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    1. c.462A > C

      All patients included in the study were VHL mutation carriers of 18 years or older examined between 1972 and 2012 in the VHL expertise centers University Medical Center Groningen (UMCG) and University Medical Center Utrecht (UMCU). Clinical data of 75 VHL mutation carriers were retrospectively retrieved from electronic and written patient record. Of these patients, one was found to harbour the c.462A>C germline mutation of the VHL gene. They presented with a cerebellar hemangioblastoma, renal cyst and pheochromocytoma. Their age at the last follow-up was 71. Previously published in: PMID 24132471.

    2.  c.241C > T2 (3%)2a/b47 (34–59)HBr, HBc,HBsc, RCC, PNET, Pheo, Cr

      PatientID: None

      KindredID: 3

      Case: Sex Unknown, 59Y0M, 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:0002666 (Retinal capillary hemangioma, Cerebellar hemangioblastoma, Spinal hemangioblastoma, Renal cell carcinoma, Pancreatic endocrine tumor, Renal cyst, Pheochromocytoma)

      CaseHPOFreeText: VHL Type 2a/b.

      CaseNotHPOs: N/A

      CaseNotHPOFreeText: N/A

      CasePreviousTesting: N/A

      PreviouslyPublished: 24132471

      SupplementalData: Table 1

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

      LegacyVariant: N/A

      CaseProblemVariantFreeText: N/A

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

      CAID: N/A

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

      VariantEvidence: N/A

      MutationType: missense_variant;transition

      CivicName: P81S (c.241C>T)

      MultipleGeneVariants: N/A

    1. GroupID: 9

      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 the mutation belonging to 1 family. This mutation was found in 1 VHL family with 3 patients.

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

      GroupHPOFreeText: 2 patients had retinal angiomas diagnosed at a mean age of 15Y, 2 patients had cerebellar hemangioblastomas diagnosed at a mean age of 15Y, and 1 patient had RCCs with an age of diagnosis of 40Y.

      GroupNotHPOs: HP:0002666 (pheochromocytoma)

      GroupNotHPOFreeText: N/A

      GroupPreviousTesting: N/A

      PreviouslyPublished: N/A

      SupplementalData: Supplementary Table S1.

      Variant: p.S72Pfs*87 (c.214del)

      CaseProblemVariantFreeText: N/A

      LegacyVariant: N/A

      ClinVarID: N/A

      CAID: CA658795180 http://reg.clinicalgenome.org/redmine/projects/registry/genboree_registry/allele?hgvsOrDescriptor=NM_000551.3%3Ac.214del

      gnomAD: N/A

      VariantEvidence: N/A

      MutationType: minus_1_frameshift_variant

      CivicName: S72fs (c.214del)

      MultipleGeneVariants: N/A

    2. GroupID: 65

      Case: 48Y0M, Sex Unknown, Ethnicity Unknown

      DiseaseAssertion: assumed VHL

      FamilyInfo: 1 of the 573 patients discussed in this paper were found to have this variant. This mutation (c.344A>C) was found in 1 VHL family with a single patient.

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

      CaseHPOFreeText: patient had cerebellar hemangioblastoma diagnosed at 48Y and a retinal angioma at 24Y

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

      CaseNotHPOFreeText: N/A

      CasePreviousTesting: N/A

      PreviouslyPublished: N/A

      SupplementalData: Supplementary Table S1.

      Variant: p.H115P (c.344A>C)

      CaseProblemVariantFreeText: N/A

      LegacyVariant: N/A

      ClinVarID: 560744 https://www.ncbi.nlm.nih.gov/clinvar/variation/560744/

      CAID: N/A

      gnomAD: N/A

      VariantEvidence: N/A

      MutationType: missense_variant;transversion

      CivicName: H115P (c.344A>C)

      MultipleGeneVariants: N/A

    3. 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). This nonsense mutation (c.481C>T) was found in 7 families with 30 affected members: 24 had retinal angiomas, 13 had cerebellar hemangioblastomas, 14 had renal cell carcinomas, and 3 had pheochromocytomas. ACMG PP4 PM4

    4. Genotype-phenotype correlations of 573 VHL patients from 200 kindreds were analyzed. Age-related risks of retinal angiomas and renal cell carcinoma were higher in patients with nonsense or frameshift mutations. This mutation (c.340+5G>C) was found in a VHL family with 3 patients. 2 had retinal hemangioblastoma at a mean age of 16Y, one had cerebellar hemangioblastoma at 16Y, and 1 had pheochromcytoma at 14Y. This mutation has a large allele frequency and therefore a polymorphism that is likely non disease causing.

    5. GroupID: 77

      Case: 23Y0M, Sex Unknown, Ethnicity Unknown

      DiseaseAssertion: assumed VHL

      FamilyInfo: 1 of the 573 patients discussed in this paper were found to have this variant. This mutation (c.491A>G) was found in 1 VHL family with a single patient.

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

      CaseHPOFreeText: patient had pheochromocytoma diagnosed at 10Y, a retinal angioma at 23Y.

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

      CaseNotHPOFreeText: N/A

      CasePreviousTesting: N/A

      PreviouslyPublished: N/A

      SupplementalData: Supplementary Table S1.

      Variant: p.Q164R (c.491A>G)

      CaseProblemVariantFreeText: N/A

      LegacyVariant: N/A

      ClinVarID: 2238 https://www.ncbi.nlm.nih.gov/clinvar/variation/2238/

      CAID: N/A

      gnomAD: N/A

      VariantEvidence: N/A

      MutationType: missense_variant;transition

      CivicName: Q164R (c.491A>G)

      MultipleGeneVariants: N/A

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

      PatientID: 3

      KindredID: 3

      Case: Sex Unknown, Age Unknown, Ethnicity Unknown

      DiseaseAssertion: renal cell carcinoma

      FamilyInfo: None

      CasePresentingHPOs: HP:0005584 (renal cell carcinoma)

      CaseHPOFreeText: N/A

      CaseNotHPOs: N/A

      CaseNotHPOFreeText: N/A

      CasePreviousTesting: N/A

      PreviouslyPublished: N/A

      SupplementalData: N/A

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

      LegacyVariant: N/A

      CaseProblemVariantFreeText: N/A

      ClinVarID: N/A

      CAID: N/A

      gnomAD: N/A

      VariantEvidence: germline deletion on chromosome 3 (>35kb, <90kb) resulting in complete loss of VHL gene. Renal cell carcinoma sample from this patient shows a missense mutation R69C(c.205C>T) in the second copy of VHL gene.

      MutationType: deletion

      CivicName: Deletion AND R69C (c.205C>T)

      MultipleGeneVariants: Somatic, VHL, c.205C>T (p.Arg69Cys)

    1. GroupID: 9

      DiseaseAssertion: VHL

      GroupSize: 3

      GroupNumberMales: N/A

      GroupNumberFemales: N/A

      GroupEthnicity: Japanese

      GroupAgeRange: N/A

      GroupInfo: The three patients are grouped based on both having the c.233A>G mutation. They are unrelated to one another.

      GroupPresentingHPOs: HP:0009711, HP:0010797 (Retinal capillary hemangioma, Hemangioblastoma)

      GroupHPOFreeText: All three patients had retinal angioma and hemangioblastoma of the CNS.

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

      GroupNotHPOFreeText:N/A

      GroupPreviousTesting: N/A

      PreviouslyPublished: N/A

      SupplementalData: N/A

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

      CaseProblemVariantFreeText: N/A

      LegacyVariant: p.N149S(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

    2. 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. 712C>T) which coincides with legacy variant nomenclature (AF010238.1) and was mapped to c.499C>T (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 hemangioblastoma (Hb) renal cell carcinoma (RCC), and pheochromocytoma was available. Case 19 had an R167W (c.499C>T) mutation. 1 member was affected with RCC, pheochromocytoma, CNS Hb, and retinal hemangioma. Other demographics of the members were not described.

    1. 8 c.241C>T p.Pro81Ser p.P81S Sporadic cHAB

      Molecular analysis of VHL gene in 146 probands, 103 with and 43 without a positive family history, resulted in the detection of 43 germline VHL mutations. Majority of mutations were found in patients with classic or multi-organ manifestations of VHL disease, but mutations were also found in patients with limited or single-organ manifestations of VHL disease. Follow-up of families with germline mutations and limited VHL manifestations was recommended. The c.241C>T (P81S) mutation was found in 5 patients from Family 8. Only one of which presented with CNS hemangioblastoma. Further family info found at PMID: 11106358; 8956040; 9829911; 8634692 as previously published.

