

      PreviouslyPublished: N/A

      SupplementalData: N/A

      Variant: p.T124Mfs*33 (c.369_375del)

      LegacyVariant: c.582_589delGACACAC

      ClinVarID: N/A

      CAID: CA913189240 https://reg.clinicalgenome.org/redmine/projects/registry/genboree_registry/allele?hgvsOrDescriptor=NM_000551.3%3Ac.369_375del

      gnomAD: N/A

      VariantEvidence: N/A

      MutationType: minus_1_frameshift_variant

      CivicName: T124Mfs*33(c.369_375del)

      MultipleGeneVariants: N/A

    1. The missense mutation p.Arg167Gln in VHL exon 3 was detected in an index female (patient #2) and her mother

      PatientID: None

      KindredID: 2

      Case: F, Age unknown, Bulgarian

      DiseaseAssertion: VHL

      FamilyInfo: Patient has a daughter (PatientID: 1) with bilateral pheo and retinal hemangioma as well.

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

      CaseHPOFreeText: bilateral pheochromocytoma

      CaseNotHPOs: N/A

      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

    1. Meanwhile, it was also found that the guanine replaced the 559th cytosine on one patient and two carriers from the third family, which made the 116th leucine replaced by valine.

      PatientID: III-7

      KindredID: 3

      Case: F, Age Unknown, Chinese

      DiseaseAssertion: asymptomatic

      FamilyInfo: The transition mutation was found and confirmed in this patient’s mother (II-3) and 2 carriers, her, and her first-cousin once removed (III-7, IV-2). 5 additional members had hemangioblastomas of the CNS, but had all passed away before genetic testing. Could be assumed and deduced the genetics due to pedigree showing future linear relations of this mutation.

      CasePresentingHPOs: N/A

      CaseHPOFreeText: Stated as carrier, however she is young (likely before the age of onset)

      CaseNotHPOs: N/A

      CaseNotHPOFreeText: N/A

      CasePreviousTesting: N/A

      PreviouslyPublished: N/A

      SupplementalData: N/A

      Variant: p.L116V (c.346C>G)

      LegacyVariant: p.L116V (c.559C>G)

      CaseProblemVariantFreeText: N/A

      ClinVarID: N/A

      CAID: CA351753642 https://reg.clinicalgenome.org/redmine/projects/registry/genboree_registry/allele?hgvsOrDescriptor=NM_000551.3%3Ac.346C%3EG

      gnomAD: N/A

      VariantEvidence: N/A

      MutationType: missense_variant;transversion

      CivicName: L116V (c.346C>G)

      MultipleGeneVariants: N/A

    2. The cytosine replaced the 716th guanine on four patients and three carriers of virulence gene from the first family, which made the 168th serine replaced by threonine.

      This study shows the clinical characteristics of three large Chinese families with VHL disease and evaluates the consequence of the genetic test for the diagnosis of VHL disease and clinical screening of the family members. DNA is extracted from peripheral blood in 43 members from three large families with VHL disease and amplified by PCR to three exons of the VHL gene. The PCR products were directly sequenced and the mutations compared with the Human Gene Mutation Database. The ages of the patients who are given the initial diagnosis ranged from 16 to 47 years (mean: 31 years), and the mean time was 17.3 months (2-30 months) from the emergence of the symptom to patients' first visit. Furthermore, the gender distribution was 20% female (4) and 80% male (16). Von Hippel-Lindau disease is seen in 12 members of a Chinese family. Molecular diagnosis is confirmed in only 7 family members. The proband (male; deceased) has retinal capillary hemangioma; hemangioblastoma, 2 of his brothers (deceased) have pancreatic cancer, a third brother has renal cancer and hemangioblastoma, and 5 nephews have hemangioblastoma. There are three members who are asymptomatic carriers, but are young and may be before the age of onset. The mutation p.S168T (c.503G>C) was referred to in the paper by c.716G>C due to a difference in transcript sequence. At least 5 additional members had VHL phenotypes, but had all passed away before genetic testing. It could be assumed their genetic mutation due to pedigree showing future linear relations of this mutation all in generation III. ACMG evidence codes: 'PP1' based on segregation results, 'PP2' because they observe a missense variant in gene where missense variants are common mechanism of disease, 'PP4' because the patients phenotypes and family history are highly specific for a disease with single genetic etiology.

    1. PatientID: None (Maternal Aunt)

      KindredID: 1

      Case: F, 30Y0M, Ethnicity Unknown

      DiseaseAssertion: VHL

      FamilyInfo: Look to proband for more information on family history.

      CasePresentingHPOs: HP:0006880; HP:0009711 (Cerebellar hemangioblastoma, Retinal capillary hemangioma)

      CaseHPOFreeText: Cerebellar/cerebral trunk hemangioblastoma. Multiple retinal hemangioblastomas.

      CaseNotHPOs: N/A

      CaseNotHPOFreeText: N/A

      CasePreviousTesting: N/A

      PreviouslyPublished: 25494863

      SupplementalData: Figure 1

      Variant: p.G114R (c.340G>C)

      LegacyVariant: N/A

      CaseProblemVariantFreeText: N/A

      ClinVarID: 223193, https://www.ncbi.nlm.nih.gov/clinvar/variation/223193/

      CAID: N/A

      gnomAD:

      VariantEvidence: N/A

      MutationType: missense_variant;transversion

      CivicName: G114R (c.340G>C)

      MultipleGeneVariants: N/A

    2. We report the case of a 15-year-old boy with the diagnosis of aggressive GH-PRL pituitary macroadenoma and a family history of VHL disease. Pituitary resection was performed, although complete excision of the lesion could not be confirmed by the neurosurgeon. A control MRI was done 6 months after surgery and the pituitary lesion was similar to the presurgical image. A second operation allowed partial resection of the tumour followed by targeted radiotherapy.

      PatientID: None (Proband)

      KindredID: 1

      Case: M, 18Y0M, Ethnicity Unknown

      DiseaseAssertion: VHL

      FamilyInfo: The family history revealed VHL in his mother, who died at the age of 40, and in his maternal aunt and grandmother, deceased at 30 and 33 years, respectively. His mother was operated on three times for cerebellar hemangioblastomas, the first at 13 years of age. She had also been treated for bilateral retinal hemangioblastomas since the age of 19. In addition, she had surgery for a renal tumor at the age of 32 and also had pancreatic cysts. She died of the diffuse hemangioblastomas in the posterior fossa. Variant is stated to be previously identified in the family but it is not clear which members have been genetically tested.

      CasePresentingHPOs: HP:0006880; HP:0002893; HP:0007663; HP:0001510; HP:0000823; HP:0009711 (Cerebellar hemangioblastoma, Pituitary adenoma, Reduced visual acuity, Growth delay, Delayed puberty, Retinal capillary hemangioma)

      CaseHPOFreeText: Referred at the age of 15 for decreased visual acuity of the right eye. Growth failure with short stature for age and lack of pubertal development was noted. This was confirmed by ophthal-mologic examination which also showed bitemporal quadranopsia. Two retinal vascular lesions had already been diagnosed and photocoagulated. Cerebral MRI examination visualized a voluminous pituitary adenoma (confirmed pathologically) with suprasellar extension compressing the optic fibres invading both cavernous sinuses. It also confirmed two small cerebellar hemangioblastomas. On follow-up, MRI showed a persistent pituitary adenoma (confirmed by pathology) with numerous mitoses. A cystic part of the main hemangioblastoma was also noted in the right cerebellum image.

      CaseNotHPOs: HP:0005584 (Renal cell carcinoma)

      CaseNotHPOFreeText: No renal lesion was found on ultrasound examination. Renal ultrasound examination was persistently normal.

      CasePreviousTesting: N/A

      PreviouslyPublished: 25494863

      SupplementalData: Figure 1

      Variant: p.G114R (c.340G>C)

      LegacyVariant: N/A

      CaseProblemVariantFreeText: N/A

      ClinVarID: 223193, https://www.ncbi.nlm.nih.gov/clinvar/variation/223193/

      CAID: N/A

      gnomAD:

      VariantEvidence: N/A

      MutationType: missense_variant;transversion

      CivicName: G114R (c.340G>C)

      MultipleGeneVariants: N/A

    1. 14F/11ASB/L PCC+sPGLVHL3c.500G>Ap.(Arg167Gln)Substitution (missense)Disease causingProbably damaging score 1.000DamagingNRNR

      PatientID: 14

      KindredID: 14

      Case: F, 11Y0M, Asian Indian

      DiseaseAssertion: assumed VHL

      FamilyInfo: None - Apparently sporadic

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

      CaseHPOFreeText: Bilateral pheochromocytoma and sympathetic PGL

      CaseNotHPOs: N/A

      CaseNotHPOFreeText: N/A

      CasePreviousTesting: RET/ SDHB/ SDHD/ NF1

      PreviouslyPublished: N/A

      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: 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

    1. three familial cases

      PatientID: 5

      KindredID: C

      Case: M, Age Unknown, Japanese

      DiseaseAssertion: Asymptomatic

      FamilyInfo: This mutation was found in a family of 10 individuals; six were found to carry the mutation NM_000551.3:c.464-1G>T the patient carried, and three presented with symptoms. They were identified with hemangioblastomas of the central nervous system and retinal angiomas. The eldest patient also had renal cell carcinoma (patient C-1).

      CasePresentingHPOs: N/A

      CaseHPOFreeText: The paper states that this patient was not yet symptomatic, suggesting they may be too young to show symptoms yet.

      CaseNotHPOs: N/A

      CaseNotHPOFreeText: N/A

      CasePreviousTesting: N/A

      PreviouslyPublished: N/A

      SupplementalData: N/A

      Variant: (c.464-1G>T)

      LegacyVariant: (c.677-1G>T)

      ClinVarID: 223221, http://www.ncbi.nlm.nih.gov/clinvar/variation/223221

      CAID: N/A

      gnomAD: N/A

      VariantEvidence: N/A

      MutationType: splice_site_variant

      CivicName: SpliceSite(c.464-1G>T)

      MultipleGeneVariants: N/A

    1. Germline mutations and genotype–phenotype correlations in patients with apparently sporadic pheochromocytoma/paraganglioma in Korea J.H. Kim, J.H. Kim Department of Internal medicine, Seoul National University College of Medicine, Seoul, South KoreaBoth the authors contributed equally to this work.Search for more papers by this authorM.-W. Seong, M.-W. Seong Department of Laboratory medicine, Seoul National University College of Medicine, Seoul, South KoreaBoth the authors contributed equally to this work.Search for more papers by this authorK.E. Lee, K.E. Lee Department of Surgery, Seoul National University College of Medicine, Seoul, South KoreaSearch for more papers by this authorH.J. Choi, H.J. Choi Department of Internal Medicine, Chungbuk National University College of Medicine, Cheongju, South KoreaSearch for more papers by this authorE.J. Ku, E.J. Ku Department of Internal medicine, Seoul National University College of Medicine, Seoul, South KoreaSearch for more papers by this authorJ.H. Bae, J.H. Bae Department of Internal medicine, Seoul National University College of Medicine, Seoul, South KoreaSearch for more papers by this authorS.S. Park, S.S. Park Department of Laboratory medicine, Seoul National University College of Medicine, Seoul, South KoreaSearch for more papers by this authorS.H. Choi, S.H. Choi Department of Internal medicine, Seoul National University College of Medicine, Seoul, South KoreaSearch for more papers by this authorS.W. Kim, S.W. Kim Department of Internal medicine, Seoul National University College of Medicine, Seoul, South KoreaSearch for more papers by this authorCS Shin, CS Shin Department of Internal medicine, Seoul National University College of Medicine, Seoul, South KoreaSearch for more papers by this authorS.Y. Kim, Corresponding Author S.Y. Kim Department of Internal medicine, Seoul National University College of Medicine, Seoul, South Korea Corresponding author: Prof Seong Yeon Kim, Department of Internal Medicine, Seoul National University College of Medicine, Seoul National University Hospital, Seoul 110-744, South Korea. Tel.: 082-02-2072-3216; fax: 082-02-762-9662; e-mail: seongyk@plaza.snu.ac.krSearch for more papers by this author

      PMID: 24134185

      Gene: VHL

      StandardizedReferenceSequence: NM_000551.3

    1. IV - 10

      PatientID: IV:10

      KindredID: 1

      Case: F, 28Y0M, Chinese

      DiseaseAssertion: VHL

      FamilyInfo: A 5-generation family with VHL in 15 members. Both second generation children (presumed), 5 third generation, and 8 further generation individuals were affected and haplotyping was conducted using three polymorphic microsatellite markers. All of the 5th generation children (9 total at time of publication) had been sequenced and haplotyped as unaffected.

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

      CaseHPOFreeText: patient had cerebellar HB; renal cysts. Age of onset was 23Y, and surgery (operation) was 28Y

      CaseNotHPOs: HP:0002666; HP:0030405; HP:0001737; HP:0002668 (pheochromocytoma, pancreatic endocrine tumor, pancreatic cysts, paraganglioma)

      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?dataset=gnomad_r2_1

      VariantEvidence: genotyped three polymorphic microsatellite markers that flanked VHL on chromosome 3p25 (D3S3691, D3S1597 and D3S1263). 

      MutationType: missense_variant;transition

      CivicName: R167W (c.499C>T)

      MultipleGeneVariants: N/A

    2. PatientsThe Chinese family study included five-generations comprising of 38 living family members, of whom nine were affected [Figure 1]. All living members were examined clinically. The clinical and radiographic images were published with the consent of the patient. The study was approved by the research Ethics Committees of Xi’an Jiaotong University School of Medicine. Written informed consents were obtained from all participants.Open in a separate windowFigure 1Haplotypes of the Chinese family affected by Von Hippel-Lindau (VHL). The open and filled blackened symbols indicated unaffected and affected individuals, respectively. The squares and circles symbolized the males and females, respectively. The proband, IV-3, was indicated by an arrow. The haplotyping was conducted using three polymorphic microsatellite markers. The marker order was determined from the Marshfield map and the UCSC Human Genome database (February 2009). The dark boxes symbolized haplotypes that cosegregated with the affected individuals and suggested linkage of VHL to disease in this family. The boxes with slash symbolized the dead family members.

      PatientID: III:10

      KindredID: 1

      Case: M, Age Unknown (deceased), Chinese

      DiseaseAssertion: VHL

      FamilyInfo: A 5-generation family with VHL in 15 members. Both second generation children (presumed), 5 third generation, and 8 further generation individuals were affected and haplotyping was conducted using three polymorphic microsatellite markers. All of the 5th generation children (9 total at time of publication) had been sequenced and haplotyped as unaffected.

      CasePresentingHPOs: N/A

      CaseHPOFreeText: unknown phenotype, however they were said to be affected

      CaseNotHPOs: N/A

      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?dataset=gnomad_r2_1

      VariantEvidence: Death before genetic diagnostic, however presumed by authors due to extensive family history (See pedigree).

      MutationType: missense_variant;transition

      CivicName: R167W (c.499C>T)

      MultipleGeneVariants: N/A

    1. Of 246 patients affected with von Hippel-Lindau disease, 64 patients (26%) from 38 families had pheochromocytoma, including 33 newly diagnosed during screening studies and 31 treated before screening at NIH. Germline mutations in the VHL gene was determined from peripheral blood. Family 3948 and family 4589 were found with c.485G>T mutations in the VHL gene (legacy notation c.698G>t converted to NM_000551.3). Family 3948: 1/4 had pheochromocytoma, 1/4 had renal cell carcinoma, 4/4 had CNS hemangioblastoma, 2/4 had retinal angiomas and 2/4 had cysts. Family 4589: 2/2 had pheochromocytoma and 1/2 had retinal angiomas. Individual patient phenotype-genotype was not described in the paper.

    2. PatientID: None

      KindredID: 6103

      Case: Sex Unknown, Age Unknown, Ethnicity Unknown

      DiseaseAssertion: VHL

      FamilyInfo: N/A

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

      CaseHPOFreeText: Diagnosed with CNS hemangioblastoma, pheochromocytoma, retinal angioma and VHL Type 2B.

      CaseNotHPOs: HP:0005584 (Renal cell carcinoma)

      CaseNotHPOFreeText: N/A

      CasePreviousTesting: N/A

      PreviouslyPublished: N/A

      SupplementalData: N/A

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

      LegacyVariant: c.712C>T

      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: Variant reported as 712, C to T (Arg to Trp), assumed to be reported in legacy nomenclature (AF010238.1) and mapped to c.499C>T, p.Arg167Trp (NM_000551.3).

      MutationType: missense_variant;transition

      CivicName: R167W (c.499C>T)

      MultipleGeneVariants: N/A

    3. Of 246 patients affected with von Hippel-Lindau disease, 64 patients (26%) from 38 families had pheochromocytoma, including 33 newly diagnosed during screening studies and 31 treated before screening at NIH. Germline mutations in the VHL gene were determined from sequencing peripheral blood using PCR, SSCP (single-strand conformation polymorphism), and Southern Blotting. Family 4578 was found with c.233A>G mutation in the VHL gene (legacy notation c.446A>G converted to NM_000551.3). It should be noted that the paper describes the amino acid change to be Asp to Ser but, there is no Asp at position 233. This is assumed to be a mistake, with the correct amino acid change being Asn to Ser. 4/8 had pheochromocytoma, 7/8 had renal cell carcinoma, 5/8 had CNS hemangioblastoma, 3/8 had retinal angiomas and 2/8 had cysts.