    1. PatientID: 2

      KindredID: 1

      Case: F, Age Unknown, German

      DiseaseAssertion: VHL

      FamilyInfo: This patient and her unaffected spouse (patient 1) had four children; one died and was affected, two (patient 5 and 7) had both mutations and presented with pheochromocytoma, and one child (patient 6) was unaffected and carried neither mutation. Patient 7 had a child (patient 9) who also carried both mutations and presented with pheochromocytoma. Furthermore, this patient's brother (patient 3) carried both mutations and presented with pheochromocytoma. He had a child with patient (4) who was unaffected. Their child (patient 8) carried both mutations and presented with pheochromocytoma. Patient 8 had two children; one that did not carry the mutation and was unaffected (patient 10) and another that carried both mutations but was disease free (patient 11). See Figure 3 for family pedigree.

      CasePresentingHPOs: HP:0002666 (pheochromocytoma)

      CaseHPOFreeText: N/A

      CaseNotHPOs: N/A

      CaseNotHPOFreeText: N/A

      CasePreviousTesting: N/A

      PreviouslyPublished: 8772572, 7563486

      SupplementalData: N/A

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

      LegacyVariant: P81S (c.454C>T)

      CaseProblemVariantFreeText: N/A

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

      CAID: CA020148 http://reg.clinicalgenome.org/redmine/projects/registry/genboree_registry/allele?hgvsOrDescriptor=NM_000551.3%3Ac.241C%3ET

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

      VariantEvidence: N/A

      MutationType: missense_variant;transition

      CivicName: P81S (c.241C>T) and L188V (c.562C>G)

      MultipleGeneVariants: Germline, VHL, c.562C>G (p.Leu188Val)

    1. 53p.L89P>18YAffectedKC, PC+ 1 Hb

      PatientID: None

      KindredID: 53

      Case: Sex and Ethnicity unknown; Age >18Y0M

      DiseaseAssertion: assumed VHL

      FamilyInfo: None

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

      CaseHPOFreeText: 1 kidney and pancreatic cyst at first screening, as well as a hemangioblastoma at final screening (5 year follow up).

      CaseNotHPOs: N/A

      CaseNotHPOFreeText: N/A

      CasePreviousTesting: N/A

      PreviouslyPublished: N/A

      SupplementalData: N/A

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

      CaseProblemVariantFreeText: N/A

      LegacyVariant: N/A

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

      CAID: N/A

      gnomAD: N/A

      VariantEvidence: N/A

      MutationType: missense_variant; transition

      CivicName: L89P(c.266T>C)

      MultipleGeneVariants: N/A

    2. p.C162F

      The genetic testing program for VHL disease included 17 families, ten of which had definite VHL disease and seven had possible VHL disease. 17 families (n=109 individuals) were tested for VHL mutations. Mutation analysis was performed by direct sequencing of the VHL gene. Mutations were identified in 36 patients. Mutations-carriers were screened for VHL disease-related tumors and were offered follow-up annual examinations. Tumor status and phenotypes were documented at initial screening and at follow ups. 1 individual from family 20 was tested positive for p.C162F mutation. 2 hemangioblastoma, unilateral retinal capillary hemangioma, kidney cysts, pancreatic cysts and 1 pheochromocytoma were diagnosed at initial screening. 1 renal cell carcinoma and 1 pheochromocytoma were detected at follow-ups. ACMG evidence codes: 'PP4' because the patient's phenotypes are highly specific for a disease with single genetic etiology.

    1. c.492G>T/c.340+574A>T

      The authors identify a new VHL cryptic exon (termed E1') deep in intron 1 that is naturally expressed in many tissues. Mutations in E1' are identified in 7 families with erythrocytosis and in 1 large family with typical VHL disease but without any alteration in the other VHL exons. In this study, the authors show that the mutations in E1' induced a dysregulation of VHL splicing with excessive retention of E1' and were associated with a downregulation of VHL protein expression. Patient II.1 of family F6, was found to have two germline mutations in the VHL gene: Q164H (c.492G>T) and c.340+574A>T. This patient was diagnosed with splenomegaly at age 6 months (DOB: 2014). This patient's asymptomatic parents were also genetically tested and her mother was found to have the germline c.340+574A>T variant of the VHL gene while her father carried the Q164H (c.492G>T) germline variant.

    1. Germline mutations were found in 20 Brazilian, VHL probands and their families. The F136S (c.407T>C) germline missense mutation was found in a VHL type 1 family of 8 affected individuals (VHL family 12). Seven had hemangioblastomas of the central nervous system, one had retinal angiomas, and 2 had renal carcinoma. One patient in this family has a renal tumor <3cm.

    1. Complete deletion*

      GroupID/ KindredID: 26

      PatientID: I

      Case: 37Y0M, Sex unknown, Polish

      DiseaseAssertion: VHL

      FamilyInfo: Family 26 consisted of 2 members; One other member (40Y) was diagnosed with a single spinal HAB, and a single cerebellar HAB at 38Y.

      CasePresentingHPOs: HP:0006880 (cerebellar hemangioblastoma)

      CaseHPOFreeText: Patient was diagnosed with a single cerebellar HAB at 32Y

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

      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

    2. 445delG149Frameshift

      A study of 34 Polish families revealed germline mutations in 30 families using DNA isolated from peripheral blood luykocytes to sequence through PCR and Quantitative Southern analysis. Mutations were not detected in 4 probands fulfilling clinical criteria for von Hippel-Lindau disease (VHLD). This mutation was found in a VHL family of 3 individuals. All 3 had retinal hemangioblastomas, 2 had hemangioblastomas of the central nervous system, and one had renal cell carcinoma (family no. 13). ACMG codes as follows: A frameshift variant in a gene where loss-of-function is a known mechanism of disease (PVS1).

    3. Exons 2, 3 deletion

      GroupID/ KindredID: 22 / S 4

      Case: Age unknown, Sex unknown, Polish

      DiseaseAssertion: VHL

      FamilyInfo: This deletion was found in Family No. 22 with 1 member affected. Germline de novo mutations confirmed by analysis of parents’ DNA. Germline mutations (of deletion of exon 2-3) was not detected in DNA extracted from blood leucocytes of the parents.

      CasePresentingHPOs: HP:0009711 (retinal capillary hemangioma)

      CaseHPOFreeText: N/A

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

      CaseNotHPOFreeText: N/A

      CasePreviousTesting: N/A

      PreviouslyPublished: N/A

      SupplementalData: N/A

      Variant: Exons 2, 3 deletion

      CaseProblemVariantFreeText: N/A

      LegacyVariant: N/A

      ClinVarID: N/A

      CAID: N/A

      gnomAD: N/A

      VariantEvidence: N/A

      MutationType: exon_loss_variant

      CivicName: EXON 2-3 DELETION

      MultipleGeneVariants: N/A

    1. PatientID: 347

      KindredID: 347

      Case: Sex Unknown, 30Y0M, Ethnicity Unknown

      DiseaseAssertion: VHL

      FamilyInfo: Family history is positive but no details provided.

      CasePresentingHPOs: HP:0010797; HP:0000107 (Hemangioblastoma, Renal cyst)

      CaseHPOFreeText: CNS hemangioblastoma and renal cyst.

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

      CaseNotHPOFreeText: N/A

      CasePreviousTesting: N/A

      PreviouslyPublished:N/A

      SupplementalData: Table S1, S2 and S3

      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; deletion

      CivicName: Exon 1 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 L188R (c.563T>G) germline mutation of the VHL gene was found in a 48 yr old VHL patient with renal cystic lesions and hemangioblastomas of the central nervous system (index case 109). The variant is noted as likely de novo. Child/children were analyzed but no details were provided.

    3. PatientID: 164

      KindredID: 164

      Case: Sex Unknown, 12Y0M, Ethnicity Unknown

      DiseaseAssertion: VHL

      FamilyInfo: N/A

      CasePresentingHPOs: HP:0002666 (Pheochromocytoma)

      CaseHPOFreeText: N/A

      CaseNotHPOs: HP:0010797; HP:0006770; HP:0001732; HP:0009711; HP:0000107 (Hemangioblastoma, Clear cell renal cell carcinoma, Abnormality of the pancreas, Retinal capillary hemangioma, Renal cyst)

      CaseNotHPOFreeText: N/A

      CasePreviousTesting: N/A

      PreviouslyPublished: N/A

      SupplementalData: Table S1, S2 and S3

      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

    4. 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 R167L (c.500G>T) germline mutation of the VHL gene, was found in two patients. Patient 24 (57Y) presented with pheochromocytoma, retinal hemangioblastoma and CNS hemangioblastoma. Their father were found to carry the R167L (c.500G>T) germline mutation of the VHL gene. Father, siblings and nephew were analyzed but no phenotype information was provided for these family members. Genotype information for siblings and nephew was not provided. Patient 232 presented with pheochromocytoma, retinal hemangioblastoma and CNS hemangioblastoma. The variant is noted as likely de novo. Mother and sibling were analyzed but no details were provided. Based on likely de novo assertion, it’s assumed that mother was negative for this mutation.

    1. F2-II1Male24p.N78S-Left, 1.0x1.0x0.8; right, 1.0x1.0x1.0Right, 4.1x3.4x3.9Right PHEO resection + right RCC resection + resection of bilateral epididymal cystRight PHEO + right RCC + bilateral epididymal cystRight PHEO + right PHEOa + bilateral epididymal cust + multiple pancreatic cystsVHL-IIB

      PatientID: II1

      KindredID: 2

      Case: M, 33Y0M, Chinese (East Asian)

      DiseaseAssertion: Assumed VHL

      FamilyInfo: Patient’s brother (symptomatic) and son (asymptomatic) tested positive for this germline mutation.

      CasePresentingHPOs: HP:0002666; HP:0005584; HP:0030424; HP:0009715 (Pheochromocytoma; Renal Cell Carcinoma; Epididymal cyst; Papillary cystadenoma of the epididymis)

      CaseHPOFreeText: Admitted at 24Y due to headache, dizziness, and palpitations. MRI showed a mass (4.1x3.4x3.9sm) in the right adrenal gland, and multiple renal tumors on both kidneys - RCC (the largest diameter of the tumors, 1.0x1.0x1.0 cm on the left; 1.0x1.0x0.8 cm on the right). The patient also had multiple pancreatic cysts, and at 27 (3Y later) underwent bilateral epididymal nodule excision due to multiple nodules in the epididymal head.

      CaseNotHPOs: HP:0009711 (retinal capillary hemangioma)

      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

    2. F1-III2

      PatientID: III2

      KindredID: 1

      Case: F, 25Y0M, Chinese (East Asian)

      DiseaseAssertion: Pheochromocytoma

      FamilyInfo: Patient’s aunt and cousin were diagnosed with the same genetic mutation and VHL-pheochromocytoma. Her father was the bloodline and he has passed away with an unknown medical history at age 38Y. It is likely that he was a VHL mutation carrier, however it was never tested.

      CasePresentingHPOs: HP:0006748 (adrenal pheochromocytoma)

      CaseHPOFreeText: bilateral synchronous adrenal pheo diagnosed at 28Y with resection (Left: 6.0x4.7x3.5cm; Right:3.5x2.8x2.5cm). (Table mixes up III2 and III6 - folllow test and pedgree for accuracy).

      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. #7bilccRCC(49–51)NAc.340+578C>Trs1396223560.05NANANANANAVUS

      PatientID: 7

      KindredID: 7

      Case: Sex Unknown, 51Y0M, Ethnicity Unknown

      DiseaseAssertion: clear cell renal cell carcinoma

      FamilyInfo: N/A - not stated

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

      CaseHPOFreeText: Bilateral clear cell RCC was first diagnosed between 49-51Y of age

      CaseNotHPOs: N/A

      CaseNotHPOFreeText: N/A

      CasePreviousTesting: N/A

      PreviouslyPublished: N/A

      SupplementalData: Yes

      Variant: c.340+578C>T

      LegacyVariant: N/A

      CaseProblemVariantFreeText: N/A

      ClinVarID: 849869 https://www.ncbi.nlm.nih.gov/clinvar/variation/849869/

      CAID: N/A

      gnomAD: 0.0005097 https://gnomad.broadinstitute.org/variant/3-10184449-C-T

      VariantEvidence: N/A

      MutationType: splice_site_variant; intron_variant

      CivicName: Splice Site (c.340+578C>T)

      MultipleGeneVariants: N/A

    1. Thirty-five unrelated patients suspected of having von Hippel-Lindau disease were analyzed and 32 VHL gene variants were found in 35 patients using PCR and SSCP by peripheral blood leukocytes. An association of clear cell renal carcinoma development with a relatively high loss of structural stability in VHL protein missense mutations was discovered. This missense mutation (D121G) was found in a 31 year old patient with retinal hemangioblastomas and renal cysts (patient no. F26). Patient had family history of pheochromocytomas and hemangioblastomas of the central nervous system.

    2. Thirty-five unrelated patients suspected of having von Hippel-Lindau disease were analyzed and 32 VHL gene variants were found in 35 patients using PCR and SSCP by peripheral blood leukocytes. An association of clear cell renal carcinoma development with a relatively high loss of structural stability in VHL protein missense mutations was discovered. VHL R167W (c.499C>T) was found in 3 unrelated patients (non-relation confirmed by haplotype analysis). Patient F34 (33 years old at onset) had retinal and cerebellar hemangioblastomas, unilateral clear cell renal carcinoma (ccRC), renal cyst, pancreatic cyst, and positive for familial antecedents; although unknown of any additional features to index case. Patient F40 (42 years old at onset) had retinal hemangioblastoma, bilateral pheochromocytoma, unilateral ccRC, and again positive for familial antecedents however unknown of any additional features. Patient F64 (24 years old at onset) had retinal hemangioblastoma, bilateral pheochromocytoma, pancreatic cyst, and no family history. Structural analysis revealed that this variant resulted in high degrees of pVHL unfolding.

    1. Mari IMANAKA, Keiji IIDA, Kentaro TAKAHASHI, Kazuo TSUJI, Hitoshi NISHIZAWA, Hidenori FUKUOKA, Ryoko TAKENO, Yutaka TAKAHASHI, Yasuhiko OKIMURA, Hidesuke KAJI, Kazuo CHIHARA

      ArticleReferenceSequence: Not specified - NM_000551.3 or AF010238.1 could have been used as author documented variant with protein number and position in codon only.

      GenotypingMethod: Exons 1, 2, and 3 of the VHL gene were then amplified by PCR. After purifying the PCR products by using the QIA quick PCR purification kit (Qiagen Corp., Valencia, CA, USA), direct sequencing was performed using the ABI Prism 310 Genetic Analyzer (model 310; Perkin-Elmer, Applied Biosystems, Foster City, CA, USA). To confirm the presence of a mutation, PCR-based restriction fragment length polymorphism (RFLP) analysis of exon 2 of the VHL gene was performed. After amplifying exon 2 in the VHL gene from the patient and normal control, the PCR products were digested with the restriction enzyme HpaI (Takara) according to the manufacturer’s instructions.

      SamplingMethod: Peripheral blood, tumour tissue

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

      GroupID/ KindredID: 3575NCI

      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 3575NCI. 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.N150Ifs*9 (c.448delA)

      LegacyVariant: FS (c.661delA)

      CaseProblemVariantFreeText: NM_000551.3:c.448delA automaps to NM_000551.3:c.449delA due to redundancy

      ClinVarID: 195093 https://www.ncbi.nlm.nih.gov/clinvar/variation/195093/

      CAID: N/A

      gnomAD: N/A

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

      MutationType: minus_1_frameshift_variant

      CivicName: N150fs (c.449delA)

      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 (G93S (c.277G>A)) was taken from multiple databases, including: the Munich, university of Freiburg and Institute of Pathology database, and the National Cancer Institute database, with an unknown number of members belonging to two family IDs: Family ID 62CE and 4873NCI. It was reported in the paper as c.490G>A due to a difference in transcript reference. As reported in Table 4, this mutation is found in VHL families with pheochromocytoma. Other phenotypes are likely, including renal cell carcinoma, however not detailed here.