    1. 239G→A Ts Exon 1 80 AGT S S80N

      A study of 103 patients with VHL retinal manifestations and 108 patients without VHL retinal manifestations extracted from the French VHL database revealed that the number of hemangioblastomas appeared higher in patients who had a substitution when compared with patients with a truncated protein. Detected by PCR and SSCP, this mutation p.S80N (c.239G>A) was found in 2 VHL patients. Both were said to have retinal hemangioblastomas, while other manifestations are not clearly stated. No family information or relation was provided. This is possibly previously published in PMID: 15300849

    2. 473T→C Ts Exon 3 158 CTG L L158P

      GroupID: 42

      Case: Age unknown, Sex unknown, French

      DiseaseAssertion: VHL

      FamilyInfo: N/A - only 1 patient reported here

      CasePresentingHPOs: HP:0009711 (retinal capillary hemangioma)

      CaseHPOFreeText: Other manifestations are possibly but not clearly reported

      CaseNotHPOs: N/A

      CaseNotHPOFreeText: N/A

      CasePreviousTesting: N/A

      PreviouslyPublished: Possibly published in PMID:15300849

      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

    3. 571delC Fs Exon 3 191 CAC H Stop201

      GroupID: 52

      Case: Age unknown, Sex unknown, French

      DiseaseAssertion: VHL

      FamilyInfo: None - one member documented here

      CasePresentingHPOs: HP:0009711 (retinal capillary hemangioma)

      CaseHPOFreeText: other manifestations are not clearly stated.

      CaseNotHPOs: N/A

      CaseNotHPOFreeText: N/A

      CasePreviousTesting: N/A

      PreviouslyPublished: Possibly published in PMID:15300849

      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: H191FS (c.571delC)

      MultipleGeneVariants: N/A

    1. 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

    2. DNA isolation DNA was isolated from peripheral blood leucocytes using proteinase K digestion and phenol/chloroform purification. Aliquots of DNA were dissolved in sterile distilled water to a working concentration of 50 ng/μl. googletag.cmd.push(function() { googletag.display("dfp-ad-mpu"); }); Sequencing The entire coding sequence of the VHL gene was amplified in a PCR reaction using primer pairs 3, 101, 102, 103, and 6, 107.28 After purification, PCR products were sequenced with the same primers, using fluorescently labelled dideoxy chain terminators from an ABI Prism kit (Applied Biosystems) in an ABI 373 automated sequencer.

      ArticleReferenceSequence: Not specified – Assumption: variants assumed to have been documented by the author under reference sequence NM_000551.3

      GenotypingMethod: The entire coding sequence of the VHL gene was amplified in a PCR reaction using primer pairs 3, 101, 102, 103, and 6, 107. Quantitative Southern analysis was then employed.

      SamplingMethod: Peripheral blood leukocytes

    3. 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. PatientID: 1 (Proband)

      KindredID: 17

      Case: F, 3Y0M, Ethnicity Unknown

      DiseaseAssertion: Asymptomatic

      FamilyInfo: 6 members of this family tested positive for the c.496_506del germline variant of the VHL gene. ID 4 presented with CNS hemangioblastoma, retinal angioma and renal and pancreatic abnormalities. ID 25 and 8 were asymptomatic.ID 22 presented with CNS hemangioblastoma. ID 5 presented with retinal angioma. 2 members were assumed to have the variant but were not genetically confirmed (ID 20 and ID 11). ID 11 and 20 presented with CNS hemangioblastoma.

      CasePresentingHPOs: N/A

      CaseHPOFreeText: N/A

      CaseNotHPOs: HP:0005584; HP:0002666; HP:0010797; HP:0000077; HP:0001732; HP:0009711 (Renal cell carcinoma, Pheochromocytoma, Hemangioblastoma, Abnormality of the kidney, Abnormality of the pancreas, Retinal capillary hemangioma)

      CaseNotHPOFreeText: N/A

      CasePreviousTesting: N/A

      PreviouslyPublished: N/A

      SupplementalData: Supplementary Table 1.

      Variant: p.V166Sfs*4 (c.496_506del)

      LegacyVariant: N/A

      CaseProblemVariantFreeText: N/A

      ClinVarID: 223229, https://www.ncbi.nlm.nih.gov/clinvar/variation/223229/

      CAID: N/A

      gnomAD: N/A

      VariantEvidence: It is unclear from the publication if this variant is reported according to legacy (AF010238.1) or NM_000551.3 reference sequence. Clinical notes from the case confirm the reference sequence to be NM_000551.3.

      MutationType: deletion; minus_2_frameshift_variant

      CivicName: V166SFS*4 (c.496_506del)

      MultipleGeneVariants: N/A

    1. c.240 T>Gap.S80R

      53 patients with a molecularly confirmed VHL mutation (by PCR through EDTA-anticoagulated blood) and a pancreatic neuroendocrine tumor (ICT) were collected from the German NET-Registry and the German VHL-registry. An additional 296 patients were stated in this paper with a VHL associated germline mutation, but without pancreatic neuroendocrine tumors. 3 patients were found to have the above mutation (c.240T>G). 1 was a VHL patient with an ICT (pancreatic neuroendocrine tumor) taken from the VHL-registry. The other 2 patients were stated to be in this study with the given mutation, however no ICT. Other clinical manifestations outside of a pancreatic neuroendocrine tumor are possible, but were not discussed. ACMG evidence codes: 'PP2' because they observe a missense variant in a gene where missense variants are a common mechanism of disease.

    2. c.482 G>Aap.R161Q

      GroupID: 22A

      DiseaseAssertion: VHL

      GroupSize: 5

      GroupNumberMales: N/A

      GroupNumberFemales: N/A

      GroupEthnicity: N/A

      GroupAgeRange: N/A

      GroupInfo: 5 VHL patients with the given VHL mutation and manifestation were grouped in this study.

      GroupPresentingHPOs: HP:0030405 (pancreatic endocrine tumor)

      GroupHPOFreeText: Patients have islet cell tumors (ICTs), or listed as pancreatic endocrine tumor. Other clinical manifestations outside of a pancreatic neuroendocrine tumor are possible, but were not discussed.

      PreviouslyPublished: N/A

      SupplementalData: N/A

      Variant: p.R161Q (c.482G>A)

      LegacyVariant: N/A

      CaseProblemVariantFreeText: N/A

      ClinVarID: 182983 https://www.ncbi.nlm.nih.gov/clinvar/variation/182983/

      CAID: N/A

      gnomAD: N/A

      VariantEvidence: N/A

      MutationType: missense_variant; transition

      CivicName: R161Q (c.482G>A)

      MultipleGeneVariants: N/A

    1. 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

    2. 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. family B, with pheochromocytoma only phenotype, we detected a previously not described c.463G>A/p.Val84Met replacement. Within this family, a prenatal diagnosis was also performed.

      PatientID: BII2

      KindredID: B

      Case: M, 40Y0M, Serbian

      DiseaseAssertion: VHL

      FamilyInfo: Families were selected based on their clinical data and family history. Patient’s father (BI1) had pheochromocytoma, but was not genetically tested. The patient’s son (BIII3) developed pheochromocytoma at the age of one, but progressed to bilateral pheochromocytoma 3 years later. Genetic testing revealed the same mutation in the patient and his son. In fact, a sample of amniotic fluid was taken from the patient’s wife (BII2) during the 16th week of pregnancy for prenatal testing, which was later confirmed to be the same point mutation as BII2. See pedigree in figure 1.

      CasePresentingHPOs: HP:0002666 (pheochromocytoma)

      CaseHPOFreeText: The first symptoms of pheochromocytoma appeared in the patient at age 40Y0M.

      CaseNotHPOs: N/A

      CaseNotHPOFreeText: N/A

      CasePreviousTesting: N/A

      PreviouslyPublished: N/A

      SupplementalData: N/A

      Variant: p.V84M (c.250G>A)

      LegacyVariant: p.V84M (c.463G>A)

      CaseProblemVariantFreeText: N/A

      ClinVarID: 428813, https://www.ncbi.nlm.nih.gov/clinvar/variation/428813/

      CAID: N/A

      gnomAD: 0.000004376, https://gnomad.broadinstitute.org/variant/3-10183781-G-A

      VariantEvidence: N/A

      MutationType: missense variant; transition

      CivicName: V84M (c.250G>A)

      MultipleGeneVariants: N/A

    1. PatientID: 5

      KindredID: 2

      Case: F, 20Y0M, Indian

      DiseaseAssertion: VHL

      FamilyInfo: Another member of this family (Gen 1) presented with the same mutation, bilateral pheochromocytoma, RCC as well as neural hemangioblastoma that ultimately caused his death.

      CohortInfo: This retrospective study was conducted at Department of Endocrinology of a tertiary care health centre in Western India. Patients presented to our institute between 2008 and 2016 were included in the study. During the study period a total of 33 patients were suspected to have VHL syndrome based on clinical features among whom 31 patients were found to have mutation in VHL gene. All patients are of Asian Indian descent.

      CasePresentingHPOs: HP:0002666 (Pheochromocytoma)

      CaseHPOFreeText: Bilateral pheochromocytoma.

      CaseNotHPOs: HP:0005584; HP:0001737; HP:0009711; HP:0010797; HP:0002668; HP:0030405 (Renal cell carcinoma, Pancreatic cysts, Retinal capillary hemangioma, Hemangioblastoma, Paraganglioma, Pancreatic endocrine tumor)

      CaseNotHPOFreeText: N/A

      CasePreviousTesting: N/A

      PreviouslyPublished: N/A

      SupplementalData: N/A

      Variant: p.R161Q (c.482G>A)

      LegacyVariant: N/A

      CaseProblemVariantFreeText: N/A

      ClinVarID: 182983, https://www.ncbi.nlm.nih.gov/clinvar/variation/182983/

      CAID: N/A

      gnomAD: N/A

      VariantEvidence: N/A

      MutationType: missense_variant;transition

      CivicName: R161Q (c.482G>A)

      MultipleGeneVariants: N/A

    1. Germline mutations in 45 unrelated Japanese VHL patients were determined from blood samples using PCR-SSCP or Southern blot analyses. The authors reported a nucleotide deletion (i.e. 746T>C) which coincides with legacy variant nomenclature (AF010238.1) and was mapped to c.533T>C (NM_000551.3). PCR-SSCP or Southern blot analyses of the DNA from family members showed that mutations were segregated with disease phenotype in VHL families, although this data was not shown. Data on the presence of retinal angioma, CNS Hb, RCC, and Pheo was available. Case 34 had an c.533T>C mutation. 1 member of this family was affected with RCC, CNS Hb, and retinal hemangioma. Other demographics of the members were not described.

    2. Germline mutations in 45 unrelated Japanese VHL patients were determined from blood samples using PCR-SSCP or Southern blot analyses. The authors used the 284 codon ORF previously described by Latif et al., 1993 and this notation was converted to NP_000542. PCR-SSCP or Southern blot analyses of the DNA from family members showed that mutations were segregated with disease phenotype in VHL families, although this data was not shown. Data on the presence of retinal angioma, CNS hemangioblastoma (Hb) renal cell carcinoma (RCC), and pheochromocytoma was available. Case 9 had p.Asn78Ser (c.233A>G) mutation. Three members were affected, and all had retinal capillary hemangioma and CNS hemangioblastoma. Other demographics of the members were not described.

    3. Germline mutations in 45 unrelated Japanese VHL patients were determined from blood samples using PCR-SSCP or Southern blot analyses. The authors reported a nucleotide deletion (i.e. 476G>C) which coincides with legacy variant nomenclature (AF010238.1) and was mapped to c.263G>C (NM_000551.3). PCR-SSCP or Southern blot analyses of the DNA from family members showed that mutations were segregated with disease phenotype in VHL families, although this data was not shown. Data on the presence of retinal angioma, CNS Hb, RCC, and Pheo was available. Case 8 had p.Trp88Ser mutation. All 5 examined family members were affected with renal cell carcinoma. Other demographics of the members were not described.

    4. GroupID: 39

      Case: Sex Unknown, Age Unknown, Japanese

      DiseaseAssertion: VHL

      FamilyInfo: N/A

      CasePresentingHPOs: HP:0009711(retinal capillary hemangioma)

      CaseHPOFreeText: N/A

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

      CaseNotHPOFreeText: N/A

      CasePreviousTesting: N/A

      PreviouslyPublished: N/A

      SupplementalData: N/A

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

      LegacyVariant: p.P157L (c.470C>T)

      CaseProblemVariantFreeText: N/A

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

      CAID: N/A

      gnomAD: N/A

      VariantEvidence: N/A

      MutationType: missense_variant;transition

      CivicName: P86L(c.257C>T)

      MultipleGeneVariants: N/A

    1. This mutation was inherited from the paternal allele

      PatientID: None (father)

      KindredID: 1

      Case: M, Age Unknown, Ethnicity Unknown

      DiseaseAssertion: Asymptomatic

      FamilyInfo: No significant family history.

      CasePresentingHPOs: N/A

      CaseHPOFreeText: N/A

      CaseNotHPOs: N/A

      CaseNotHPOFreeText: N/A

      CasePreviousTesting: N/A

      PreviouslyPublished: N/A

      SupplementalData: N/A

      Variant: p.V194G (c.581T>G)

      LegacyVariant: N/A

      CaseProblemVariantFreeText: N/A

      ClinVarID: 428810, https://www.ncbi.nlm.nih.gov/clinvar/variation/428810/

      CAID: N/A

      gnomAD: N/A

      VariantEvidence: In silico analysis was performed using the PolyPhen-2 program and SIFT analysis. In the PolyPhen-2 analysis, the prediction score was 1.000, which indicated “probably damaging.” In addition, SIFT analysis of V194G indicated a SIFT score of 0, which indicates a seriously damaging mutation.

      MutationType: missense_variant;transversion

      CivicName: V194G (c.581T>G)

      MultipleGeneVariants: N/A

    1. Germline mutations were identified in 300/469 (63%) of the families tested; 137 distinct intragenic germline mutations were detected.

      GroupID/ KindredID: 11BMS

      DiseaseAssertion: VHL

      GroupSize: N/A

      GroupNumberMales: N/A

      GroupNumberFemales: N/A

      GroupEthnicity: N/A

      GroupAgeRange: N/A

      GroupInfo: This germline familial VHL mutation was taken from the Bristol Myers Squibb database, with an unknown number of members belonging to Family ID 11BMS. Table 3 lists all ID and mutations associated with individuals possessing renal carcinoma, without pheochromocytoma.

      GroupPresentingHPOs: HP:0005548 (renal cell carcinoma)

      GroupHPOFreeText: Described as a VHL family with RCC, without pheochromocytoma. Other phenotypes are likely, however not detailed in this publication

      GroupNotHPOs: HP:0002666 (pheochromocytoma)

      GroupNotHPOFreeText: N/A

      GroupPreviousTesting: N/A

      PreviouslyPublished: N/A

      SupplementalData: N/A

      Variant: p.T152Hfs*22 (c.452_453insA)

      LegacyVariant: FS (c.665insA)

      CaseProblemVariantFreeText: N/A

      ClinVarID: N/A

      CAID: CA2573131771 https://reg.clinicalgenome.org/redmine/projects/registry/genboree_registry/allele?hgvsOrDescriptor=NM_000551.3%3Ac.452_453insA

      gnomAD: N/A

      VariantEvidence: This paper declares this variant is predicted to compromise the Elongin-binding site by truncating the protein.

      MutationType: plus_1_frameshift_variant

      CivicName: T152fs (c.452_453insA)

      MultipleGeneVariants: N/A

    2. Germline mutations were identified in 300/469 (63%) of the families tested; 137 distinct intragenic germline mutations were detected.

      Germline mutational data on VHL was gathered from various countries to assess variation in germline mutations that produce disease within different populations. Families were grouped according to three possible outcomes of disease: renal cell carcinoma without pheochromocytoma, renal cell carcinoma with pheochromocytoma, or pheochromocytoma alone. SSCP and denaturing gradient gel electrophoresis identified mutations in 300/469 (63%) of families affected with VHL. This germline familial VHL mutation (S72Pfs*87 (c.214delT)) was taken from the Cambridge, Department of Pathology database, with an unknown number of members belonging to Family ID 112CA. It was reported in the paper as c.427delT due to a difference in transcript reference. As reported in Table 3, this mutation is found in VHL family without pheochromocytoma, and with renal cell carcinoma.

    3. Germline mutations were identified in 300/469 (63%) of the families tested; 137 distinct intragenic germline mutations were detected.