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

      GroupID/ KindredID: 4486NCI

      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 4486NCI. 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.H115Q (c.345C>A)

      LegacyVariant: p.H115Q (c.558C>A)

      CaseProblemVariantFreeText: N/A

      ClinVarID: 496057 https://www.ncbi.nlm.nih.gov/clinvar/variation/496057/

      CAID: N/A

      gnomAD: N/A

      VariantEvidence: N/A

      MutationType: missense_variant; transversion

      CivicName: H115Q (c.345C>A)

      MultipleGeneVariants: N/A

    4. 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 (Q195* (c.583C>T)) was taken from two databases: the Cambridge, Department of Pathology database and the Munich, university of Freiburg and Institute of Pathology database. There was an unknown number of members belonging to Family IDs: 21CA and 56CE. It was reported in the paper as c.796C>T 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.

    5. 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 (C77fs (c.228dupC)) was taken from the Cambridge, Department of Pathology database, with an unknown number of members belonging to Family ID 85CA (reported in Table 3, found in VHL families with renal cell carcinoma), and 71CA (reported in Table 4, found in VHL families with pheochromocytoma). Other phenotypes are likely, however not detailed here. It was reported in the paper as c.441insC due to a difference in transcript reference.

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

      GroupID/ KindredID: 39CA

      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 Cambridge, Department of Pathology database, with an unknown number of members belonging to family ID: Family 39CA. Table 5 lists all ID and mutations associated with individuals without detailed clinical information.

      GroupPresentingHPOs: N/A

      GroupHPOFreeText: Described as multiple VHL families without detailed clinical information. Other phenotypes are possible, however not detailed here.

      GroupNotHPOs: N/A

      GroupNotHPOFreeText: N/A

      GroupPreviousTesting: 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: N/A

      gnomAD: N/A

      VariantEvidence: N/A

      MutationType: missense_variant; transversion

      CivicName: S65W (c.194C>G)

      MultipleGeneVariants: N/A

    7. 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 (F76del (c.227_229delTCT)) was taken from various families from multiple databases: including: the National Cancer Institute database, the Bristol Myers Squibb database, Department of Uroglogy, Yokohama database, and the Cambridge, Department of Pathology; with an unknown number of members belonging to each. It was reported in the paper as both c.439delTTC and c.440delTCT, 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, including IDs: 2693NCI, 2956NCI, 20BMS, 2YO, 27BMS, 75CA, 48CA, and 144CA. Additionally, table 5 lists all ID and mutations associated with individuals without detailed clinical information, and was found in one family: family ID 134CA. Other phenotypes are possible, however not detailed here. Later publications reference this cohort as being reported in PMIDs: 7728151 and 9829911.

    1. PatientID: S6150

      KindredID: S6150

      Case: Sex Unknown, Age Unknown, Ethnicity Unknown

      DiseaseAssertion: VHL

      FamilyInfo: N/A

      CohortInfo: 92 unrelated patients with VHL disease.

      CasePresentingHPOs: N/A

      CaseHPOFreeText: N/A

      CaseNotHPOs: N/A

      CaseNotHPOFreeText: N/A

      CasePreviousTesting: N/A

      PreviouslyPublished: N/A

      SupplementalData: N/A

      Variant: p.G104A(c.311G>C)

      LegacyVariant:N/A

      CaseProblemVariantFreeText: N/A

      ClinVarID: 411966 https://www.ncbi.nlm.nih.gov/clinvar/variation/411966/

      CAID: N/A

      gnomAD: N/A

      VariantEvidence: N/A

      MutationType: missense_variant;transversion

      CivicName:G104A(c.311G>C)

      MultipleGeneVariants: N/A

    2. PatientID: V287

      KindredID: V287

      Case: Sex Unknown, Age Unknown, French

      DiseaseAssertion: VHL

      FamilyInfo: N/A

      CasePresentingHPOs: N/A

      CaseHPOFreeText: Diagnosed with VHL Type 1.

      CaseNotHPOs: HP:0002666 (Pheochromocytoma)

      CaseNotHPOFreeText: N/A

      CasePreviousTesting: N/A

      PreviouslyPublished: N/A

      SupplementalData: N/A

      Variant: p.N67_V74del (c.198_221del)

      LegacyVariant: N/A

      CaseProblemVariantFreeText: N/A

      ClinVarID: N/A

      CAID: CA645524685, https://reg.clinicalgenome.org/redmine/projects/registry/genboree_registry/allele?hgvsOrDescriptor=NM_000551.3%3Ac.198_221del

      gnomAD: N/A

      VariantEvidence: Variant was reported as c.197del24 which was mapped to c.198_221del.

      MutationType: inframe_deletion; deletion

      CivicName: N67_V74del (c.198_221del)

      MultipleGeneVariants: N/A

    3. Screening of 92 unrelated patients with VHL disease revealed 61 DNA variants. Blood samples were isolated and sequenced by direct sequencing using prism-ready reaction dye primer cycle sequencing kits (Applied Biosystem Roissy CDG France) and an ABI 373A automated sequencer (AppliedBiosystem Roissy CDG France). No variants were found in 96 control cases. This missense mutation, c.393C>A, was found in a VHL type 2A patient (patient no. V233). Type 2A VHL families were described as having pheochromocytomas. A single unaffected family member available for screening did not have the N131K mutation.

    4. 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 E73* (c.217C>T) mutation was found in a VHL type 1 (no pheochromocytoma) patient (patient no. V64).

    1. PatientID: 26

      KindredID: 26

      Case: F, 46Y0M, Korean

      DiseaseAssertion: VHL

      FamilyInfo: Family history positive for 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:0010797; HP:0005584; HP:0002666 (Hemangioblastoma, Renal cell carcinoma, Pheochromocytoma)

      CaseHPOFreeText: CNS hemangioblastomas. Diagnosed with VHL Type 2B.

      CaseNotHPOs: HP:0009711 (Retinal capillary hemangioma)

      CaseNotHPOFreeText: N/A

      CasePreviousTesting: N/A

      PreviouslyPublished: N/A

      SupplementalData: N/A

      Variant: p.V87A (c.260T>C)

      LegacyVariant: N/A

      CaseProblemVariantFreeText: coding DNA and protein position (c.341T>C, p.Val114Arg) do not match reference sequence. “We found our error of changing the nucleotide code "A" to the three-letter code "Arg", which should be corrected to "ALA" based on the reference NM_001354723.1(VHL). It could be corrected as follows; NM_000551.3(VHL): c.260T>C (p.Val87Ala).” (Author Rhee comment)

      ClinVarID: N/A

      CAID: CA351750654, https://reg.clinicalgenome.org/redmine/projects/registry/genboree_registry/by_canonicalid?canonicalid=CA351750654

      gnomAD: N/A

      VariantEvidence: N/A

      MutationType: missense_variant;transition

      CivicName: V87A (c.260T>C)

      MultipleGeneVariants: N/A

    2. PatientID: 33

      KindredID: 33

      Case: M, 33Y0M, 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:0010797; HP:0005584 (Hemangioblastoma, Renal cell carcinoma)

      CaseHPOFreeText: Multiple or bilateral CNS hemangioblastomas and renal cell carcinoma. 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 (Pheochromocytoma, Retinal capillary hemangioma)

      CaseNotHPOFreeText: N/A

      CasePreviousTesting: N/A

      PreviouslyPublished: N/A

      SupplementalData: N/A

      Variant: p.L140Sfs*4 (c.417dup)

      LegacyVariant: N/A

      CaseProblemVariantFreeText: N/A

      ClinVarID: N/A

      CAID: CA2573051216, https://reg.clinicalgenome.org/redmine/projects/registry/genboree_registry/by_canonicalid?canonicalid=CA2573051216

      gnomAD: N/A

      VariantEvidence: Stated as c.417_418insT by the authors.

      MutationType: duplication; plus_1_frameshift_variant

      CivicName: L140Sfs*4 (c.417dup)

      MultipleGeneVariants: N/A

    3. Medical records of 26 patients with germline mutations of the VHL gene who had been diagnosed with VHL disease in Severance Hospital (Seoul, Republic of Korea) and Samsung Medical Center (Seoul, Republic of Korea) between 2003 and 2012 were respectively reviewed. Peripheral blood leukocytes were isolated and directly sequenced. One 38Y male patient (Patient 32) presented with renal cell carcinoma and retinal hemangioblastoma. He had a germline missense mutation in the VHL gene (c.416C>T; Ser139Phe). Family history of this patient is unknown. The patient was previously reported by Kim et al., in 2005 (reference 9 in the current paper).