      Germline mutational data on VHL was gathered from various countries to assess variation in germline mutations that produce disease within different populations. Families were grouped according to three possible outcomes of disease: renal cell carcinoma without pheochromocytoma, renal cell carcinoma with pheochromocytoma, or pheochromocytoma alone. SSCP and denaturing gradient gel electrophoresis identified mutations in 300/469 (63%) of families affected with VHL. This germline familial VHL mutation (Q96P (c.287A>C)) was taken from the Cambridge, Department of Pathology database, with an unknown number of members belonging to Family ID 98CA. It was reported in the paper as c.500A>C due to a difference in transcript reference. As reported in Table 3, this mutation is found in VHL families without pheochromocytoma, and with renal cell carcinoma.

    4. Germline mutations were identified in 300/469 (63%) of the families tested; 137 distinct intragenic germline mutations were detected.

      GroupID/ KindredID: 3786NCI

      DiseaseAssertion: VHL

      GroupSize: N/A

      GroupNumberMales: N/A

      GroupNumberFemales: N/A

      GroupEthnicity: N/A

      GroupAgeRange: N/A

      GroupInfo: This germline familial VHL mutation was taken from the National Cancer Institute database, with an unknown number of members belonging to Family ID 3786NCI. Table 4 lists all ID and mutations associated with individuals with pheochromocytoma.

      GroupPresentingHPOs: HP:0002666 (pheochromocytoma)

      GroupHPOFreeText: Described as a VHL family with pheochromocytoma. Other phenotypes are likely, including renal cell carcinoma, however not detailed here.

      GroupNotHPOs: N/A

      GroupNotHPOFreeText: N/A

      GroupPreviousTesting: N/A

      PreviouslyPublished: 7728151

      SupplementalData: N/A

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

      LegacyVariant: p.L178P (c.746T>C)

      CaseProblemVariantFreeText: N/A

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

      CAID: N/A

      gnomAD: N/A

      VariantEvidence: This paper declares this variant is predicted to compromise the Elongin-binding site by location between codons 157 and 189.

      MutationType: missense_variant; transition

      CivicName: L178P (c.533T>C)

      MultipleGeneVariants: N/A

    5. Germline mutations were identified in 300/469 (63%) of the families tested; 137 distinct intragenic germline mutations were detected.

      GroupID/ KindredID: 53CE

      DiseaseAssertion: VHL

      GroupSize: N/A

      GroupNumberMales: N/A

      GroupNumberFemales: N/A

      GroupEthnicity: N/A

      GroupAgeRange: N/A

      GroupInfo: This germline familial VHL mutation was taken from the Munich, university of Freiburg and Institute of Pathology database, with an unknown number of members belonging to Family ID 53CE. Table 3 lists all ID and mutations associated with individuals possessing renal carcinoma, without phechromocytoma.

      GroupPresentingHPOs: HP:0005548 (renal cell carcinoma)

      GroupHPOFreeText: Described as a VHL family with RCC, without pheochromocytoma. Other phenotypes are likely, however not detailed in this publication

      GroupNotHPOs: HP:0002666 (pheochromocytoma)

      GroupNotHPOFreeText: N/A

      GroupPreviousTesting: N/A

      PreviouslyPublished: N/A

      SupplementalData: N/A

      Variant: p.V74G (c.221T>G)

      LegacyVariant: p.V74G (c.434T>G)

      CaseProblemVariantFreeText: N/A

      ClinVarID: N/A

      CAID: CA70042528 https://reg.clinicalgenome.org/redmine/projects/registry/genboree_registry/allele?hgvsOrDescriptor=NM_000551.3%3Ac.221T>G

      gnomAD: N/A

      VariantEvidence: N/A

      MutationType: missense_variant; transversion

      CivicName: V74G (c.221T>G)

      MultipleGeneVariants: N/A

    1. 16 different families

      PatientID: 2

      KindredID: 5

      Case: Sex Unknown, Age Unknown, Ethnicity Unknown

      DiseaseAssertion: VHL

      FamilyInfo: Patient’s father is presented with renal cell carcinoma, renal cysts, adrenal pheochromocytoma, spinal hemangioblastoma, pancreatic cysts, endolymphatic sac tumor and salivary gland neoplasm at age 19Y0M. This patient is 1 of 3 carrier children of this mutation, without any further phenotypic information.

      CasePresentingHPOs: N/A

      CaseHPOFreeText: N/A

      CaseNotHPOs: N/A

      CaseNotHPOFreeText: N/A

      CasePreviousTesting: N/A

      PreviouslyPublished: N/A

      SupplementalData: N/A

      Variant: p.G93R (c.277G>C)

      LegacyVariant: N/A

      CaseProblemVariantFreeText: N/A

      ClinVarID: 223174, https://www.ncbi.nlm.nih.gov/clinvar/variation/223174

      CAID: N/A

      gnomAD: N/A

      VariantEvidence: N/A

      MutationType: missense_variant, transversion

      CivicName: G93R (c.277G>C)

      MultipleGeneVariants: N/A

    2. In 1996, we described a 3 generation VHL 2A kindred with 11 mutation carriers. We aim to share our experience regarding the long-term follow-up of this family

      PatientID: 19

      KindredID: 1

      Case: F, 17Y0M, Ethnicity Unknown

      DiseaseAssertion: VHL

      FamilyInfo: This patient was a member of family 1, where 14/32 total patients were diagnosed with VHL. One of which (I-32) was a mutational carrier with down syndrome. The other 13 patients had varying phenotypes, including adrenal pheochromocytoma, pancreatic endocrine tumors, liver and bone metastases, paraganglioma, cerebellar, spinal, and retinal hemangioblastomas, polycythemia, and chondrosarcoma. See Fig. 1 for family pedigree.

      CasePresentingHPOs: HP:0006748; HP:0030405 (adrenal pheochromocytoma; pancreatic endocrine tumor)

      CaseHPOFreeText: Patient presented with his initial VHL-related clinical manifestations at 17Y0M. She had adrenal pheochromocytoma and pancreatic endocrine tumor. She was diagnosed with VHL subtype 2A at age 18Y0M (see table 1).

      CaseNotHPOs: HP:0002668 (paraganglioma)

      CaseNotHPOFreeText: Patient does not have paraganglioma.

      CasePreviousTesting: N/A

      PreviouslyPublished: 8550742

      SupplementalData: N/A

      Variant: p.V166F (c.496G>T)

      LegacyVariant: N/A

      CaseProblemVariantFreeText: N/A

      ClinVarID: 2224, https://www.ncbi.nlm.nih.gov/clinvar/variation/2224/

      CAID: N/A

      gnomAD: N/A

      VariantEvidence: N/A

      MutationType: missense_variant; transversion

      CivicName: V166F (c.496G>T)

      MultipleGeneVariants: N/A

    3. 16 different families

      PatientID: IX-I

      KindredID: 9

      Case: M, 68Y0M, Ethnicity Unknown

      DiseaseAssertion: VHL

      FamilyInfo: No family history reported.

      CasePresentingHPOs: HP:0006748; HP:0002668; HP:0030405; HP:0001737; HP:0006880 (adrenal pheochromocytoma, paraganglioma, pancreatic endocrine tumor, pancreatic cyst, cerebellar hemangioblastoma)

      CaseHPOFreeText: Patient presented with adrenal pheochromocytoma, paraganglioma, pancreatic endocrine tumor, pancreatic cyst, and cerebellar hemangioblastoma at age 55Y0M and was diagnosed with VHL type 2A (see table 2).

      CaseNotHPOs: HP:0000107; HP:0005584 (renal cyst; renal cell carcinoma)

      CaseNotHPOFreeText: Patient negative for renal cell carcinoma and renal cysts.

      CasePreviousTesting: N/A

      PreviouslyPublished: N/A

      SupplementalData: N/A

      Variant: complete deletion

      LegacyVariant: N/A

      CaseProblemVariantFreeText: N/A

      ClinVarID: N/A

      CAID: N/A

      gnomAD: N/A

      VariantEvidence: N/A

      MutationType: deletion

      CivicName: NULL (deletion)

      MultipleGeneVariants: N/A

    1. PatientID: VII-2

      KindredID: 1

      Case: M, Age Unknown, Ethnicity Unknown

      DiseaseAssertion: VHL

      FamilyInfo: Family’s roots were traced to the German town of Leipzig in Saxony, from whence the original 11 siblings had immigrated to America around 1670. The following report is a 2011 updated pedigree on the previously reported Tisherman kindred. At the time of this study, 43/49 patients have undergone mutational analysis revealing the VHL familial mutation (Y112H) and 35/49 patients have clinical VHL manifestations. Phenotypic cumulative lifetime risk was 71% for Pheo/PGL, 15% for hemangioblastoma, 33% for retinal angioma, 3% for renal cell carcinoma, and 3% for pancreatic cysts. 6 members of the family (all deceased; 4 males, 2 females) had suspected VHL and 2 (males) of these were suspected to have had Pheo/PGL.

      CasePresentingHPOs: HP:0009711 (Retinal capillary hemangioma)

      CaseHPOFreeText: Phenotype noted as: Pheo/PGL (unclear which of the two or if both apply to this patient).

      CaseNotHPOs: HP:0005584; HP:0002666; HP:0002668 (Renal cell carcinoma, Pheochromocytoma, Paraganglioma)

      CaseNotHPOFreeText: N/A

      CasePreviousTesting: N/A

      PreviouslyPublished: 9201016; 8239848 (no genetic information; only phenotypes)

      SupplementalData: N/A

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

      LegacyVariant: N/A

      CaseProblemVariantFreeText: N/A

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

      CAID: N/A

      gnomAD: N/A

      VariantEvidence: N/A

      MutationType: missense_variant;transition

      CivicName: Y112H (c.334T>C)

      MultipleGeneVariants: N/A

    2. PatientID: VI-6

      KindredID: 1

      Case: F, Age Unknown, Ethnicity Unknown

      DiseaseAssertion: VHL (Asymptomatic)

      FamilyInfo: Family’s roots were traced to the German town of Leipzig in Saxony, from whence the original 11 siblings had immigrated to America around 1670. The following report is a 2011 updated pedigree on the previously reported Tisherman kindred. At the time of this study, 43/49 patients have undergone mutational analysis revealing the VHL familial mutation (Y112H) and 35/49 patients have clinical VHL manifestations. Phenotypic cumulative lifetime risk was 71% for Pheo/PGL, 15% for hemangioblastoma, 33% for retinal angioma, 3% for renal cell carcinoma, and 3% for pancreatic cysts. 6 members of the family (all deceased; 4 males, 2 females) had suspected VHL and 2 (males) of these were suspected to have had Pheo/PGL.

      CasePresentingHPOs: N/A

      CaseHPOFreeText: N/A

      CaseNotHPOs: HP:0005584; HP:0009711; HP:0002666; HP:0002668 (Renal cell carcinoma, Retinal capillary hemangioma, Pheochromocytoma, Paraganglioma)

      CaseNotHPOFreeText: N/A

      CasePreviousTesting: N/A

      PreviouslyPublished: 9201016; 8239848 (no genetic information; only phenotypes)

      SupplementalData: N/A

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

      LegacyVariant: N/A

      CaseProblemVariantFreeText: N/A

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

      CAID: N/A

      gnomAD: N/A

      VariantEvidence: N/A

      MutationType: missense_variant;transition

      CivicName: Y112H (c.334T>C)

      MultipleGeneVariants: N/A

    1. The genotype and phenotype in the large Chinese family with VHL disease. a The pedigree of the family 6 with 18 affected patients. b DNA sequence analysis showing a A–G transition at nucleotide 446. The change results in the mutation from Asn to Ser in codon78.

      PatientID: IV-13

      GroupID/ KindredID: 6

      Case: Age unknown, M, Chinese

      DiseaseAssertion: asymptomatic

      FamilyInfo: Positive - 22 family members were recorded with the given mutation. 18 had VHL manifestations while 4, including this patient, are asymptomatic carriers. See pedigree (Fig 3.), or follow GroupID/KindredID: 6

      CasePresentingHPOs: None

      CaseHPOFreeText: N/A

      CaseNotHPOs: HP:0010797; HP:0002666; HP:0009711; HP:0005584; HP:0001732 (hemangioblastoma, pheochromocytoma, retinal capillary hemangioma, Renal cell carcinoma,abnormality of the pancreas)

      CaseNotHPOFreeText: N/A

      CasePreviousTesting: N/A

      PreviouslyPublished: N/A

      SupplementalData: N/A

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

      CaseProblemVariantFreeText: Named a carrier as positively tested without symptoms

      LegacyVariant: p.N78S (c.446A>G)

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

      CAID: N/A

      gnomAD: N/A

      VariantEvidence: N/A

      MutationType: missense_variant; transition

      CivicName: N78S (c.233A>G)

      MultipleGeneVariants: N/A

    1. Screening of 92 unrelated patients with VHL disease revealed 61 DNA variants. No variants were found in 96 control cases. Direct sequencing on peripheral blood was systematically performed on exon 1 PCR products. Southern blotting was used to search for larger alterations to the gene. The W117C (c.351G>T) missense mutation was found in 4 VHL type 1 (no pheochromocytoma) family members (patient/proband no. V13).

    2. GroupID: V43

      DiseaseAssertion: VHL

      GroupSize: 4

      GroupNumberMales: N/A

      GroupNumberFemales: N/A

      GroupEthnicity: French

      GroupAgeRange: N/A

      GroupInfo: Patients are grouped by family.

      FamilyInfo: 4/7 members of this family that underwent genetic testing had the same mutation.

      GroupPresentingHPOs: N/A

      GroupHPOFreeText: Diagnosed with VHL Type 1.

      GroupNotHPOs: HP:0002666 (Pheochromocytoma)

      GroupNotHPOFreeText: N/A

      GroupPreviousTesting: N/A

      PreviouslyPublished: Likely 15300849

      SupplementalData: N/A

      Variant: p.L158dup (c.473_474insTTT)

      LegacyVariant: N/A

      CaseProblemVariantFreeText: N/A

      ClinVarID: N/A

      CAID: CA2573320246, https://reg.clinicalgenome.org/redmine/projects/registry/genboree_registry/by_caid?caid=CA2573320246

      gnomAD: N/A

      VariantEvidence: N/A

      MutationType: inframe_insertion

      CivicName: L158dup (c.473_474insTTT)

      MultipleGeneVariants: N/A

    1. Deletion p.(Phe76del)

      VHL germline mutation carriers who had an ophthalmologic examination at the Erasmus Medical Centre or the Rotterdam Eye Hospital between 1984 and 2017, and were diagnosed with retinal hemangioblastoma (RH) were included in this study. A diagnosis of RH was based on the clinical appearance of a vasoproliferative retinal tumour. Peripheral blood samples from every member that had clinically suspected VHL disease of each family were collected for VHL mutation analysis. A total of 21 patients from 10 families were included on the basis of both a VHL germline mutation and ocular manifestations. Copy number analyses were carried out by multiplex ligation dependent probe amplification (MLPA) and fluorescence in situ hybridization (FISH). Mutations were described as one of the following two groups: truncating (complete deletion, partial deletion, nonsense mutation, splice site mutation, duplication and insertion) or missense. Ocular manifestations were not reported on an individual level, but rather were broken down based on the two groups. From Pedigree (family) 3, one individual was suspected of VHL disease and mutational analysis revealed an in-frame germline P76del(c.227_229del) deletion. This individual had RH development.

    1. Mutation analysisAll germ-line mutations were documented by the results of genetic testing performed in Florence according to standardized protocols. DNA was extracted from the peripheral blood leukocytes of each patient using the NucleoSpin Blood L kit (Macherey-Nagel, Düren, Germany) and analyzed for germ-line mutations of SDHA (all exons), SDHB (all exons), SDHC (all exons), SDHD (all exons), SDHAF2 (all exons), MAX (all exons), TMEM127 (all exons), and VHL (all exons). For each gene, coding regions and exon–intron boundaries were amplified by PCR as described previously (Astuti et al. 2001). PCR products, purified using a commercial kit (PCR purification kit, Qiagen), were subjected to 2% agarose gel electrophoresis with ethidium bromide staining and subsequently sequenced with a genetic analyzer (ABI PRISM 310; Applied Biosystems, Milan, Italy).Multiplex ligation-dependent probe amplification reactionsPatients younger than 50 years, whose DNA sequencing was wild type for SDHB, SDHC, SDHD, SDHAF2, and VHL, underwent analysis for genomic rearrangements in these genes. For this purpose, we used commercial kits for multiplex ligation-dependent probe amplification (MLPA)-based assays (SALSA MLPA P016B VHL and SALSA MLPA P226 SDHD; MRC-Holland, Amsterdam, The Netherlands) following the manufacturers' instructions.Amplification products were diluted in HiDi formamide containing 500TAMRA internal size standards (MRC-Holland) and then separated by size using an ABI PRISM 310 Genetic Analyser (Applied Biosystems). Electropherograms were analyzed using Coffalyser MLPA DAT software (MRC-Holland).