    1. missense mutations

      PatientID: None

      KindredID: 42

      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 42

      CasePresentingHPOs: N/A

      CaseHPOFreeText: Unknown

      CaseNotHPOs: HP:0002666 (pheochromocytoma)

      CaseNotHPOFreeText: No presence of phaeochromocytoma in family

      CasePreviousTesting: N/A

      PreviouslyPublished: N/A

      SupplementalData: N/A

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

      CaseProblemVariantFreeText: N/A

      LegacyVariant: p.C162Y (c.698G>A)

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

      CAID: N/A

      gnomAD: N/A

      VariantEvidence: N/A

      MutationType: missense_variant; transition

      CivicName: C162Y (c.485G>A)

      MultipleGeneVariants: N/A

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

      PatientID: None

      KindredID: 38

      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 38

      CasePresentingHPOs: N/A

      CaseHPOFreeText: Unknown or unstated.

      CaseNotHPOs: HP:0002666 (pheochromocytoma)

      CaseNotHPOFreeText: No presence of phaeochromocytoma in family

      CasePreviousTesting: N/A

      PreviouslyPublished: N/A

      SupplementalData: N/A

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

      CaseProblemVariantFreeText: N/A

      LegacyVariant: p.Q73* (c.430C>T)

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

      CAID: N/A

      gnomAD: N/A

      VariantEvidence: N/A

      MutationType: stop_gained

      CivicName: Q73* (c.217C>T)

      MultipleGeneVariants: N/A

    3. 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 R177* (c.499C>T) was referred to in the paper by c.712C>T due to a difference in transcript sequence. This missense mutation was found in one of the VHL families (family ID 153).

    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. The p.P158L (c.473T>C) mutation was detected in the patient, referred to in the paper by c.686T>C due to a difference in transcript sequence. This missense mutation was found in two VHL type 2A families of 55 individuals altogether (family IDs 3476, 3127). 26 of 55 individuals were identified with retinal hemangioblastomas, 5 with CNS hemangioblastomas, and 30 with pheochromocytomas. Supporting evidence of pathogenicity because cosegregation with disease in multiple affected family members in a gene definitively known to cause the disease (ACMG code: PP1).

    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 detected in VHL type 1 patient (Family ID 3618), using PCR and SSCP sequencing. The mutation of c.486C>G was referred to in the paper by c.699C>G due to a difference in transcript sequence. The patient had CNS hemangioblastomas.

    3. 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 nonsense mutation was found in a VHL type 1 family of 6 individuals (family ID 3710), using PCR and SSCP sequencing. The mutation of c.404T>A was referred to in the paper by c.617T>A due to a difference in transcript sequence. All 6 individuals were identified with CNS hemangioblastomas, 4 with retinal angiomas and 3 with renal cell carcinoma. Supporting evidence of pathogenicity because cosegregation with disease in multiple affected family members in a gene definitively known to cause the disease (ACMG code: PP1).

    4. GroupID: 3969

      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:0002666 (retinal capillary hemangioma, pheochromocytoma)

      GroupHPOFreeText: both (2) members had retinal angiomas (hemangiomas), and 1 had pheochromocytoma

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

      GroupNotHPOFreeText: N/A

      GroupPreviousTesting: N/A

      PreviouslyPublished: 8956040 (type 2 3969NCI)

      SupplementalData: N/A

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

      CaseProblemVariantFreeText: N/A

      LegacyVariant: p.A220T (c.658G>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. PatientID: 8

      KindredID: Unknown

      Case: F, 28Y0M, Dutch

      DiseaseAssertion: VHL

      FamilyInfo: Unknown - study sampled 15 patients from 5 families

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

      CaseHPOFreeText: retinal capillary hemangioma of the right eye

      CaseNotHPOs: N/A

      CaseNotHPOFreeText: N/A

      CasePreviousTesting: N/A

      PreviouslyPublished: N/A

      SupplementalData: N/A

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

      LegacyVariant: p.V241D

      CaseProblemVariantFreeText: Variant determined through the assumption of the authors using Latif et al 1993 (AF010238.1) transcript and adding 71bp to the protein sequence.

      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. PatientID: 11

      KindredID: Unknown

      Case: M, 38Y0M, Dutch

      DiseaseAssertion: VHL

      FamilyInfo: Unknown - study sampled 15 patients from 5 families

      CasePresentingHPOs: HP:0001737; HP:0009711; HP:0006880; HP:0009713; HP:0000107; HP:0006706 (pancreatic cyst, retinal capillary hemangioma, cerebellar hemangioblastoma, spinal hemangioblastoma, renal cyst, cystic liver disease)

      CaseHPOFreeText: retinal capillary hemangioma of the right eyes, pancreatic, renal and liver cysts (cystic liver disease), and cerebellar and spinal hemangioblastoma

      CaseNotHPOs: N/A

      CaseNotHPOFreeText: N/A

      CasePreviousTesting: N/A

      PreviouslyPublished: N/A

      SupplementalData: N/A

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

      LegacyVariant: p.V241D

      CaseProblemVariantFreeText: Variant determined through the assumption of the authors using Latif et al 1993 (AF010238.1) transcript and adding 71bp to the protein sequence.

      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. p.Arg161X29F+CHB, RCC, pancreatic cyst

      PatientID: 8

      KindredID: 5

      Case: F, 29Y0M, Ethnicity unknown

      DiseaseAssertion: VHL

      FamilyInfo: Familial VHL mutation - unknown relatives

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

      CaseHPOFreeText: With an age of diagnosis of VHL at 29

      CaseNotHPOs: N/A

      CaseNotHPOFreeText: N/A

      CasePreviousTesting: Patients with clinical manifestations suggestive of VHL or MEN2 were first screened for VHL or RET mutation, respectively. Possible screening of RET, SDHB and SDHD as well

      PreviouslyPublished: N/A

      SupplementalData: Yes

      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: 49

      KindredID: N/A

      Case: Sex Unknown, Age Unknown, Ethnicity Unknown

      DiseaseAssertion: VHL

      FamilyInfo: N/A

      CohortInfo: The authors evaluated 64 VHL patients (32 women and 32 men) with renal involvement of whom 54/64 had undergone renal surgery or a radiofrequency thermal ablation procedure for RCC. In 10/64 VHL patients, at least one or more RCC were diagnosed, however at the time of diagnosis an indication for treatment was not yet present. For all patients several CT/MRI scans existed for retrospective description of tumour growth kinetics.

      CasePresentingHPOs: HP:0005584 (Renal cell carcinoma)

      CaseHPOFreeText: This is a tumor resolution study (VHL patients were investigated based on the presence of renal tumors.) No other phenotypic information is available.

      CaseNotHPOs: N/A

      CaseNotHPOFreeText: N/A

      CasePreviousTesting: N/A

      PreviouslyPublished: N/A

      SupplementalData: Supplementary Table S5 describes 8 patients with small deletions, including this patient.

      Variant: p.R177Dfs*25 (c.528del)

      LegacyVariant: c.740delG

      CaseProblemVariantFreeText: N/A

      ClinVarID: N/A

      CAID: CA432423454

      gnomAD: N/A

      VariantEvidence: N/A

      MutationType: minus_1_frameshift_variant; deletion

      CivicName: R177fs(c.528del)

      MultipleGeneVariants: N/A

    2. PatientID: 7

      KindredID: N/A

      Case: Sex Unknown, Age Unknown, Ethnicity Unknown

      DiseaseAssertion: VHL

      FamilyInfo: N/A

      CohortInfo: The authors evaluated 64 VHL patients (32 women and 32 men) with renal involvement of whom 54/64 had undergone renal surgery or a radiofrequency thermal ablation procedure for RCC. In 10/64 VHL patients, at least one or more RCC were diagnosed, however at the time of diagnosis an indication for treatment was not yet present. For all patients several CT/MRI scans existed for retrospective description of tumour growth kinetics.

      CasePresentingHPOs: HP:0005584 (Renal cell carcinoma)

      CaseHPOFreeText: This is a tumor resolution study (VHL patients were investigated based on the presence of renal tumors.) No other phenotypic information is available.

      CaseNotHPOs: N/A

      CaseNotHPOFreeText: N/A

      CasePreviousTesting: N/A

      PreviouslyPublished: N/A

      SupplementalData: Supplementary Table S1 describes 19 patients with missense mutations, including this patient.