      ArticleReferenceSequence: Not specified – Assumption: variants assumed to have been documented by the author under reference sequence NM_000551.3

      GenotypingMethod: For each gene (MAX, SDHA, SDHB, SDHC, SDHD, SDHAF2, TMEM127, VHL), all coding regions and exon–intron boundaries were amplified by PCR. Multiplex ligation-dependent probe amplification (MLPA)-based assays (SALSA MLPA P016B VHL and SALSA MLPA P226 SDHD; MRC-Holland, Amsterdam, The Netherlands).

      SamplingMethod: peripheral blood leukocytes

    1. 2/M 10 Yes 63 271 Hypersensitive NI 376G>T/wt 

      PatientID: 2

      KindredID: 1

      Case: M, 10Y0M, Ukrainian

      DiseaseAssertion: Asymptomatic

      FamilyInfo: His sister (patient 1) also had polycythemia and was heterozygeous for the mutation. Mutation inherited from father. The father was not polycythemic, but his BFU-Es were hypersensitive to Epo.

      CasePresentingHPOs: HP:0001901 (polycythemia)

      CaseHPOFreeText: Patient had a hematocrit of 63%, erythropoietin level of 271 mIU/mL, and had hypersensitivity of erythroid progenitors to Epo.

      CaseNotHPOs: N/A

      CaseNotHPOFreeText: No tumor masses were detected by repeated CT scans of his abdomen or chest and by magnetic resonance imaging (MRI) of the head.

      CasePreviousTesting: N/A

      PreviouslyPublished: N/A

      SupplementalData: N/A

      Variant: p.D126Y(c.376G>T)

      LegacyVariant: N/A

      CaseProblemVariantFreeText: N/A

      ClinVarID: 2230 https://www.ncbi.nlm.nih.gov/clinvar/variation/2230/

      CAID: CA020319 http://reg.clinicalgenome.org/redmine/projects/registry/genboree_registry/allele?hgvsOrDescriptor=NM_000551.3%3Ac.376G%3ET

      gnomAD: N/A

      VariantEvidence: Patient was heterozygous for the mutation.

      MutationType: missense_variant;transversion

      CivicName: D126Y(c.376G>T)

      MultipleGeneVariants: N/A

    1. F119 18 F left 3 23  2 VHL R64P VHL

      PatientID: F119

      KindredID: 1

      Case: F, 20Y0M, Ethnicity Unknown

      DiseaseAssertion: VHL

      FamilyInfo: N/A

      CasePresentingHPOs: HP:0002666 (pheochromocytoma)

      CaseHPOFreeText: The patient had a pheochromocytoma in the left adrenal gland. It was measured to be 3 cm in size and 23 grams in weight.

      CaseNotHPOs: N/A

      CaseNotHPOFreeText: N/A

      CasePreviousTesting: RET/SDHB/SDHD

      PreviouslyPublished: N/A

      SupplementalData: N/A

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

      LegacyVariant: N/A

      CaseProblemVariantFreeText: N/A

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

      CAID: N/A

      gnomAD: N/A

      VariantEvidence: N/A

      MutationType: missense_variant;transversion

      CivicName: R64P(c.191G>C)

      MultipleGeneVariants: N/A

    1. PatientID: 10

      KindredID: 10

      Case: M, 26Y0M, Ethnicity Unknown

      DiseaseAssertion: VHL

      FamilyInfo: N/A

      CasePresentingHPOs: HP:0009713 (spinal hemangioblastoma)

      CaseHPOFreeText: The patient had a spinal hemangioblastoma at the C4/C5 boundary. The patient showed an high-normal Hb values (18.6) which fits the polyglobulia disease criteria. After the spinal hemangioblastoma was removed, the Hb normalized.

      CaseNotHPOs: N/A

      CaseNotHPOFreeText: N/A

      CasePreviousTesting: N/A

      PreviouslyPublished: N/A

      SupplementalData: N/A

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

      LegacyVariant: p.S65W(c.407C>G)

      CaseProblemVariantFreeText: 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

    1. PatientID: None (Proband)

      KindredID: 1

      Case: F, 24Y0M, Ethnicity Unknown

      DiseaseAssertion: VHL

      FamilyInfo: Aunt had a metastatic and progressinve pNET in the context of VHL.

      CasePresentingHPOs: HP:0002666; HP:0030405 (Pheochromocytoma, Pancreatic endocrine tumor)

      CaseHPOFreeText: Underwent bilateral adrenalectomies for pheochromocytomas and a distal pancreatectomy and splenectomy for a grade 2 well-differentiated pNET. Post-operation, 3 new pNET’s developed and continued to grow. Due to the rate of growth of the lesion, her family history of malignant disease and concerns about her ability to manage resultant pancreatic endocrine insufficiency, she underwent a trial of primary somatostatin analog therapy. After 6 months, imaging showed significant decrease in size of all of the pNETs

      CaseNotHPOs: N/A

      CaseNotHPOFreeText: N/A

      CasePreviousTesting: N?A

      PreviouslyPublished: N/A

      SupplementalData: N/A

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

      LegacyVariant: N/A

      CaseProblemVariantFreeText:

      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-

      VariantEvidence: N/A

      MutationType: missense_variant;transition

      CivicName: R167W (c.499C>T)

      MultipleGeneVariants: N/A

    1. nt 665 T/C* 151 Ile→Thr I151T Missense 2

      A cohort of 141 patients with hemangioblastomas of the central nervous system was analyzed. 81 patients had germline mutations in the VHL gene, analyzed through peripheral blood by Southern blotting and SSCP analysis. This missense mutation (c.452T>C) was recorded in the paper as c.665T>C due to a difference in transcript sequence. It was found in 2 patients with hemangioblastomas of the central nervous system. Any family information or relations is unknown. No other phenotypes described. This (member) was published in a future publication: PMID: 32179488.

    1. c.232A > Gp.Asn78Asp

      Direct sequencing and multiplex ligation dependent probe amplification were performed on thirteen unrelated subjects with VHL mutations. The clinical manifestations and family histories of the subjects were evaluated. An 11 year old Korean male patient presented with nausea, vomiting and spinal and cerebellar hemangioblastomas (11Y), multiple pancreatic neuroendocrine tumors (20Y), and renal cysts (20Y). Genetic testing confirmed a missense mutation at c.232A>G of the VHL gene. Family history is unknown.

    2. 7M–1c.233A > Gp.Asn78Ser11414––14, M14, B4

      PatientID: 7

      KindredID: 7

      Case: M, 14Y0M, Korean

      DiseaseAssertion: VHL

      FamilyInfo: None

      CohortInfo: Thirteen unrelated patients with germline VHL mutations who were diagnosed with VHL disease were evaluated.

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

      CaseHPOFreeText: The patient was found to have a CNS hemangioblastoma, retinal capillary hemangioma, multiple pancreatic cysts and bilateral renal cysts at age 14. MRI of the brain showed a tiny well-enhanced nodule at the cervicomedullary junction with an adjacent prominent vascular structure.

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

      CaseNotHPOFreeText: N/A

      CasePreviousTesting: N/A

      PreviouslyPublished: N/A

      SupplementalData: N/A

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

      CaseProblemVariantFreeText: N/A

      LegacyVariant: N/A

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

      CAID: N/A

      gnomAD: N/A

      VariantEvidence: N/A

      MutationType: missense_variant; transition

      CivicName: N78S (c.233A>G)

      MultipleGeneVariants: N/A

    1. 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. We identified deletions ranging from 0.5 kb to 250 kb affecting part of or the entire VHL and flanking genes in 54 families.

      GroupID: 7

      DiseaseAssertion: VHL

      GroupSize: N/A GroupNumberMales: N/A GroupNumberFemales: N/A GroupEthnicity: N/A GroupAgeRange: N/A

      GroupInfo: 54 VHL deletion families from the Freiburg registry were selected in order to assist in the correlation of VHL deletions to clinical phenotypes.

      GroupPresentingHPOs: HP:0005584; HP:0000107; HP:0002666; HP:0009711; HP:0010797; HP:0009713; HP:0001737 (Renal cell carcinoma, Renal cyst, Pheochromocytoma, Retinal capillary hemangioma, Hemangioblastoma, Spinal hemangioblastoma, Pancreatic cysts)

      GroupHPOFreeText: # of affected individuals: Renal cell carcinoma (1), Renal cyst (1), Pheochromocytoma (1), Retinal capillary hemangioma (1), Hemangioblastoma/brain/cerebellum (1), Spinal hemangioblastoma (1), Pancreatic cysts (1)

      GroupNotHPOs: N/A

      GroupNotHPOFreeText: N/A

      GroupPreviousTesting: N/A

      PreviouslyPublished: N/A

      SupplementalData: Supplemental Table 2, Table 1, Table 3

      Variant: Exon 1 Deletion (c.1-?_340+?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 1 Deletion

      MultipleGeneVariants: N/A

    1. VHL kindreds for germline mutations and calculated the age related tumour risks for different classes of VHL gene mutations.

      PatientID: None

      KindredID: 134

      Case: Age, sex ethnicity unknown

      DiseaseAssertion: unknown; paper focused only on pheochromocytoma

      FamilyInfo: No specific family info was present; although this was recorded as a family germline mutation belonging to Family ID 134

      CasePresentingHPOs: N/A

      CaseHPOFreeText: Unknown

      CaseNotHPOs: N/A

      CaseNotHPOFreeText: N/A

      CasePreviousTesting: N/A

      PreviouslyPublished: 32179488, 17024664

      SupplementalData: N/A

      Variant: p.F76del (c.227_229delTCT)

      CaseProblemVariantFreeText: N/A

      LegacyVariant: p.F76del (c.440delTCT)

      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_229delTTC)

      MultipleGeneVariants: N/A

    2. VHL kindreds for germline mutations and calculated the age related tumour risks for different classes of VHL gene mutations.

      In a study of 138 unrelated VHL families, 109 germline mutations were found. Missense mutations were more frequently found in families with pheochromocytoma (PC). Deletions, nonsense, and frameshift mutations were more frequently found in families without PC. Large deletions and mutations predicted to cause truncated protein were associated with lower risk of PC. The mutation D121Mfs*38 (c.361delG) was referred to in the paper by c.574delG due to a difference in transcript sequence. This FS mutation found in a VHL family without PC (family ID 147).

    3. missense mutations

      PatientID: None

      KindredID: 77

      Case: Age, sex ethnicity unknown

      DiseaseAssertion: unknown; paper focused only on pheochromocytoma

      FamilyInfo: No specific family info was present; although this was recorded as a family germline mutation belonging to Family ID 77

      CasePresentingHPOs: Unknown

      CaseHPOFreeText: N/A

      CaseNotHPOs: N/A

      CaseNotHPOFreeText: N/A

      CasePreviousTesting: N/A

      PreviouslyPublished: N/A

      SupplementalData: N/A

      Variant: p.V170D (c.509T>A)

      CaseProblemVariantFreeText: N/A

      LegacyVariant: p.V170D (c.722T>A)

      ClinVarID: 625256 https://www.ncbi.nlm.nih.gov/clinvar/variation/625256/

      CAID: N/A

      gnomAD: N/A

      VariantEvidence: N/A

      MutationType: missense_variant; transversion

      CivicName: V170D (c.509T>A)

      MultipleGeneVariants: N/A

    1. One hundred and sixteen unrelated VHL disease patients have been investigated by molecular genetic analysis. Twenty-two of these were previously shown to have germline deletions on Southern analysis, and in the present study the remaining 94 patients were screened for intragenic mutations via SSCP and heteroduplex analysis of 855 bp of the VHL coding sequence and 800 bp of the 3' UTR. An intragenic mutation was identified in 55 (59%) out of 94 patients without germline deletions on Southern analysis. In all patients with multiple affected family members the missense mutation segregated with the disease. Large deletions or intragenic mutations predicted to cause a truncated protein were found in 36 of 53 families without pheochromocytoma (VHL type 1) and 2 of 12 families with pheochromocytoma (VHL type 2). This study also investigated the frequency of different mutation classes between kindreds with and without pheochromocytoma. The p.N131Pfs*3 (c.390_391delTA) deletion (noted as p.201FS (c.603delTA) in the paper due to a difference in reference transcript used) was found in at least one patient in kindred 64. Pheochromocytoma was not observed in any members of this kindred (implying the affected patient(s) had VHL disease type 1). No other familial phenotypic information could be inferred from the paper.

    2. One hundred and sixteen unrelated VHL disease patients have been investigated by molecular genetic analysis. Twenty-two of these were previously shown to have germline deletions on Southern analysis, and in the present study the remaining 94 patients were screened for intragenic mutations via SSCP and heteroduplex analysis of 855 bp of the VHL coding sequence and 800 bp of the 3' UTR. An intragenic mutation was identified in 55 (59%) out of 94 patients without germline deletions on Southern analysis. In all patients with multiple affected family members the missense mutation segregated with the disease. Large deletions or intragenic mutations predicted to cause a truncated protein were found in 36 of 53 families without pheochromocytoma (VHL type 1) and 2 of 12 families with pheochromocytoma (VHL type 2). This study also investigated the frequency of different mutation classes between kindreds with and without pheochromocytoma. The L153Cfs*6 (c.457del) deletion (noted as p.224fs (c.670delC) in the paper due to a difference in reference transcript used) was found in at least one patient in kindred 41, and at least one patient in kindred 99. Pheochromocytoma was not observed in any members of kindred 41 (implying the affected patient(s) had VHL disease type 1). No familial phenotypic information could be inferred from the paper for kindred 99.

    3. KindredID: 21

      GroupID: 55

      GroupSize: Unknown

      GroupNumberMales: Unknown

      GroupNumberFemales: Unknown

      GroupEthnicity: Unknown

      GroupAgeRange: Unknown

      DiseaseAssertion: VHL

      GroupInfo: Kindred no.21 describes a family where at least one member (unspecified how many) had this mutation in the VHL gene. Family history indicates that pheochromocytoma is not present in this kindred.

      GroupPresentingHPOs: N/A

      GroupHPOFreeText: No phenotypic information is listed for this kindred.

      GroupNotHPOs: HP:0002666 (Pheochromocytoma)

      GroupNotHPOFreeText: Pheochromocytoma was not observed in any members of the affected patient(s)' family (VHL type 1).

      GroupPreviousTesting: N/A

      PreviouslyPublished: N/A

      SupplementalData: N/A

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

      LegacyVariant: c.796C>T (p.Q266*)

      CaseProblemVariantFreeText: N/A

      ClinVarID: 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

    1. 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. Molecular and clinical analysis of 126 French VHL families tested for renal involvement revealed 92 different mutations. 90 of these families had renal involvement. The p.Y156* (c.468T>G) germline variant of the VHL gene was detected in a family (ID 3). Member 37 had no renal involvement. Member 38 presented with moderate renal disease (RCC). Members 47 and 3 presented with severe renal disease (RCC). The paper states that this family is previously reported in PMID 12202531 and/or 9829912.

    2. GroupID: 44

      DiseaseAssertion: VHL

      GroupSize: 5

      GroupNumberMales: N/A

      GroupNumberFemales: N/A

      GroupEthnicity: French

      GroupAgeRange: N/A

      GroupInfo: 5 members of this family were found to have the germline c.226_228del variant of the VHL gene. Member 4975 presented with moderate renal disease (RCC), members 4978, 4977 and 4976 presented with mild renal disease and member 5283 had unknown renal involvement. Families were recruited from the French VHL Registry. Enrolment in the study required identification of the germline VHL mutation (currently 85% of the families included in the French VHL Registry) and available data regarding renal phenotype. A total of 126 families fulfilled these criteria.

      GroupPresentingHPOs: HP:0009726; HP:0005584 (Renal neoplasm, Renal cell carcinoma)

      GroupHPOFreeText: Mild renal disease (simple renal cyst, multicystic kidney[s], small lesion [less than 10 mm in size] of unknown significance, or small solid tumor without indication for surgical removal [less than 30 mm in size]). Moderate renal disease (less than five solid lesions requiring surgical treatment, either unilateral or bilateral).

      GroupNotHPOs: N/A

      GroupNotHPOFreeText: N/A

      GroupPreviousTesting: N/A

      SupplementalData: Phenotype and genotype information can be found in Supplementary Table S1.

      Variant: p.F76del (c.226_228del)

      LegacyVariant: N/A

      CaseProblemVariantFreeText: N/A

      ClinVarID: N/A

      CAID: CA357012, https://reg.clinicalgenome.org/redmine/projects/registry/genboree_registry/allele?hgvsOrDescriptor=NM_000551.3%3Ac.226_228del

      gnomAD: N/A

      VariantEvidence: N/A

      MutationType: inframe_deletion; deletion

      CivicName: F76del (c.226_228del)

      MultipleGeneVariants: N/A

    3. Molecular and clinical analysis of 126 French VHL families tested for renal involvement revealed 92 different mutations. 90 of these families had renal involvement. The p.P71Lfs*61 (c.211_212insT) germline variant of the VHL gene was detected in a family (ID 96). Members 5997 and 5993 have unknown renal involvement. Member 5999 presented with mild renal disease. The paper states that this family is previously reported in PMID 12202531, where 1 patient with this mutation is reported and assumed to be part of this family.

    4. GroupID: 411

      DiseaseAssertion: VHL

      GroupSize: 2

      GroupNumberMales: N/A

      GroupNumberFemales: N/A

      GroupEthnicity: French

      GroupAgeRange: N/A

      GroupInfo: 3 members of this family were found to have the c.500G>A germline variant of the VHL gene. Member 9710 presented with mild renal disease (RCC) and members 13888 and 12271 had unknown renal involvement. Families were recruited from the French VHL Registry. Enrolment in the study required identification of the germline VHL mutation (currently 85% of the families included in the French VHL Registry) and available data regarding renal phenotype. A total of 126 families fulfilled these criteria.

      GroupPresentingHPOs: HP:0005584 (Renal cell carcinoma)

      GroupHPOFreeText: Mild renal disease (simple renal cyst, multicystic kidney[s], small lesion [less than 10 mm in size] of unknown significance, or small solid tumor without indication for surgical removal [less than 30 mm in size]).

      GroupNotHPOs: N/A

      GroupNotHPOFreeText: N/A

      GroupPreviousTesting: N/A

      PreviouslyPublished: N/A

      SupplementalData: Phenotype and genotype information can be found in Supplementary Table S1.

      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

    5. GroupID: 313

      DiseaseAssertion: VHL

      GroupSize: 3

      GroupNumberMales: N/A

      GroupNumberFemales: N/A

      GroupEthnicity: French

      GroupAgeRange: N/A

      GroupInfo: 3 members of this family were found to harbor the c.340+1_340+5delGTACG germline variant of the VHL gene. Members 7171 and 7170 had unknown renal involvement. Member 5545 presented with severe renal disease (RCC). Families were recruited from the French VHL Registry. Enrolment in the study required identification of the germline VHL mutation (currently 85% of the families included in the French VHL Registry) and available data regarding renal phenotype. A total of 126 families fulfilled these criteria.

      GroupPresentingHPOs: HP:0005584 (Renal cell carcinoma)

      GroupHPOFreeText: Moderate renal disease (less than five solid lesions requiring surgical treatment, either unilateral or bilateral).

      GroupNotHPOs: N/A

      GroupNotHPOFreeText: N/A

      GroupPreviousTesting: N/A

      PreviouslyPublished: Paper states that this family is previously reported in PMID 9829912, where 1 individual is reported to have the “IVS1+1del5” splice site variant which is assumed to correspond to a member of the current family.

      SupplementalData: Phenotype and genotype information can be found in Supplementary Table S1.

      Variant: c.340+2_340+6del

      LegacyVariant: N/A

      CaseProblemVariantFreeText: N/A

      ClinVarID: N/A

      CAID: CA357098, https://reg.clinicalgenome.org/redmine/projects/registry/genboree_registry/allele?hgvsOrDescriptor=NM_000551.3%3Ac.340%2B1_340%2B5del

      gnomAD: N/A

      VariantEvidence: Variant is reported as c.340+1_340+5del and was mapped to c.340+2_340+6del. Authors state that this mutation is predicted to disturb the splicing process.

      MutationType: splice_site_variant; deletion; minus_2_frameshift_variant

      CivicName: Splice Site (c.340+2_340+6del)

      MultipleGeneVariants: N/A

    6. PatientID: 13773

      KindredID: 599

      Case: Sex Unknown, Age Unknown, French

      DiseaseAssertion: VHL

      FamilyInfo: N/A

      CohortInfo: Families were recruited from the French VHL Registry. Enrolment in the study required identification of the germline VHL mutation (currently 85% of the families included in the French VHL Registry) and available data regarding renal phenotype. A total of 126 families fulfilled these criteria.

      CasePresentingHPOs: HP:0005584 (Renal cell carcinoma)

      CaseHPOFreeText: Moderate renal disease (less than five solid lesions requiring surgical treatment, either unilateral or bilateral). Individual RCC phenotype is noted as positive.

      CaseNotHPOs: N/A

      CaseNotHPOFreeText: N/A

      CasePreviousTesting: N/A

      PreviouslyPublished: N/A

      SupplementalData: Phenotype and genotype information can be found in Supplementary Table S1.

      Variant: p.F76_C77del (c.226_231del)

      LegacyVariant: N/A

      CaseProblemVariantFreeText: N/A

      ClinVarID: N/A

      CAID: CA2573130179, https://reg.clinicalgenome.org/redmine/projects/registry/genboree_registry/by_caid?caid=CA2573130179

      gnomAD: N/A

      VariantEvidence: N/A

      MutationType: inframe_deletion; deletion

      CivicName: F76_C77del (c.226_231del)

      MultipleGeneVariants: N/A

    7. PatientID: 5730

      KindredID: 269

      Case: Sex Unknown, Age Unknown, French

      DiseaseAssertion: VHL

      FamilyInfo: N/A

      CohortInfo: Families were recruited from the French VHL Registry. Enrolment in the study required identification of the germline VHL mutation (currently 85% of the families included in the French VHL Registry) and available data regarding renal phenotype. A total of 126 families fulfilled these criteria.

      CasePresentingHPOs: HP:0005584 (Renal cell carcinoma)

      CaseHPOFreeText: Severe renal disease (any solid lesion before 25 years of age, five or more solid lesions within one or two kidneys, or metastasis of renal cell carcinoma). Individual RCC phenotype is noted as positive.

      CaseNotHPOs: N/A

      CaseNotHPOFreeText: N/A

      CasePreviousTesting: N/A

      PreviouslyPublished: Paper states that this family is previously reported in PMID 12202531 and/or 9829912, where 1 and 1 individuals respectively with this mutation are reported. It is unclear if one or both of these previously reported groups are the same as the current family. These previously published individuals could alternatively correspond to family 1005.

      SupplementalData: Phenotype and genotype information can be found in Supplementary Table S1.

      Variant: p.L188P (c.563T>C)

      LegacyVariant: N/A

      CaseProblemVariantFreeText: N/A

      ClinVarID: 625266, https://www.ncbi.nlm.nih.gov/clinvar/variation/625266/

      CAID: N/A

      gnomAD: N/A

      VariantEvidence: N/A

      MutationType: missense_variant;transition

      CivicName: L188P (c.563T>C)

      MultipleGeneVariants: N/A

    1. VHL-19c.500G > Ap.Arg167Gln[2]noA2MultipleBilateral––––

      PatientID: VHL-19

      KindredID: 19

      Case: Sex Unknown, Age Unknown, Italian

      DiseaseAssertion: VHL

      FamilyInfo: None.

      CohortInfo: Forty-three index cases were referred to the Service of Medical Genetics, Genova, for germline mutation analysis in the VHL gene between 1995 and 2008.

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

      CaseHPOFreeText: Multiple hemangioblastoma of the CNS and spinal cord. Bilateral renal cell carcinoma.

      CaseNotHPOs: HP:0001737, HP:0002666, HP:0009711 (pancreatic cysts, pheochromocytoma, retinal capillary hemangioma)

      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.500 G >A)

      MultipleGeneVariants: N/A

    1. 194C>T Ser65Leu Germline mutation

      Tissues embedded in paraffin blocks were collected from 203 cHAB patients operated in different Medical Centres in Poland. Eight of these harboured germline mutations in unrelated patients from distinct undiagnosed VHL families. Various variants were unverified as somatic or germline as they were detected in tumour but blood samples were not tested. Other phenotypes and demographic information is not known. Patient 30 was found with a germline p.Ser65Leu mutation in the VHL gene. This patient also had a somatic mutation (c.266T>C p.Leu89Pro) in the tumour.

    1. c.341 G > T G114V 

      The patient cohort consisted of 57 patients (26 male and 31 female) from Southern Italy, most of whom (55 of 57) presented with solitary HGB of the CNS: 6 were syndromic and 51 were apparently sporadic. 8 patients had germline VHL mutations. Both peripheral blood and tumor tissue samples were sequenced using Big Dye Terminator Ready Reaction mix v.1.1 (Life Technologies, Foster City, CA). Sequencing reactions were loaded on an ABI 3100 capillary sequencer (Life Technologies) and analyzed using the Sequencing Analysis software v.3.7 (PE Applied Biosystems, Grand Island, NY). One Italian patient (Case ID HGB-19) with a germline missense mutation (c.341G>T; p.Gly114Val) in the VHL gene was diagnosed at age 32 with cerebellar hemangioblastoma, and developed spinal hemangioblastoma at 40Y. The patient had no family history of VHL disease.

    1. 4 16.1 Retinal angioma, cervical spine hemangioblastoma, cysts of pancreas and kidney No Germline G to A base change at −1 position of splice acceptor sequence for exon 2

      PatientID: 4

      KindredID: 4

      Case: 16Y1M, sex unknown ethnicity unknown

      DiseaseAssertion: assumed VHL

      FamilyInfo: None

      CasePresentingHPOs: HP:0006880; HP:0009711; HP:0009713; HP:0001737; HP:0000107 (cerebellar hemangioblastoma; retinal capillary hemangioma; spinal hemangioblastoma; pancreatic cysts; renal cyst)

      CaseHPOFreeText: spinal hemangioma was cervical.

      CaseNotHPOs: N/A

      CaseNotHPOFreeText: N/A

      CasePreviousTesting: N/A

      PreviouslyPublished: N/A

      SupplementalData: N/A

      Variant: c.341-1G>A

      CaseProblemVariantFreeText: N/A

      LegacyVariant: N/A

      ClinVarID: 823743 https://www.ncbi.nlm.nih.gov/clinvar/variation/823743/

      CAID: N/A

      gnomAD: N/A

      VariantEvidence: Germline G to A base change at 1 position of splice acceptor sequence for exon 2

      MutationType: splice_site_variant

      CivicName: Splice Site (c.341-1G>A)

      MultipleGeneVariants: N/A

    1. A 32-year old man was invited to our centre for a consultation at the Polish VHL Registry as a member of a family with suspected von Hippel-Lindau disease (VHL). He had a history of left facial nerve palsy at the age of 19 years due to tumour of the temporal bone. The patient was operated on a few months later and a histopathological diagnosis of choroid plexus papilloma was made. Two years later he was reoperated on due to recurrence and treated with adjunctive radiotherapy. Three years later the patient developed ataxia and was treated surgically because of a cerebellar tumour that was histopathologically diagnosed as haemangioblastoma. Due to recurrence of this tumour the patient was reoperated on two years later. He also had a history of retinal capillary angioma treated by cryo- and laser therapy.

      PatientID: None

      KindredID: 1

      Case: M, 32Y0M, Ethnicity Unknown

      DiseaseAssertion: Assumed VHL

      FamilyInfo: Many of the patient’s family members developed lesions in sites suggesting VHL including multiple central nervous system tumours (probable hemangioblastomas), renal tumours (probable renal cell carcinomas), pancreatic tumours (probable cysts and neuroendocrine tumours), temporal bone tumours (probable ELST), and some of the family members have lost their sight because of retinal detachment (probably in the case of retinal haemangiomas). However, the diagnosis of VHL has not been established in the family. Two of his children were also found to have the NM_000551.3:c.194C>T(S65L) mutation after analysis of blood samples.

      CasePresentingHPOs: HP:0030393; HP:0010797; HP:0009711 (Endolymphatic sac tumour, hemangioblastoma, retinal capillary hemangioma)

      CaseHPOFreeText: The patient had a history of left facial nerve palsy at the age of 19 years due to tumour of the temporal bone with a recurrence two years later (at 21Y). The patient was originally histopathologically diagnosed with choroid plexus papilloma, but was re-diagnosed with an endolymphatic sac tumour on reexamination of the sample. Three years later (24Y) the patient developed ataxia because of a cerebellar tumour that was histopathologically diagnosed as hemangioblastoma. He had a recurrence two years later (26Y). He also had a history of retinal capillary angioma.

      CaseNotHPOs: N/A

      CaseNotHPOFreeText: N/A

      CasePreviousTesting: N/A

      PreviouslyPublished: N/A

      SupplementalData: N/A

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

      LegacyVariant: p.S65L (c.407C>T)

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

      gnomAD: 0.000, https://gnomad.broadinstitute.org/variant/3-10183725-C-T

      VariantEvidence: N/A

      MutationType: missense_variant;transition

      CivicName: S65L(c.194C>T)

      MultipleGeneVariants: N/A

    1. complete vhl gene deletion in 2 patients

      PatientID: 19

      KindredID: 19

      Case: 43Y0M, sex unknown, ethnicity unknown

      DiseaseAssertion: VHL

      FamilyInfo: N/A

      CasePresentingHPOs: HP:0010797; HP:0005584; HP:0030405; HP:0009711 (hemangioblastoma; renal cell carcinoma; pancreatic endocrine tumor; retinal capillary hemangioma)

      CaseHPOFreeText: See Table 1&2 for retinal capillary hemangioma information

      CaseNotHPOs: N/A

      CaseNotHPOFreeText: N/A

      CasePreviousTesting: N/A

      PreviouslyPublished: N/A

      SupplementalData: N/A

      Variant: Null (Complete deletion)

      CaseProblemVariantFreeText: N/A

      LegacyVariant: N/A

      ClinVarID: N/A

      CAID: N/A

      gnomAD: N/A

      VariantEvidence: Stated in paper as “del VHL”; complete vhl gene deletion

      MutationType: deletion (exon_loss_variant)

      CivicName: DELETION

      MultipleGeneVariants: N/A

    2. detected point germline vhl mutations in 14 patients

      PatientID: 17

      KindredID: 17

      Case: 20Y0M, sex unknown, ethnicity unknown

      DiseaseAssertion: VHL

      FamilyInfo: N/A

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

      CaseHPOFreeText: See Table 1&2 for retinal capillary hemangioma information

      CaseNotHPOs: N/A

      CaseNotHPOFreeText: N/A

      CasePreviousTesting: N/A

      PreviouslyPublished: N/A

      SupplementalData: N/A

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

      CaseProblemVariantFreeText: N/A

      LegacyVariant: 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: N/A

      MutationType: missense_variant;transition

      CivicName: S65L (c.194C>T)

      MultipleGeneVariants: N/A

    1. 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. PatientID: 8

      KindredID: 8

      Case: M,35Y0M, Ethnicity Unknown

      DiseaseAssertion: VHL

      FamilyInfo: N/A

      CohortInfo: Thirteen patients with a supratentorial hemangioblastoma.

      CasePresentingHPOs: HP:0010797 (hemangioblastoma)

      CaseHPOFreeText: The patient had a meckel cave hemangioblastoma at age 28. The patient had a papillary edema and pituitary stalk hemangioblastoma at age 34. The patient died of VHL disease.

      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

    1. PatientID: 1

      KindredID: 1

      Case: M, 68Y0M, Ethnicity unknown

      DiseaseAssertion: VHL

      FamilyInfo: None.

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

      CaseHPOFreeText: Patient was found observed to have retinal angioma (retinal capillary hemangioma) and a right kidney cortex cyst (30mm). Patient's pheochromocytoma was found incidentally and he remained asymptomatic with steady weight.

      CaseNotHPOs: N/A

      CaseNotHPOFreeText: N/A

      CasePreviousTesting: RET, SDHB, SDHC and SDHD

      PreviouslyPublished: N/A

      SupplementalData: N/A

      Variant: p.P25L (c.74C>T)

      CaseProblemVariantFreeText: N/A

      LegacyVariant: N/A

      ClinVarID: 93330 https://www.ncbi.nlm.nih.gov/clinvar/variation/93330/

      CAID: N/A

      gnomAD: 0.002988 https://gnomad.broadinstitute.org/variant/3-10183605-C-T

      VariantEvidence: N/A

      MutationType: missense_variant;transition

      CivicName: P25L (c.74C>T)

      MultipleGeneVariants: N/A

    1. PatientID: None

      KindredID: VHL23

      Case: M, 13Y0M, Ethnicity Unknown

      DiseaseAssertion: VHL

      FamilyInfo: N/A

      CohortInfo: A total of 190 patients recruited by the COMETE network over 15 years were included in the study.

      CasePresentingHPOs: HP:0002666 (Pheochromocytoma)

      CaseHPOFreeText: The patient had one malignant pheochromocytoma.

      CaseNotHPOs: N/A

      CaseNotHPOFreeText: N/A

      CasePreviousTesting: RET/SDHB/SDHC/SDHD

      PreviouslyPublished: N/A

      SupplementalData: Table 1 of Supplementary

      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: The patient had LOH found in the BAC array CGH data.

      MutationType: missense_variant;transition

      CivicName: L178P (c.533T>C)

      MultipleGeneVariants: N/A

    2. PatientID: None

      KindredID: VHL10

      Case: F, 65Y0M, Ethnicity Unknown

      DiseaseAssertion: VHL

      FamilyInfo: N/A

      CohortInfo: A total of 190 patients recruited by the COMETE network over 15 years were included in the study.