      Variant: p.V130F(c.388G>T)

      LegacyVariant: c.601G>T

      CaseProblemVariantFreeText: N/A

      ClinVarID: 496061, https://www.ncbi.nlm.nih.gov/clinvar/variation/496061/

      CAID: N/A

      gnomAD: N/A

      VariantEvidence: N/A

      MutationType: missense_variant;transversion

      CivicName: V130F(c.388G>T)

      MultipleGeneVariants: N/A

    3. PatientID: 23

      KindredID: N/A

      Case: Sex Unknown, Age Unknown, Ethnicity Unknown

      DiseaseAssertion: VHL

      FamilyInfo: N/A

      CohortInfo: The authors evaluated 64 VHL patients (32 women and 32 men) with renal involvement of whom 54/64 had undergone renal surgery or a radiofrequency thermal ablation procedure for RCC. In 10/64 VHL patients, at least one or more RCC were diagnosed, however at the time of diagnosis an indication for treatment was not yet present. For all patients several CT/MRI scans existed for retrospective description of tumour growth kinetics.

      CasePresentingHPOs: HP:0005584 (Renal cell carcinoma)

      CaseHPOFreeText: This is a tumor resolution study (VHL patients were investigated based on the presence of renal tumors.) No other phenotypic information is available.

      CaseNotHPOs: N/A

      CaseNotHPOFreeText: N/A

      CasePreviousTesting: N/A

      PreviouslyPublished: N/A

      SupplementalData: Supplementary Table S1 describes 19 patients with missense mutations, including this patient.

      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: N/A

      MutationType: missense_variant;transition

      CivicName: R167W(c.499C>T)

      MultipleGeneVariants: N/A

    4. The authors described the growth kinetics of 96 renal tumours in 64 VHL patients (32 males, 32 females). All patients had VHL disease with renal involvement. 54/64 had undergone renal surgery or a radiofrequency thermal ablation procedure for RCC. In 10/64 patients, at least one or more RCC was diagnosed. However, at the time of diagnosis, an indication for treatment was not yet present. For all patients, several CT/MRI scans existed for retrospective description of tumour growth kinetics. 10-ml EDTA anticoagulated blood samples were available from each patient for mutation screening of all exons of the VHL gene. Genomic DNA from blood samples was extracted using standard methods. Small deletions/insertions or point mutations were identified by DNA sequencing followed by complete mutation screening using PCR/single-strand conformation polymorphism and denaturing high-performance liquid chromatography. A germline deletion p.L129Wfs*30 (c.384del) was identified in patient #15. This mutation was noted as c.597delT in the paper due to a difference in reference transcript used (see Table S5). No family information is available for this patient.

    1. ConclusionsIn this case of VHL syndrome presenting with aneurysmal SAH, the patient was heterozygous for a germline point mutation at nucleotide 469 in the VHL gene. A possible molecular link may exist through HIF, MMP, VEGF, and a disorganized fibronectin ECM. Although a single point mutation is unlikely to be responsible for a complex phenotype such as an intracranial aneurysm, further research on aneurysm domes and VHL gene expression may prove illuminating.

      A 17-year-old female (the proband, designated arbitrarily as 'Patient 1' in this annotation) underwent endovascular coiling for an aneurysmal subarachnoid hemorrhage. Six years later (at age 23), she presented with cystic lesions in the cerebellar vermis and cervicomedullary region, diagnosed as spinocerebellar hemangioblastomas through tumor biopsy. She underwent a total excision of these tumors. At the 12-month follow-up examination, no neuroimaging evidence of residual or recurrent disease was found. Sequencing of genomic DNA extracted from this patient's peripheral blood revealed that she was heterozygous for a missense mutation in the VHL gene: p.Pro86Ser (c.256C>T). This missense mutation is noted as c.469C>T in the paper due to a difference in the VHL reference sequence notation used. The patient's mother (designated as 'Patient 2') also tested positive for the same point mutation, but neuroimaging showed that she was unaffected by the same disease (spinocerebellar hemangioblastomas) as her daughter. There was no other family history of similar diseases/complaints.

    1. GroupID/ KindredID: VHL 57

      Case: Sex unknown, Age unknown, German

      DiseaseAssertion: assumed VHL

      FamilyInfo: One patient with the given mutation is stated to belong to VHL family 57

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

      CaseHPOFreeText: N/A

      CaseNotHPOs: N/A

      CaseNotHPOFreeText: N/A

      CasePreviousTesting: N/A

      PreviouslyPublished: N/A

      SupplementalData: N/A

      Variant: c.464-2A>T

      CaseProblemVariantFreeText: N/A

      LegacyVariant: c.677-2A>T

      ClinVarID: N/A

      CAID: CA70052157 https://reg.clinicalgenome.org/redmine/projects/registry/genboree_registry/allele?hgvsOrDescriptor=NM_000551.3%3Ac.464-2A%3ET

      gnomAD: N/A

      VariantEvidence: N/A

      MutationType: splice_site_variant

      CivicName: Splice Site (c.464-2A>T)

      MultipleGeneVariants: N/A

    2. Of 65 VHL families from central Europe, 53 were identified with germline mutations using SSCP analysis of PCR products by peripheral blood. This nonsense mutation was found in 3 Italian, VHL type 1 family members. Two had retinal angiomas, 2 had hemangioblastomas of the central nervous system, 2 had renal cysts, 1 had renal cell carcinoma, and all three had pancreatic cysts. The S183* (c.548C>A) mutation was detected in the patient, referred to in the paper by c.761C>A due to a difference in transcript sequence. This study contains very strong evidence of pathogenicity in the form of a nonsense variant in a gene where loss-of-function is a known mechanism of disease (ACMG code: PVS1).

    3. Of 65 VHL families from central Europe, 53 were identified with germline mutations using SSCP analysis of PCR products by peripheral blood. This nonsense mutation was found in a German, VHL type 1 patient with retinal angiomas, hemangioblastomas of the central nervous system, pancreatic cysts, and liver cysts (family VHL 30). The Q132* (c.394C>T) mutation was detected in the patient, referred to in the paper by c.607C>T due to a difference in transcript sequence. This study contains very strong evidence of pathogenicity in the form of a nonsense variant in a gene where loss-of-function is a known mechanism of disease (ACMG code: PVS1).

    4. GroupID/ KindredID: VHL23

      Case: Sex unknown, Age unknown, German

      DiseaseAssertion: assumed VHL

      FamilyInfo: One patient with the given mutation is stated to belong to VHL family 23. Although the patient had multiple VHL lesions, there was no family history of the disease.

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

      CaseHPOFreeText: N/A

      CaseNotHPOs: N/A

      CaseNotHPOFreeText: N/A

      CasePreviousTesting: N/A

      PreviouslyPublished: N/A

      SupplementalData: N/A

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

      CaseProblemVariantFreeText: N/A

      LegacyVariant: p.P81S (c.454C>T)

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

      CAID: CA020148 http://reg.clinicalgenome.org/redmine/projects/registry/genboree_registry/allele?hgvsOrDescriptor=NM_000551.3%3Ac.241C%3ET

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

      VariantEvidence: N/A

      MutationType: missense_variant;transition

      CivicName: P81S (c.241C>T)

      MultipleGeneVariants: N/A

    1. c.462A>C1 (1)2a/b71HBc, Pheo, Cr

      GroupID: None

      Case: Sex Unknown, 71Y0M, Dutch

      DiseaseAssertion: VHL

      FamilyInfo: N/A

      CasePresentingHPOs: HP:0006880; HP:0002666; HP:0000107 (Cerebellar hemangioblastoma, Pheochromocytoma, Renal cyst)

      CaseHPOFreeText: This individual was classified as 2a/b meaning that it included de novo VHL mutation carriers or VHL mutation carriers having a family history with diagnosis of pheochromocytoma and other VHL related manifestations.