      CasePresentingHPOs: HP:0002666 (Pheochromocytoma)

      CaseHPOFreeText: The patient had one malignant pheochromocytoma.

      CaseNotHPOs: N/A

      CaseNotHPOFreeText: N/A

      CasePreviousTesting: RET/SDHB/SDHC/SDHD

      PreviouslyPublished: N/A

      SupplementalData: Table 1 of Supplementary

      Variant: p.Y156H (c.466T>C)

      LegacyVariant: N/A

      CaseProblemVariantFreeText: N/A

      ClinVarID: N/A

      CAID: CA351756040, https://reg.clinicalgenome.org/redmine/projects/registry/genboree_registry/allele?hgvsOrDescriptor=NM_000551.3%3Ac.466T%3EC

      gnomAD: N/A

      VariantEvidence: The patient had LOH found in the BAC array CGH data.

      MutationType: missense_variant;transition

      CivicName: Y156H (c.466T>C)

      MultipleGeneVariants: N/A

    1. PatientID: 6 (tumour 8)

      KindredID: 7

      Case: Sex Unknown, Age Unknown, Ethnicity Unknown

      DiseaseAssertion: VHL

      FamilyInfo: N/A

      CasePresentingHPOs: HP:0002666 (pheochromocytoma)

      CaseHPOFreeText: Patient had one benign pheochromocytoma.

      CaseNotHPOs: N/A

      CaseNotHPOFreeText: N/A

      CasePreviousTesting: RET

      PreviouslyPublished: 7759077, 9681856

      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: CA020246 http://reg.clinicalgenome.org/redmine/projects/registry/genboree_registry/allele?hgvsOrDescriptor=NM_000551.3%3Ac.292T%3EC

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

      VariantEvidence: Refer to Table 1 for LOH information.

      MutationType: missense_variant;transition

      CivicName: Y98H (c.292T>C)

      MultipleGeneVariants: N/A

    1. Case reportA 19-year-old woman was referred to our psychiatric inpatient service in June 2017, with the suspicion of AN. At the time of hospital admission, the patient's weight was 28 kg, her height was 1.55 m and her body mass index (BMI) was 11.6 kg/m2. The patient had had no menstrual cycle for at least 1 year. Over the previous 2 years, her food intake had progressively diminished, without an immediately apparent cause. The patient was hungry but felt satiated after ingesting only a small amount of food, and had difficulty swallowing.

      PatientID: N/A (case)

      KindredID: 1

      Case: F, 19Y0M, Ethnicity Unknown

      DiseaseAssertion: VHL

      FamilyInfo: Non-consanguineous parental relationship; second child; no mention of VHL in the family.

      CasePresentingHPOs: HP:0010797; HP:0001713; HP:0002039; HP:0001824 (Hemangioblastoma; pancreatic cysts; anorexia; weight loss)

      CaseHPOFreeText: Healthy from birth, this patient was referred to a psychiatric inpatient at 19Y with the weight loss and weakness, and the suspicion on anorexia nervosa. AN was not met according to the DSM-5 or ICD-10 (despite anorexic tendencies). There were also no tendencies towards an eating disorder. Patient developed progressive gait abnormality, along with bilateral dysmetria. MRI revealed a massive lesion with vascular characteristics suggestive of a HB in the fourth ventricle causing hypertensive hydrocephalus. Abdominal CT scan revealed cystic lesions throughout the parenchymatous portion of the pancreas, suspected to be related to VHLs. Together, supported the diagnosis of VHL. The patient underwent surgery of the brain, and radiotherapy which proved to work in small degrees.

      CaseNotHPOs: HP:0002666 (pheochromocytoma)

      CaseNotHPOFreeText: All blood tests, urinalysis and chest X‑ray were unremarkable. She also had no pheochromocytoma.

      CasePreviousTesting: N/A

      PreviouslyPublished: N/A

      SupplementalData: N/A

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

      LegacyVariant: N/A

      CaseProblemVariantFreeText: 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

    1. PatientID: 6

      KindredID: 6

      Case: F, 29Y0M, Korean

      DiseaseAssertion: VHL

      FamilyInfo: N/A

      CohortInfo: 55 patients treated at Asan Medical Center in Korea treated between January 1995 and February 2013 clinically diagnosed with VHL disease and presenting with pancreatic lesions.

      CasePresentingHPOs: HP:0001737, HP:0030405 (pancreatic cysts, pancreatic endocrine tumor)

      CaseHPOFreeText: The patient presented with serous cystadenoma and pancreatic endocrine tumour at age 26. She was followed up 35.8 months later when her disease was reported to have progressed.

      CaseNotHPOs: N/A

      CaseNotHPOFreeText: N/A

      CasePreviousTesting: 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

    1. PatientID: None

      KindredID: 1

      Case: M, 11Y0M, Ethnicity unknown

      DiseaseAssertion: assumed VHL

      FamilyInfo: Familial/syndromic (FS) association

      CasePresentingHPOs:HP:0002666; HP:0009711 (Pheochromocytoma; retinal capillary hemangioma)

      CaseHPOFreeText: Benign bilateral pheochromocytoma and retinal angioma at age 11

      CaseNotHPOs: N/A

      CaseNotHPOFreeText: N/A

      CasePreviousTesting: SDHB,SDHC, SDHD, and exons 10, 11, 13, 14, 15 and 16 of RET proto-oncogene

      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

    1. Genotype-phenotype correlations of 573 VHL patients from 200 kindreds were analyzed and confirmed that higher risk of pheochromocytoma is associated with missense mutations that result in substitution of a surface amino acid or that disrupt the structural integrity of the VHL gene product (pVHL). Age-related risks of retinal hemangoblastomas and renal cell carcinoma were higher in patients with nonsense or frameshift mutations. Southern blot and/or MLPA analysis by whole blood detected this mutation. c.194delC was found in a VHL type 2 family of 7 individuals. Three family members had retinal angiomas, 2 had hemangioblastomas of the cerebellum, 2 had renal cell carcinoma, and one had pheochromocytoma.

    2. Genotype-phenotype correlations of 573 VHL patients from 200 kindreds were analyzed. Higher risk of pheochromocytoma was associated with missense mutations that result in substitution of a surface amino acid (p<=0.004) than for patients with missense mutations that disrupt the structural integrity of the VHL gene product (pVHL) or other loss of function mutations (either germline deletions or truncating mutations). A missense mutation (c.383T>G), affecting residue within the pVHL protein core, was found in a VHL type 1 family of 3 with 1 patient with retinal hemangioblastomas at 19Y and 1 patient with cerebellar hemangioblastomas at 24Y. ACMG codes as follows: Supporting evidence of pathogenicity because missense variant in a gene that has a low rate of benign missense variation and where missense variants are a common mechanism of disease (PP2).

    3. GroupID: 42

      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 identical variants. This mutation was found in 1 VHL family with 3 patients.

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

      GroupHPOFreeText: 2 had retinal hemangioblastoma at a mean age of 16Y, one had cerebellar hemangioblastoma at 16Y, and 1 had pheochromcytoma at 14Y.

      GroupNotHPOs: HP:0005584 (renal cell carcinoma)

      GroupNotHPOFreeText: N/A

      GroupPreviousTesting: N/A

      PreviouslyPublished: N/A

      SupplementalData: Supplementary Table S1.

      Variant: c.340+5G>C

      LegacyVariant: N/A

      CaseProblemVariantFreeText: N/A

      ClinVarID: 36901, https://www.ncbi.nlm.nih.gov/clinvar/variation/36901/

      CAID: N/A

      gnomAD: 0.01119 https://gnomad.broadinstitute.org/variant/3-10183876-G-C

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

      MutationType: splice_site_variant

      CivicName: Splice Region (c.340+5G>C)

      MultipleGeneVariants: N/A

    1. VHL_3Frozenc.482G>Ap.Arg161GlnM37AdrenalPCCB

      PatientID: VHL_3 (tumor ID)

      KindredID: 3

      Case: M, 37Y0M, Ethnicity Unknown

      DiseaseAssertion: Adrenal pheochromocytoma

      FamilyInfo: N/A

      CasePresentingHPOs: HP:0006748 (Adrenal pheochromocytoma)

      CaseHPOFreeText: The patient had a benign adrenal pheochromocytoma at 37Y.

      CaseNotHPOs: N/A

      CaseNotHPOFreeText: N/A

      CasePreviousTesting: N/A

      PreviouslyPublished: N/A

      SupplementalData: N/A

      Variant: p.R161Q (c.482G>A)

      LegacyVariant: N/A

      CaseProblemVariantFreeText: N/A

      ClinVarID: 182983, https://www.ncbi.nlm.nih.gov/clinvar/variation/182983/

      CAID: N/A

      gnomAD: N/A

      VariantEvidence: N/A

      MutationType: missense_variant;transition

      CivicName: R161Q (c.482G>A)

      MultipleGeneVariants: N/A

    1. Missense VHL gene mutation Arg161Gln (695G-A) was found in two families

      PatientID: (mother)

      KindredID: 2

      Case: F, Age unknown, Chinese

      DiseaseAssertion: unknown

      FamilyInfo: There is a history of non-syndromic familial pheochromocytoma in this patient’s family history as well as a confirmed presence of this same germline mutation in their daughter

      CasePresentingHPOs: N/A

      CaseHPOFreeText: N/A

      CaseNotHPOs: N/A

      CaseNotHPOFreeText: No clinical manifestations of hereditary syndromes, including MEN2A, MEN2B, VHL, and NF1 were found

      CasePreviousTesting: N/A

      PreviouslyPublished: N/A

      SupplementalData: N/A

      Variant: p.R161Q (c.482G>A)

      LegacyVariant: p.R161Q (c.695G>A)

      CaseProblemVariantFreeText: N/A

      ClinVarID: 182983 https://www.ncbi.nlm.nih.gov/clinvar/variation/182983/

      CAID: N/A

      gnomAD: N/A

      VariantEvidence: N/A

      MutationType: missense_variant;transition

      CivicName: R161Q (c.482G>A)

      MultipleGeneVariants: N/A

    1. We performed WES in 3 different regions of the primary tumor obtained before treatment, in the skull metastasis resected 7 years after temsirolimus treatment initiation, and in the germline DNA obtained from the patient's blood. The mean depth of coverage was >80x for the 3 regions of the primary tumors, 136x for the metastasis, and 94x for the blood (see supplemental eAppendix 1 for details regarding methodology, available online with this article at JNCCN.org)

      ArticleReferenceSequence: Not specified – Assumption: variants assumed to have been documented by the author under reference sequence NM_000551.3

      GenotypingMethod: WES (whole-exome sequencing), Sanger sequencing

      SamplingMethod: peripheral blood, tumor resection (primary tumor obtained before treatment, in the skull metastasis resected 7 years after temsirolimus treatment initiation)

    1. PatientID: V-14

      KindredID: 2

      Case: M, Age Unknown, German

      DiseaseAssertion: VHL

      FamilyInfo: Family 2 is comprised of 131 individuals over six generations including 65 members (50% of those at risk) with VHL type 2A (72% clinically affected, 12% obligate carriers, and 15% positive genetic analysis alone) and nearly equal gender distribution for affected status (54% male). An additional six members (II-3, II-4, II -5, III-1, III-2, and III-3) are suspected to have VHL without confirmation. Of note, the nuclear family (branch IV-13) contains 13 siblings, of whom 12 have been diagnosed with pheo. The presenting tumor types in Family 2 were pheo (70%), HB (17%), and RA (13%). No Family 2 member had RCC as the initial manifestation. Distribution of HB and RA are not described except for patient IV-8.

      CasePresentingHPOs: HP:0002666 (Pheochromocytoma)

      CaseHPOFreeText: N/A

      CaseNotHPOs: HP:0005584 (Renal cell carcinoma)

      CaseNotHPOFreeText: N/A

      CasePreviousTesting: N/A

      PreviouslyPublished: 7759077

      SupplementalData: N/A

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

      LegacyVariant: N/A

      CaseProblemVariantFreeText: N/A

      ClinVarID: 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. PatientID: V-23

      KindredID: 2

      Case: M, Age Unknown, German

      DiseaseAssertion: VHL

      FamilyInfo: Family 2 is comprised of 131 individuals over six generations including 65 members (50% of those at risk) with VHL type 2A (72% clinically affected, 12% obligate carriers, and 15% positive genetic analysis alone) and nearly equal gender distribution for affected status (54% male). An additional six members (II-3, II-4, II -5, III-1, III-2, and III-3) are suspected to have VHL without confirmation. Of note, the nuclear family (branch IV-13) contains 13 siblings, of whom 12 have been diagnosed with pheo. The presenting tumor types in Family 2 were pheo (70%), HB (17%), and RA (13%). No Family 2 member had RCC as the initial manifestation. Distribution of HB and RA are not described except for patient IV-8.

      CasePresentingHPOs: HP:0002666 (Pheochromocytoma)

      CaseHPOFreeText: N/A

      CaseNotHPOs: HP:0005584 (Renal cell carcinoma)

      CaseNotHPOFreeText: N/A

      CasePreviousTesting: N/A

      PreviouslyPublished: 7759077

      SupplementalData: N/A

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

      LegacyVariant: N/A

      CaseProblemVariantFreeText: N/A

      ClinVarID: 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. No abstract available

      PatientID: V-1

      KindredID: 1

      Case: M, 46Y0M, Ethnicity Unknown

      DiseaseAssertion: Assumed VHL

      FamilyInfo: The patient’s grandmother and two uncles had died with cerebellar hemangioblastoma, although genetic testing was not performed. The patient’s father presented with cerebellar hemangioblastoma, retinal hemangioblastoma, clear cell renal cell carcinoma, and serous cystadenoma at 68Y, adrenal pheochromocytoma at 73Y, and clear cell renal cell carcinoma metastasis in the thyroid at 74Y; he was found to carry the same mutation the patient carried. One of the patient’s sons, a 10Y male, was also found to carry the same mutation as the patient but was asymptomatic. Genealogical inquiry also revealed that the patient was distantly related to a known VHL family; one member, a 47Y male, was previously operated on for CNS hemangioblastoma, RCC and symptomatic pheochromocytoma and was found to carry the same mutation as the proband. Another female member had previously presented with retinal hemangioblastoma before becoming deceased at 37Y. The paper also asserted that the patient’s grandmother and two distant relatives carried the mutation, although genotyping was not performed and phenotypic information was not provided.

      CasePresentingHPOs: HP:0009726; HP:0000107; HP:0001737 (Renal tumour, renal cyst, pancreatic cyst)

      CaseHPOFreeText: N/A

      CaseNotHPOs: N/A

      CaseNotHPOFreeText: N/A

      CasePreviousTesting: N/A

      PreviouslyPublished: N/A

      SupplementalData: N/A

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

      LegacyVariant: N/A

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

      gnomAD: N/A

      VariantEvidence: N/A

      MutationType: missense_variant;transversion

      CivicName: R82P(c.245G>C)

      MultipleGeneVariants: N/A

    1. Interestingly, one carrier of the deletion developed bilateral breast cancer at age 46 and 49. First cancer was diagnosed at the age of 46 in her right breast. The patient was treated by mastectomy with postoperative chemotherapy (CMF). Histopathological examination revealed invasive ductal breast carcinoma of 1.8 cm size. The tumor was ER- negative, and PR-negative (HER2 was not analyzed). A metastasis in 1 axillary lymph node was found. There was no evidence of distant metastases. The tumor was classified as T1c pN1a M0, stage IIA; grade G2. Three years later, at the age of 49, she was diagnosed with cancer of her left breast. It was an invasive ductal carcinoma of 2.0 cm size. The tumor was ER-positive, PR-positive, and HER2-negative. There was no evidence for lymph-node or distant metastases. The tumor was classified as T1c pN 0 M0, stage IA, grade G2 and treated with mastectomy and tamoxifen. Ki67 expression was not tested. At present, 9 and 6 years after treatment of the breast cancers there is no evidence of breast cancer recurrence. However at age of 54, lesions typical for VHL disease including cerebellar haemangioblastoma and renal cell carcinoma were diagnosed in the patient.

      PatientID: 2

      KindredID: 1

      Case: F, 54Y0M, Ethnicity Unknown

      DiseaseAssertion: VHL

      FamilyInfo: Son (id:1) with the same variant, presenting with cerebellar hemangioblastoma at age 18, spinal hemangioblastomas at ages 19 and 31 and renal cysts but the age of onset for these is not noted. Father (id: 3) presented with cerebellar hemangioblastoma at age 65. Paternal uncle (id: 4) presented with prostate cancer at age 65. Paternal grandfather (id: 5) presented with cerebellar hemangioblastomas at age 69. Mother and daughter did not have the mutation. Her father was not tested. No family history of retinal capillary hemangiomas or pheochromocytoma.

      CasePresentingHPOs: HP:0006880; HP:0005584; HP:0003002 (Cerebellar hemangioblastoma, Renal cell carcinoma, Breast carcinoma)

      CaseHPOFreeText: Bilateral breast cancer at age 46 and 49. First cancer was diagnosed at the age of 46 in her right breast. The patient was treated by mastectomy with postoperative chemotherapy (CMF). Histopathological examination revealed invasive ductal breast carcinoma. A metastasis in 1 axillary lymph node was found. There was no evidence of distant metastases. Three years later, at the age of 49, she was diagnosed with cancer of her left breast. It was an invasive ductal carcinoma. There was no evidence for lymph-node or distant metastases. At present, 9 and 6 years after treatment of the breast cancers there is no evidence of breast cancer recurrence. However at age of 54, lesions typical for VHL disease including cerebellar haemangioblastoma and renal cell carcinoma were diagnosed in the patient.

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

      CaseNotHPOFreeText: N/A

      CasePreviousTesting: N/A

      PreviouslyPublished: N/A

      SupplementalData: Figure 1 (pedigree) and Table 1 (phenotype and age of onset data).

      Variant: Exon 1 Deletion (c.1-?_340+?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 1 Deletion

      MultipleGeneVariants: Germline, FANCD2, Partial Deletion

    1. PatientID: None

      KindredID: 8

      Case: M, 8Y0M, Chinese

      DiseaseAssertion: Asymptomatic

      FamilyInfo: His father had the same VHL mutation and presented with hemangioblastoma, clear cell renal cell carcinoma, and abnormality of the pancreas.

      CohortInfo: 16 Chinese patients clinically diagnosed with VHL disease.

      CasePresentingHPOs: N/A

      CaseHPOFreeText: N/A

      CaseNotHPOs: HP:0009711, HP:0002666, HP:0030393, HP:0010797, HP:0006770, HP:0001732 (retinal capillary hemangioma, pheochromocytoma, endolymphatic sac tumor, hemangioblastoma, clear cell renal cell carcinoma, abnormality of the pancreas)

      CaseNotHPOFreeText: N/A

      CasePreviousTesting: N/A

      PreviouslyPublished: N/A

      SupplementalData: N/A

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

      LegacyVariant:N/A

      CaseProblemVariantFreeText: 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

    2. Genomic DNA was isolated from peripheral blood samples by Qiagen DNA Blood mini kit (Qiagen, Hilden, Germany) following the manufacturer’s instruction. Genomic DNA (50–100 ng) was amplified by PCR in a standard PCR buffer containing 200 μM per each dNTPs, 1.5 mM MgCl2, 0.25 units of Taq polymerase and 0.2 μM per each primers with the thermal cycling program of 95 °C for 30 s, 60 °C for 30 s and 72 °C for 30 s for 30 cycles. PCR products were purified and sequenced in an ABI 3730 automated sequencer (ABI, Foster City, CA, USA). The primer pairs used for the amplification of the three exons and their flanking introns of VHL gene were 1F: 5′-IndexTermggtggtctggatcgcgga-3′ and 1R: 5′-IndexTermggcttcagaccgtgctatcg-3′ (product size 418bp), 2F: 5′-IndexTermgtggctctttaacaacctttgc-3′ and 2R: 5′-IndexTermcctgtacttaccacaacaaccttatc-3′ (product size 208 bp), and 3F: 5′-IndexTermgcaaagcctcttgttcgttc-3′ and 3R: 5′-IndexTermcaaaaatgccaccaccttct-3′ (product size 504 bp).

      ArticleReferenceSequence: Not specified – Assumption: variants assumed to have been documented by the author under reference sequence NM_000551.3

      GenotypingMethod: Genomic DNA was amplified by PCR and the products were purified and sequenced in an ABI 3730 automated sequencer (ABI, Foster City, CA, USA). UPQFM-PCR was also used to detect large deletions and insertions in the three exons of the VHL gene.

      SamplingMethod: peripheral blood

    1. p.N78S

      Between 1985 and 2017, the clinical materials of patients with VHL disease were collected from 3 different families. Peripheral blood was obtained from each patient for genetic analysis. The VHL gene was amplified by PCR and mutations were confirmed by bi-directional sequencing. Of 22 patients from 3 VHL pedigrees, 10 exhibited VHL gene mutations (3 genotypes) at the germline level. The genotypes of each of the three families were p.R161Q (c.482G>A), p.N78S (c.233A>G), and p.R167Q (c.500G>A), respectively. Family 2: Male proband was admitted at 24Y to the Second Affiliated Hospital due to paroxysmal headache, dizziness and palpitation with hyperhidrosis. MRI results revealed a mass at the right adrenal gland, multiple renal tumors and multiple cysts in the pancreas. Resection of the right adrenal tumor and the upper pole of the right kidney were performed. 3 years later, the patient underwent bilateral epididymal nodule excision and postoperative pathology confirmed patient suffered from papillary cystadenoma of the bilateral epididymal head. The proband's brother (at age 27Y) presented with multiple masses in both kidneys, multiple cysts in both kidneys, and pancreas and epididymal nodules. The patient underwent laparoscopic right radical nephrectomy. The postoperative pathology results confirmed the patient suffered from multiple RCC in the right kidney. The brother's daughter (5Y) was noted to be a germline carrier without any symptoms.

    1. In 2012, A blood DNA sequencing analysis revealed a pathogenic VHL mutation c. 232A>T; p. Asn78Tyr in this patient. The same point mutation of VHL was identified in three family members including one sister, one brother and one nephew.

      PatientID: N/A (proband's nephew)

      KindredID: 2

      Case: M, Age Unknown, Ethnicity Unknown

      DiseaseAssertion: assumed VHL

      FamilyInfo: The same point mutation of VHL (c. 232A>T; p.Asn78Tyr) was identified in three family members: 2 female and 1 male (one of which is his parent). His grandmother died of stroke at early of 50 years.

      CasePresentingHPOs: unknown

      CaseHPOFreeText: refused for further examinations for VHL-related lesions.

      CaseNotHPOs: N/A

      CaseNotHPOFreeText: N/A

      CasePreviousTesting: N/A

      PreviouslyPublished: N/A

      SupplementalData: N/A

      Variant: p.N78Y (c.232A>T)

      LegacyVariant: N/A

      ClinVar: 223167 https://www.ncbi.nlm.nih.gov/clinvar/variation/223167/

      CAID: CA357056 http://reg.clinicalgenome.org/redmine/projects/registry/genboree_registry/allele?hgvsOrDescriptor=NM_000551.3%3Ac.232A%3ET

      gnomAD: N/A

      VariantEvidence: N/A

      MutationType: missense_variant; transversion

      CivicName: N78Y (c.232A>T)

      MultipleGeneVariants: N/A

    1. Genomic DNA was extracted from peripheral blood leukocytes. Mutation analysis involved DNA sequencing, while large deletions were determined by universal primer quantitative fluorescent multiplex polymerase chain reaction (UPQFM-PCR) and multiplex ligation-dependent probe amplification (MLPA) analysis.

      ArticleReferenceSequence: NM_000551.3

      GenotypingMethod: The three exons and flanking regions of the VHL gene were amplified by PCR. Universal primer quantitative fluorescent multiplex polymerase chain reaction (UPQFM-PCR) and multiplex ligation-dependent probe amplification (MLPA) analysis

      SamplingMethod: peripheral blood leukocytes

    1. In a study of 114 unrelated VHL families, 85 germline mutations were found. VHL mutations were detected in affected family members, but not in unaffected family members or 96 normal individuals. This frameshift mutation was found in 2 VHL type 1 family of 8 and of 7 individuals (family ID 2956; 2693), using PCR and SSCP sequencing. The mutation of c.226_228delTTC was referred to in the paper by c.439delTTC due to a difference in transcript sequence. In the first, Family 2956, 2/8 members had a retinal angioma (hemangioma), 4 had RCC, and 5 members had CNS hemangioblastoma. In Family 2693 3/7 members had a retinal angioma (hemangioma), 3 had RCC, and 3 members had CNS hemangioblastoma. This is possibly previously published in PMID 9829911, as well as one member in a future publication: PMID: 32179488

    2. In a study of 114 unrelated VHL families, 85 germline mutations were found. VHL mutations were detected in affected family members, but not in unaffected family members or 96 normal individuals. This missense mutation was found in 4 VHL type 1 family members (family ID 3315), using PCR and SSCP sequencing. The mutation of c.332G>A was referred to in the paper by c.545G>A due to a difference in transcript sequence. 1 of 4 individuals were identified with retinal hemangioblastomas, 2 with CNS hemangioblastomas, and 2 with renal cell carcinoma. This was possibly previously published in PMID 9829911

    3. GroupID: 4480

      DiseaseAssertion: assumed VHL

      GroupSize: 2

      GroupNumberMales: N/A

      GroupNumberFemales: N/A

      GroupEthnicity: N/A

      GroupAgeRange: N/A

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

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

      GroupHPOFreeText: both (2) members had CNS hemangioblastoma, and 1 member had retinal angioma (hemangioma)

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

      GroupNotHPOFreeText: N/A

      GroupPreviousTesting: N/A

      PreviouslyPublished: N/A

      SupplementalData: N/A

      Variant: p.V166D (c.497T>A)

      CaseProblemVariantFreeText: N/A

      LegacyVariant: p.L237D (c.710T>A)

      ClinVarID: 625254 https://www.ncbi.nlm.nih.gov/clinvar/variation/625254/

      CAID: N/A

      gnomAD: N/A

      VariantEvidence: N/A

      MutationType: missense_variant; transversion

      CivicName: V166D (c.497T>A)

      MultipleGeneVariants: N/A

    1. PatientID: A-V5

      KindredID: A-V5

      Case: F, 37Y0M, Korean

      DiseaseAssertion: VHL

      FamilyInfo: N/A

      CasePresentingHPOs: HP:0002666; HP:0030405 (Pheochromocytoma, Pancreatic endocrine tumor)

      CaseHPOFreeText: Bilateral pheochromocytoma and pancreatic islet cell carcinoma. Diagnosed with VHL type 2.

      CaseNotHPOs: HP:0010797; HP:0009711; HP:0001737; HP:0005584 (Hemangioblastoma, Pancreatic cysts, Renal cell carcinoma)

      CaseNotHPOFreeText: N/A

      CasePreviousTesting: N/A

      PreviouslyPublished: 25078357

      SupplementalData: N/A

      Variant: p.A149T (c.445G>A)

      LegacyVariant: N/A

      CaseProblemVariantFreeText: N/A

      ClinVarID: 223213, https://www.ncbi.nlm.nih.gov/clinvar/variation/223213/

      CAID: N/A

      gnomAD: N/A

      VariantEvidence: N/A

      MutationType: missense_variant;transition

      CivicName: A149T (c.445G>A)

      MultipleGeneVariants: N/A

    1. In four families, partial deletions of one or more exons were detected by Southern blot analysis

      PatientID: unknown (brother)

      KindredID: A

      Case: M (deceased), Age unknown, Turkish

      DiseaseAssertion: assumed VHL

      FamilyInfo: 5 family members are grouped with this deletion (ages 16-37Y; mean 31Y). VHL was clinically diagnosed in, at minimum, the proband. See Fig. 2 for family pedigree. This patient and his one brother were not tested for the DNA deletion however it is assumed by the authors due to the segregation observed.

      CasePresentingHPOs: HP:0010797 (hemangioblastoma)

      CaseHPOFreeText: N/A

      CaseNotHPOs: HP:0009711; HP:0002666; HP:0005584 (retinal capillary hemangioma; pheochromocytoma; renal cell carcinoma)

      CaseNotHPOFreeText: N/A

      CasePreviousTesting: N/A

      PreviouslyPublished: N/A

      SupplementalData: N/A

      Variant: Deletion of exons 1 and 2

      CaseProblemVariantFreeText: N/A

      LegacyVariant: N/A

      ClinVarID: N/A

      CAID: N/A

      gnomAD: N/A

      VariantEvidence: not tested for the DNA deletion however it is assumed by the authors due to the segregation observed.

      MutationType: exon_loss_variant

      CivicName: exon 1-2 deletion

      MultipleGeneVariants: N/A

    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%.

      Patients presenting with cerebellar hemangioblastomas at the Mexican National institute of Neurology and Neurosurgery to were prospectively enrolled alongside family members, resulting in 84 patients in 7 families with VHL mutations, and subjected to peripheral blood draw and PCR-based mutation screening, as well as full clinical screening for symptomatic individuals. 19 individuals across two families (Family B and Family C) presented with a c.298dupA mutation, leading to a frameshift (p.T100Nfs 32). Among these individuals, 2 in Family B and 6 in Family C were asymptomatic at the time of screening (ages 2, 7, 9, 12, 13, 17, 20, and 29). Of the 4 symptomatic individuals in Family B, one presented at 44 with cerebellar hemangioblastoma and bilateral retinal angiomas; one presented at 16 with 4 cerebellar hemangioblastomas, 1 bulbar hemangioblastoma, 1 spinal hemangioblastoma, bilateral retinal angiomas, pancreatic cysts, and kidney cysts; one presented at age 26 with cerebellar hemangioblastoma, bilateral retinal angiomas, pancreatic cysts, kidney cysts, and renal cell carcinoma; and one presented at 28 with 1 cerebellar hemangioblastoma. Of the 7 symptomatic individuals in Family C, one presented at 45 with cerebellar hemangioblastoma, pancreatic cysts, kidney cysts, and renal cell carcinoma; one presented at age 21 with epididymal cystadenoma; one presented at 36 with 2 cerebellar hemangioblastomas, pancreatic cysts, kidney cysts, hepatic cysts, adrenal cysts, and bilateral renal cell carcinomas; one presented at 20 with spinal hemangioblastoma, pancreatic cysts, and kidney cysts; one presented at 13 with 2 spinal hemangioblastomas, one presented at 13 with cerebellar hemangioblastoma, one presented at 30 with cerebellar hemangioblastoma, pancreatic cysts, and kidney cysts. They were previously published in PMID: 20064270, however with a reportedly different variant: p.G34Rfs98 (c.99_100insA).

    1. c.500G > A p.Arg167Gln

      GroupID: 19

      DiseaseAssertion: assumed VHL

      GroupSize: 24

      GroupNumberMales: N/A

      GroupNumberFemales: N/A

      GroupEthnicity: Chinese

      GroupAgeRange: 47.8Y +/- 12.7Y

      GroupInfo: Clinical characteristics of 258 patients from 80 unrelated Chinese families were reported in this study. Grouped by the 21 mutations found, 10 families with 24 members total were described, and phenotypic information was given for this group.

      GroupPresentingHPOs: HP:0010797; HP:0009711; HP:0005584; HP:0001737; HP:0002666 (hemangioblastoma, retinal capillary hemangioma, renal cell carcinoma, pancreatic cysts, pheochromocytoma)

      GroupHPOFreeText: 15 of the 24 members presented with CNS hemangioblastoma (with a mean age of onset of 35.6Y), retinal capillary hemangioma in 4 members (at the mean age of 23.0Y), renal cell carcinoma in 10 members (at the mean age of 38.3Y), pancreatic cysts in 5 members (at the mean age of 37.2Y), and pheochromocytoma in 9 members (at the mean age of 36.3Y)

      GroupNotHPOs: HP:0009715 (papillary cystadenoma of the epididymis)

      GroupNotHPOFreeText: No members had a papillary cystadenoma of the epididymis genital system tumor (epididymis or broad ligament)

      GroupPreviousTesting: N/A

      PreviouslyPublished: 24581539 (family #11); 29330336 (as 7 families of 18 people); 28388566 (family #78, 79, 80, 81, 82, 83)

      SupplementalData: N/A

      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

    1. 1138Y38Y38NNNNNc.340G>AExon 1p.Gly114SerMissense

      PatientID: 1

      KindredID: 1

      Case: Sex Unknown, 38Y0M, Brazilian (Latino/Admixed American)

      DiseaseAssertion: VHL

      FamilyInfo: Also belonging to family 1, patients 2 and 3 had VHL diagnoses and phenotypes. Their relation is not clear.

      CasePresentingHPOs: HP:0002668, HP:0002666; HP:0030405 (Paraganglioma, pheochromocytoma, pancreatic endocrine tumor)

      CaseHPOFreeText: The patient developed PPGL at 38Y of age, and a PNET at 38Y.

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

      CaseNotHPOFreeText: N/A

      CasePreviousTesting: N/A

      PreviouslyPublished: N/A

      SupplementalData: N/A

      Variant: p.G114S (c.340G>A)

      CaseProblemVariantFreeText: N/A

      LegacyVariant: N/A

      ClinVarID: 583094 https://www.ncbi.nlm.nih.gov/clinvar/variation/583094/

      CAID: N/A

      gnomAD: N/A

      VariantEvidence: N/A

      MutationType: missense_variant;transition

      CivicName: G114S (c.340G>A)

      MultipleGeneVariants: N/A

    2. 312232N—N—YYYYNc.481 C>T

      PatientID: 31

      KindredID: 22

      Case: Sex Unknown, 32Y0M, Brazilian (Latino/Admixed American)

      DiseaseAssertion: VHL

      FamilyInfo: stated as a familial VHL. 1 other family member (patient 30) with that same mutation was stated with an age of 56. This patient has RCC, renal cysts, pancreatic cysts, and CNS hemangioblastoma and retinal capillary hemangioblastomas.