      CaseNotHPOs: N/A

      CaseNotHPOFreeText: N/A

      CasePreviousTesting: N/A

      PreviouslyPublished: 31087189

      SupplementalData: N/A

      Variant: p.P154= (c.462A>C)

      LegacyVariant: N/A

      CaseProblemVariantFreeText: N/A

      ClinVarID: N/A

      CAID: CA16621934, https://reg.clinicalgenome.org/redmine/projects/registry/genboree_registry/allele?hgvsOrDescriptor=NM_000551.3%3Ac.462A%3EC

      gnomAD: N/A

      VariantEvidence: N/A

      MutationType: missense_variant;transversion; synonymous_variant

      CivicName: P154= (c.462A>C)

      MultipleGeneVariants: N/A

    2.  c.259_260-insA1 (1)142HBr, HBc, HBsc, RCC, Cr, Cp

      GroupID: None

      Case: Sex Unknown, 42Y0M, Dutch

      DiseaseAssertion: VHL

      FamilyInfo: N/A

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

      CaseHPOFreeText: Diagnosed with VHL Type 1.

      CaseNotHPOs: N/A

      CaseNotHPOFreeText: N/A

      CasePreviousTesting: N/A

      PreviouslyPublished: 31087189

      SupplementalData: N/A

      Variant: p.V87Dfs*45 (c.259_260insA)

      LegacyVariant: N/A

      CaseProblemVariantFreeText: N/A

      ClinVarID: N/A

      CAID: CA913189242, https://reg.clinicalgenome.org/redmine/projects/registry/genboree_registry/by_canonicalid?canonicalid=CA913189242

      gnomAD: N/A

      VariantEvidence: N/A

      MutationType: insertion; plus_1_frameshift_variant

      CivicName: V87fs (c.259_260insA)

      MultipleGeneVariants: N/A

    1. 3 large gene rearrangements.

      PatientID: 18

      KindredID: 355

      Case: Sex unknown, Age unknown, French

      DiseaseAssertion: VHL

      FamilyInfo: N/A

      CasePresentingHPOs: HP:0002666; HP:0030405 (pheochromocytoma, pancreatic endocrine tumour)

      CaseHPOFreeText: N/A

      CaseNotHPOs: HP:0005584 (renal cell carcinoma)

      CaseNotHPOFreeText: N/A

      CasePreviousTesting: N/A

      PreviouslyPublished: N/A

      SupplementalData: N/A

      Variant: NONE (unspecified large rearrangement)

      LegacyVariant: N/A

      CaseProblemVariantFreeText: N/A

      ClinVar: N/A

      CAID: N/A

      gnomAD: N/A

      VariantEvidence:N/A

      MutationType: rearrangement_region

      CivicName: rearrangement

      MultipleGeneVariants: N/A

    2. 5 nonsense mutations

      PatientID: 19

      KindredID: 63

      Case: Sex unknown, Age unknown, French

      DiseaseAssertion: VHL

      FamilyInfo: One other member belonging to family 63 was mentioned (Patient: 11). This patient was found to have a pancreatic endocrine tumour, without pheochromocytoma, or renal cell carcinoma.

      CasePresentingHPOs: HP:0030405; HP:0002666; HP:0005584 (pancreatic endocrine tumour, pheochromocytoma, renal cell carcinoma)

      CaseHPOFreeText: N/A

      CaseNotHPOs: N/A

      CaseNotHPOFreeText: N/A

      CasePreviousTesting: N/A

      PreviouslyPublished: N/A

      SupplementalData: N/A

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

      CaseProblemVariantFreeText: N/A

      LegacyVariant: N/A

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

      CAID: N/A

      gnomAD: N/A

      VariantEvidence: N/A

      MutationType: stop_gained

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

      MultipleGeneVariants: N/A

    1. PatientID: 151

      KindredID: 55

      Case: M, 28Y0M, Chinese

      DiseaseAssertion: VHL

      FamilyInfo: The proband (patient 150) has a father (patient 151) who was also confirmed with this germline mutation, and presented at 22 with a CNS hemangioblastoma and 28 with renal cell carcinoma. The proband presented with a CNS hemangioblastoma at 14 and multiple pancreatic cysts/tumors at 17. The proband also has a grandmother (patient 153) who presented with a CNS hemangioblastoma at 43, but who passed away before diagnosis/ genetic testing.

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

      CaseHPOFreeText: The proband's father presented with a CNS hemangioblastoma at 22 and renal cell carcinoma at 28.

      CaseNotHPOs: HP:0009711; HP:0002666; HP:0001737; HP:0001732 (Retinal capillary hemangioma, Pheochromocytoma, Pancreatic cysts, Abnormality of the pancreas)

      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.I151S (c.452T>G)

      LegacyVariant: N/A

      CaseProblemVariantFreeText: N/A

      ClinVarID: 223215, https://www.ncbi.nlm.nih.gov/clinvar/variation/223215/

      CAID: N/A

      gnomAD: N/A

      VariantEvidence: N/A

      MutationType: missense_variant;transversion

      CivicName: I151S (c.452T>G)

      MultipleGeneVariants: N/A

    2. PatientID: 43

      KindredID: 15

      Case: F , 21Y0M, Chinese

      DiseaseAssertion: VHL

      FamilyInfo: Proband (patient 42) has four family members confirmed with the mutation, and two family members who passed away before diagnosis/ genetic confirmation of the mutation. Family members confirmed with the mutation include: the proband's daughter (patient 43) who had retinal angioma (age 17), renal cell carcinoma (21), multiple pancreatic cysts/tumors (18), and a pheochromocytoma (19). His son (patient 44) who was asymptomatic at the time of assessment. His niece 1 (patient 47) who had a retinal angioma and renal cell carcinoma (22). And his niece 2 (patient 28) who had a CNS hemangioblastoma (19) and a retinal angioma (18). Family members who passed away before diagnosis and were not genetically confirmed include: his sister (oatient 45) who had a CNS hemangioblastoma (22), and his brother (patient 46) who had a retinal angioma and renal cell carcinoma at 52.

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

      CaseHPOFreeText: The proband's daughter (patient 43) presented with retinal angioma at 17, multiple pancreatic cysts/tumors at 18, pheochromocytoma at 19, and renal cell carcinoma at 21.

      CaseNotHPOs: HP:0010797 (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.S80Tfs*77 (c.239_245del)

      LegacyVariant: N/A

      CaseProblemVariantFreeText: N/A

      ClinVarID: N/A

      CAID: CA913189246; https://reg.clinicalgenome.org/redmine/projects/registry/genboree_registry/allele?hgvsOrDescriptor=NM_000551.3%3Ac.239_245del

      gnomAD: N/A

      VariantEvidence: N/A

      MutationType: minus_1_frameshift_variant

      CivicName: S80fs (c.239_245del)

      MultipleGeneVariants: N/A

    3. PatientID: 23

      KindredID: 7

      Case: M, 31Y0M, Chinese

      DiseaseAssertion: VHL

      FamilyInfo: The proband, patient 23, had a brother (patient 24) and father (patient 25) who were both genetically confirmed with the mutation. The brother presented with a CNS hemangioblastoma, renal cell carcinoma, and pancreatic cysts/tumors at age 32. The father presented with renal cell carcinoma and pancreatic cysts/tumors at age 58.

      CasePresentingHPOs: HP:0010797 (Hemangioblastoma)

      CaseHPOFreeText: The proband, patient 23, presented with a CNS hemangioblastoma at age 31.

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

      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.R69Afs*63 (c.204_205insG)

      LegacyVariant: N/A

      CaseProblemVariantFreeText: N/A

      ClinVarID: N/A

      CAID: CA913189244; https://reg.clinicalgenome.org/redmine/projects/registry/genboree_registry/allele?hgvsOrDescriptor=NM_000551.3%3Ac.204_205insG

      gnomAD: N/A

      VariantEvidence: N/A

      MutationType: plus_1_frameshift_variant

      CivicName: R69AFS*63 (c.204_205insG)

      MultipleGeneVariants: N/A

    4. A retrospective cohort study included all the VHL patients diagnosed at Peking University First Hospital (Beijing, China) prior to June 1 2016. A total of 291 patients from 115 different families were included for analysis. This familial mutation was confirmed in family #55, with two members genetically confirmed for the mutation. A male proband (patient 150) was diagnosed with a CNS hemangioblastoma at 14Y, and multiple pancreatic cysts/tumors at 17Y. His father (patient 151) was diagnosed with a CNS hemangioblastoma at 22Y and renal cell carcinoma at 28Y. His grandmother (patient 152) was diagnosed with CNS hemangioblastoma at 43Y, but passed away before diagnosis/ before genetic testing. This cohort was also published in a paper by Wang et al., 2018 (PMID: 29330336).