      CasePresentingHPOs: HP:0010797; HP:0001737; HP:0005584; HP:0000107 (hemangioblastoma, pancreatic cyst, renal cell carcinoma, renal cyst)

      CaseHPOFreeText: N/A

      CaseNotHPOs: HP:0002668, HP:0002666; HP:0009711; HP:0030405; (Paraganglioma, pheochromocytoma, retinal capillary hemangioma, pancreatic endocrine tumor)

      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

    1. His father (Patient II‐3) died of advanced RCCC in the previous year

      PatientID: II-3

      KindredID: 1

      Case: M, Age Unknown, Ethnicity Unknown

      DiseaseAssertion: VHL

      FamilyInfo: Both of the patient’s brothers (Patient II-4 and II-1), the patient’s sister (II-5), and the patient’s son (III-3) were clinically diagnosed with VHL disease. Patient II-1 presented with RCCC at age 33 and CH at age 41. He carried the mutation NM_000551.3:c.269A>T. Patient II-4 presented with RCCC at age 53, and carried the same mutation. Patient III-3 presented with CH and carried the same mutation. The patient’s sister (Patient II‐5) was deceased and had an undetermined mutation. Patient II‐5 died of a ruptured CH. The patient’s parents (Patient I-1 and I-2) were also deceased from other causes. The patient’s grandson (Patient IV‐1) was healthy and did not carry the mutation.

      CasePresentingHPOs: HP:0006770 (Renal clear cell carcinoma)

      CaseHPOFreeText: The patient died from advanced RCCC.

      CaseNotHPOs: N/A

      CaseNotHPOFreeText: N/A

      CasePreviousTesting: N/A

      PreviouslyPublished: N/A

      SupplementalData: N/A

      Variant: N/A

      LegacyVariant: N/A

      ClinVarID: N/A

      gnomAD: N/A

      VariantEvidence: N/A

      MutationType: N/A

      CivicName:N/A

      MultipleGeneVariants: N/A

    1. PatientID: None

      KindredID: 6

      Case: Sex Unknown, Age Unknown, Ethnicity Unknown

      DiseaseAssertion: VHL

      FamilyInfo: No family history of VHL. Parents underwent genetic testing and were not found to harbor the P102Rfs*57 (c.305del) germline variant of the VHL gene, confirming a de novo mutation in the current patient.

      CasePresentingHPOs: HP:0010797; HP:0005584; HP:0002894 (Hemangioblastoma, Renal cell carcinoma, Neoplasm of the pancreas)

      CaseHPOFreeText: CNS hemangioblastoma, pancreatic cystadenoma and Renal carcinoma.

      CaseNotHPOs: HP:0009711; HP:0002894; HP:0002666 (Retinal capillary hemangioma, Neoplasm of the pancreas, Pheochromocytoma)

      CaseNotHPOFreeText: N/A

      CasePreviousTesting: N/A

      PreviouslyPublished: N/A

      SupplementalData: N/A

      Variant: p.P102Rfs*57 (c.305del)

      LegacyVariant: N/A

      CaseProblemVariantFreeText:

      ClinVarID: N/A

      CAID: CA658820710, https://reg.clinicalgenome.org/redmine/projects/registry/genboree_registry/allele?hgvsOrDescriptor=NM_000551.3%3Ac.305del

      gnomAD: N/A

      VariantEvidence: This variant was not found in 120 alleles from normal subjects in the Brazilian population.

      MutationType: deletion; minus_1_frameshift_variant

      CivicName: P102fs (c.305del)

      MultipleGeneVariants: N/A

    2. Germline mutations were found in 20 Brazilian VHL probands and their families. The F76del (c.226_228del) germline mutation was found in a VHL type 1 family of 5 affected individuals (VHL family 1). Of the 5 affected family members four patients had hemangioblastomas of the central nervous system and 2 had renal carcinoma. In family 1 genetic testing was performed in a non-symptomatic boy, since no relatives were alive for testing. Although many members of this family had already presented with HB, the diagnosis of VHL was confirmed after necropsy of the proband’s father, who died at 37 years from complications following emergency surgery for cerebellar HB. The necropsy showed many occult lesions related to VHL, including RC, multiple pancreatic and renal cysts, and cystadenoma of the epididymis. This variant was not found in 120 alleles from normal subjects in the Brazilian population.

    1. . Of the 13 individuals tested, V:2, IV:4, IV:6, III:2, III:3, and III:11 were all found to carry the P25L mutation in the VHL gene. With the exception of family member IV:2, none of these individuals reported any features characteristic of VHL disease.

      PatientID: III:11

      KindredID: 1

      Case: F, 75, Ethnicity Unknown

      DiseaseAssertion: Asymptomatic

      FamilyInfo: The patient's father (II:3) had a brain tumour at age 53 and died at age 78. The patient's paternal aunt (II:1) died of stomach cancer at age 80. The patient's paternal grandfather died at age 50 due to a brain tumour. The patient had seven siblings, five of whom underwent genetic testing. Two were found to carry the mutation but both were asymptomatic (patient III:2 and III:3). The patient's sister (III:2) had three children all of whom carried the P25L mutation and were asymptomatic (IV:4 and IV:6) except patient IV:2 who presented with a retinal hemangioma and renal cyst. Her niece, (IV:2) had three children and one was found to carry the mutation. The patient's brother (III:3) had six children one of whom died due to clear cell renal carcinoma at age 48 but did not carry the P25L mutation (IV:7). The patient had three unaffected children who did not carry the mutation. Of the 13 family members tested, V:2, IV:4, IV:6, III:3, and III:11 were all found to carry the P25L mutation in the VHL gene. Refer to Figure 1 for pedigree.

      CasePresentingHPOs: N/A

      CaseHPOFreeText: N/A

      CaseNotHPOs: N/A

      CaseNotHPOFreeText: Ongoing clinical follow up of the individuals with P25L over a period of 5 years has continued to show no evidence of additional clinical involvement of VHL disease.

      CasePreviousTesting: N/A

      PreviouslyPublished: N/A

      SupplementalData: N/A

      Variant: p.P25L (c.74C>T)

      LegacyVariant: N/A

      CaseProblemVariantFreeText: N/A

      ClinVarID: 93330 https://www.ncbi.nlm.nih.gov/clinvar/variation/93330/

      CAID: N/A

      gnomAD: 0.002988 https://gnomad.broadinstitute.org/variant/3-10183605-C-T

      VariantEvidence: N/A

      MutationType: missense_variant;transition

      CivicName:P25L (c.74C>T)

      MultipleGeneVariants: N/A

    1. GroupID/ KindredID: VHL 43

      DiseaseAssertion: assumed VHL

      GroupSize: 5

      GroupNumberMales: N/A

      GroupNumberFemales: N/A

      GroupEthnicity: German

      GroupAgeRange: N/A

      GroupInfo: 5 patients with the given mutation belonging to VHL family 43

      GroupPresentingHPOs: HP:0009711; HP:0010797; HP:0000107 (retinal capillary hemangioma, hemangioblastoma, renal cyst)

      GroupHPOFreeText: 5 patients have retinal angioma, 2 with hemangioblastoma and 2 with renal cyst

      GroupNotHPOs: N/A

      GroupNotHPOFreeText: N/A

      GroupPreviousTesting: N/A

      PreviouslyPublished: N/A

      SupplementalData: N/A

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

      CaseProblemVariantFreeText: N/A

      LegacyVariant: p.R167Q (c.713G>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

    2. GroupID/ KindredID: VHL54

      Case: Sex unknown, Age unknown, German

      DiseaseAssertion: assumed VHL

      FamilyInfo: One patient with the given mutation is stated to belong to VHL family 54

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

      CaseHPOFreeText: N/A

      CaseNotHPOs: N/A

      CaseNotHPOFreeText: N/A

      CasePreviousTesting: N/A

      PreviouslyPublished: 7759077

      SupplementalData: N/A

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

      CaseProblemVariantFreeText: N/A

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

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

      CAID: CA020246 http://reg.clinicalgenome.org/redmine/projects/registry/genboree_registry/allele?hgvsOrDescriptor=NM_000551.3%3Ac.292T%3EC

      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. 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. 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. c.509T>A

      Data was collected from 82 VHL mutation carriers in the Dutch VHL surveillance program. 15 patients were found with this missense variant in the VHL gene. The ages of the patients were represented as a range, 16-71Y (mean 45). The phenotypes were presented together: retinal hemangioblastoma, cerebellar hemangioblastoma, spinal cord hemangioblastoma, renal cell carcinoma, pancreatic neuroendocrine tumor, pheochromocytoma, renal cysts, and pancreatic cysts. Family history was not described. This cohort was published later in PMID 31087189.

    1. PatientID: None

      KindredID: 39

      Case: Sex Unknown, Age Unknown, Japanese

      DiseaseAssertion: VHL

      FamilyInfo: N/A

      CasePresentingHPOs: HP:0009711 (Retinal capillary hemangioma)

      CaseHPOFreeText: Retinal angioma.

      CaseNotHPOs: HP:0005584; HP:0001732; HP:0010797 (Renal cell carcinoma, Abnormality of the pancreas, Hemangioblastoma)

      CaseNotHPOFreeText: N/A

      CasePreviousTesting: N/A

      PreviouslyPublished: 8634692

      SupplementalData: N/A

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

      LegacyVariant: c.470C>T

      CaseProblemVariantFreeText: N/A

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

      CAID: N/A

      gnomAD: N/A

      VariantEvidence: N/A

      MutationType: missense_variant;transition

      CivicName: P86L (c.257C>T)

      MultipleGeneVariants: N/A

    1. A 37-year-old woman and 78-year-old man who were daughter and father, respectively, and had multiple cysts in both kidneys, were enrolled in this study. In addition, a 28-year-old healthy male subject was enrolled as a normal control. The study was in accordance with the ethical standards as formulated in the Helsinki Declaration of 1975 (revised in 1983). Both patients had c.349T>A mutation (p.Trp117Arg) in exon 2 of the VHL gene. Histopathological examination revealed clear cell type renal

      PatientID: None (father)

      KindredID: 1

      Case: M, 78Y0M, Ethnicity Unknown

      DiseaseAssertion: assumed VHL

      FamilyInfo: 37Y old daughter had multiple cysts (RCC) in both kidneys and the same (c.349T>A) mutation

      CasePresentingHPOs: HP:0000107; HP:0005584; HP:0006770 (renal cysts; renal cell carcinoma, clear cell renal cell carcinoma)

      CaseHPOFreeText: VHL patient underwent left nephrectomy and right partial nephrectomy (subtotal nephrectomy). Histopathological examination revealed clear cell type renal cell carcinoma (RCC)

      CaseNotHPOs: N/A

      CaseNotHPOFreeText: N/A

      CasePreviousTesting: N/A

      PreviouslyPublished: N/A

      SupplementalData: N/A

      Variant: p.W117R (c.349T>A)

      LegacyVariant: N/A

      CaseProblemVariantFreeText: N/A

      ClinVarID: N/A

      CAID: CA351753664 https://reg.clinicalgenome.org/redmine/projects/registry/genboree_registry/allele?hgvsOrDescriptor=NM_000551.3%3Ac.349T%3EA

      gnomAD: N/A

      VariantEvidence: N/A

      MutationType: missense_variant;transversion

      CivicName: W117R (c.349T>A)

      MultipleGeneVariants: N/A

    1. 2bF““““PPGL, HBA CNS/Ret, RCC, PanNET

      PatientID: 2b

      KindredID: 2

      Case: Sex Unknown, Age Unknown, Ethnicity Unknown

      DiseaseAssertion: VHL

      FamilyInfo: An unspecified relative (proband - 2a) had the same mutation with renal cell carcinoma, hemangioblastoma, retinal capillary hemangioma, pancreatic cysts and pancreatic endocrine tumors.

      CasePresentingHPOs: HP:0005584; HP:0010797; HP:0009711; HP:0002668; HP:0030405 (renal cell carcinoma; hemangioblastoma; retinal capillary hemangioma; pancreatic cyst; pancreatic endocrine tumor)

      CaseHPOFreeText: N/A

      CaseNotHPOs: N/A

      CaseNotHPOFreeText: N/A

      CasePreviousTesting: MEN1/ RET

      PreviouslyPublished: N/A

      SupplementalData: N/A

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

      LegacyVariant: N/A

      CaseProblemVariantFreeText: N/A

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

      CAID: N/A

      gnomAD: N/A

      VariantEvidence: N/A

      MutationType: missense_variant; transition

      CivicName: N78S (c.233A>G)

      MultipleGeneVariants: N/A

    1. her mother

      PatientID: None

      KindredID: 1

      Case: F, Age Unknown, Ethnicity Unknown

      DiseaseAssertion: Asymptomatic

      FamilyInfo: The heterozygous missense variant NM_000551.3:c.311G>T was identified on two of her daughters; one was 21Y and one was 17Y. The 21Y daughter had hypertension and a paraganglioma, and the 17Y daughter had a retinal hemangioblastoma.

      CasePresentingHPOs: N/A

      CaseHPOFreeText: The patient refused a complete staging.

      CaseNotHPOs: N/A

      CaseNotHPOFreeText: N/A

      CasePreviousTesting: N/A

      PreviouslyPublished: N/A

      SupplementalData: N/A

      Variant: p.G104V(c.311G>T)

      LegacyVariant: N/A

      ClinVarID: 223183, http://www.ncbi.nlm.nih.gov/clinvar/variation/223183

      CAID: N/A

      gnomAD: N/A

      VariantEvidence: N/A

      MutationType: missense_variant;transversion

      CivicName: G104V(c.311G>T)

      MultipleGeneVariants: N/A

    1. missense

      A cohort of 314 patients with pheochromocytoma and functional paraganglioma had blood samples collected and all five major pheo-pgl susceptibility genes (RET, VHL, SDHB, SDHD, and SDHC) were screened for mutations. 25 patients had germline VHL mutations, 16 of which had a family history and 9 patients had an apparently sporadic presentation, 11 were male and 14 were female, the median age of diagnosis is 23.9 and range of diagnosis was 4-49. Out of the 25 patients 23 had adrenal tumours, 4 had para-adrenal tumours, and 9 had other VHL lesions (renal tumours and hemangioblastomas). 1 patient with postive family history and/or a syndromic presentation and 1 patient with an apparently sporadic presentation were found with pheochromocytoma or functional paraganglioma and a germline missense VHL mutation (c.533T>C). Other phenotypes unique to the patient are unknown. ACMG: PP4

    1. PatientID: 1

      KindredID: 86

      Case: Sex, Age, Ethnicity Unknown

      DiseaseAssertion: VHL

      FamilyInfo: N/A

      CasePresentingHPOs: HP:0005584 (Renal cell carcinoma)

      CaseHPOFreeText: two RCC tumors were detected in this patient

      CaseNotHPOs: N/A

      CaseNotHPOFreeText: N/A

      CasePreviousTesting: N/A

      PreviouslyPublished: N/A

      SupplementalData: N/A

      Variant: p.C77Lfs*55 (c.227_228insC)

      CaseProblemVariantFreeText: NM_000551.3:c.227_228insC automapped to NM_000551.3:c.228dupC

      LegacyVariant: p.76 FS (c.441insC)

      ClinVarID: N/A

      CAID: CA658795177 http://reg.clinicalgenome.org/redmine/projects/registry/genboree_registry/allele?hgvsOrDescriptor=NM_000551.3%3Ac.227_228insC

      gnomAD: N/A

      VariantEvidence: Tested the tumors for somatic mutations but did not detect any

      MutationType: plus_1_frameshift_variant

      CivicName: C77fs (c.228dup)

      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: 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. 33M F NK M A VHL 854insC X > Cys+ 128AA

      PatientID: 33M

      KindredID: 33M

      Case: F, Age Unknown, Ethnicity Unknown

      DiseaseAssertion: VHL

      FamilyInfo: None

      CohortInfo: Patients with apparently sporadic pheochromocytomas.

      CasePresentingHPOs: HP:0006748 (Adrenal pheochromocytoma)

      CaseHPOFreeText: The patient had a malignant adrenal pheochromocytoma.

      CaseNotHPOs: N/A

      CaseNotHPOFreeText: N/A

      CasePreviousTesting: N/A

      PreviouslyPublished: N/A

      SupplementalData: N/A

      Variant: p.*214C(c.641_642insC)

      LegacyVariant: p.X > Cys+ 128AA (c.854insC)

      CaseProblemVariantFreeText: N/A

      ClinVarID: N/A

      CAID: CA913189243 http://reg.clinicalgenome.org/redmine/projects/registry/genboree_registry/allele?hgvsOrDescriptor=NM_000551.3%3Ac.641_642insC

      gnomAD: N/A

      VariantEvidence: N/A

      MutationType: plus_1_frameshift_variant

      CivicName: *214C (c.641_642insC)

      MultipleGeneVariants: N/A

    1. 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. 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

    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