    5. A retrospective cohort study included all the VHL patients diagnosed at Peking University First Hospital (Beijing, China) prior to June 1 2016. A total of 291 patients from 115 different families were included for analysis. This mutation was confirmed in kindred 56. A male proband, patient 154, presented with a retinal angioma, renal cell carcinoma, and multiple pancreatic cysts/tumors at age 34. No family information was given. This kindred 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).

    6. PatientID: 59

      KindredID: 22

      Case: M, 14Y0M, Chinese

      DiseaseAssertion: VHL

      FamilyInfo: N/A

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

      CaseHPOFreeText: The proband presented with multiple pancreatic cysts/tumors at 14 and pheochromocytoma at 11.

      CaseNotHPOs: HP:0010797; HP:0009711; HP:0005584 (Hemangioblastoma, Retinal capillary hemangioma, Renal cell carcinoma)

      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.V87E (c.260T>A)

      LegacyVariant: N/A

      CaseProblemVariantFreeText: N/A

      ClinVarID: N/A

      CAID: CA351750651; https://reg.clinicalgenome.org/redmine/projects/registry/genboree_registry/allele?hgvsOrDescriptor=NM_000551.3%3Ac.260T%3EA

      gnomAD: N/A

      VariantEvidence: N/A

      MutationType: missense_variant;transition

      CivicName: V87E (c.260T>A)

      MultipleGeneVariants: N/A

    7. PatientID: 154

      KindredID: 57

      Case: M, 34Y0M, Chinese

      DiseaseAssertion: VHL

      FamilyInfo: N/A

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

      CaseHPOFreeText: The proband presented at age 34 with retinal angioma, multiple pancreatic cysts/tumors, and renal cell carcinoma.

      CaseNotHPOs: HP:0010797; HP:0002666 (Hemangioblastoma, Pheochromocytoma)

      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.V155Dfs*17 (c.464_468del)

      LegacyVariant: N/A

      CaseProblemVariantFreeText: N/A

      ClinVarID: N/A

      CAID: CA2499306942; https://reg.clinicalgenome.org/redmine/projects/registry/genboree_registry/by_caid?caid=CA2499306942

      gnomAD: N/A

      VariantEvidence: N/A

      MutationType: minus_2_frameshift_variant

      CivicName: V155fs (c.464_468delTGTAT)

      MultipleGeneVariants: N/A

    Tags

    Annotators

    URL

    1. Of 16 patients presenting with clinical VHL features that underwent genetic testing, one presented with the c.463G>A mutation of the VHL gene (stated as c.676G>A in the paper which used the Latif sequence as reference). Peripheral blood lymphocytes were collected and products of the polymerase chain reaction performed on this sample were analyzed with single-stranded conformational polymorphism analysis (SSCP), PCR sequencing and Southern analysis. This missense mutation was confirmed using restriction fragment length polymorphism or allele-specific oligonucleotide analysis. This patient has a family history of multiple tumor types indicative of VHL disease. The patient presented with retinal angiomata and hemangioblastoma(s).

    1. Genetic analysis showed that there were 13 families in the partial deletion group

      GroupID: None

      DiseaseAssertion: VHL

      GroupSize: 35

      GroupNumberMales: 23

      GroupNumberFemales: 12

      GroupEthnicity: Chinese

      GroupAgeRange: N/A

      GroupInfo: 13 families (35 patients total, 33 of which are alive) in the partial deletion group had a CNS hemangioblastoma (see table 1)

      GroupPresentingHPOs: HP:0010797 (Hemangioblastoma

      GroupHPOFreeText: N/A

      GroupNotHPOs: N/A

      GroupNotHPOFreeText: N/A

      GroupPreviousTesting: N/A

      PreviouslyPublished: 32432044 (Potential overlap, same authors)

      SupplementalData:  N/A

      Variant: Partial Deletion

      LegacyVariant: N/A

      CaseProblemVariantFreeText: N/A

      ClinVarID: N/A

      CAID: N/A

      gnomAD: N/A

      VariantEvidence: N/A

      MutationType: deletion

      CivicName: Null (Partial Deletion)

      MultipleGeneVariants: N/A

    1. II 0 1 No manifestations T c.464-?_642 + ?del

      PatientID: II

      KindredID: 19

      Case: Sex Unknown, 1Y0M, Danish

      DiseaseAssertion: Asymptomatic

      FamilyInfo: 3 other family members presented with this VHL variant. Patients 19-I and 19-III were asymptomatic. Patient 19-IV presented with 2 retinal hemangioblastomas (10Y and 12Y) and kidney disease (17Y).

      CasePresentingHPOs: N/A

      CaseHPOFreeText: Diagnosed with VHL at age 0Y. Age at the end of study: 1Y.

      CaseNotHPOs: N/A

      CaseNotHPOFreeText: N/A

      CasePreviousTesting: N/A

      PreviouslyPublished: N/A

      SupplementalData: N/A

      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

      CivicName: Null (c.464-?_642+?del)

      MultipleGeneVariants: N/A

    2. III 15 60 2 pheo (15 years) M c.496G > T (p.Val166Phe)

      PatientID: III

      KindredID: 15

      Case: Sex Unknown, 60Y0M, Danish

      DiseaseAssertion: VHL

      FamilyInfo: 2 other family members presented with the same VHL variant. Patient 15-II presented with 2 pheochromocytoma (8Y) 2 CNS hb (12Y and 13Y) and 2 retinal hemangioblastomas (8Y, 12Y). Patient 15-I was asymptomatic.

      CasePresentingHPOs: HP:0002666 (Pheochromocytoma)

      CaseHPOFreeText: Diagnosed with VHL at age 15Y. Presented with 2 pheochromocytoma (15Y). Age at the end of study: 60Y.

      CaseNotHPOs: N/A

      CaseNotHPOFreeText: N/A

      CasePreviousTesting: N/A

      PreviouslyPublished: N/A

      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. 13 I 13 Dead at age 48 years 8 retinal hb (13 + 16 + 17 + 18 years) 1 PC (17 years) 1 CNS hb (17 years) M c.194C > G (p.Ser65Trp)

      PatientID: I

      KindredID: 13

      Case: Sex Unknown, 48Y0M, Danish

      DiseaseAssertion: VHL

      FamilyInfo: N/A

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

      CaseHPOFreeText: The patient was diagnosed with VHL at age 13. The patient had 8 retinal hemangioblastomas at ages 13, 16,17,18. The patient had 1 pancreatic cyst at age 17 and one CNS hemangioblastoma at age 17. The patient died at age 48.

      CaseNotHPOs: N/A

      CaseNotHPOFreeText: N/A

      CasePreviousTesting: N/A

      PreviouslyPublished: 19863552, 25834951, 27966541, 27539272

      SupplementalData: N/A

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

      LegacyVariant: N/A

      CaseProblemVariantFreeText: N/A

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

      CAID: N/A

      gnomAD: N/A

      VariantEvidence: N/A

      MutationType: missense_variant;transversion

      CivicName:S65W(c.194C>G)

      MultipleGeneVariants: N/A

    1. 07MPARAMediastinum24noNoVHL: c.376G>A, p.Asp126Asn

      PatientID: 10

      KindredID: 10

      Case: M, 7Y0M, Ethnicity Unknown

      DiseaseAssertion: paraganglioma

      FamilyInfo: No details on family information provided.

      CasePresentingHPOs: HP:0002668 (paraganglioma)

      CaseHPOFreeText: Patient had mediastinum paraganglioma.

      CaseNotHPOs: N/A

      CaseNotHPOFreeText: N/A

      CasePreviousTesting: N/A

      PreviouslyPublished: N/A

      SupplementalData: N/A

      Variant: p.D126N (c.376G>A)

      LegacyVariant: N/A

      CaseProblemVariantFreeText: N/A

      ClinVarID: 141044, https://www.ncbi.nlm.nih.gov/clinvar/variation/141044/

      CAID: N/A

      gnomAD: 0.00001988, https://gnomad.broadinstitute.org/variant/3-10188233-G-A

      VariantEvidence: N/A

      MutationType: missense_variant; transition

      CivicName: D126N (c.376G>A)

      MultipleGeneVariants: N/A

    1. To achieve more comprehensive genome-level analysis in our pediatric oncology patients, we utilized three CLIA-certified, CAP (College of American Pathologists), and New York State Department of Health approved assays. When possible, we utilized a cancer whole exome sequencing test (cWES) comprising WES of tumor and normal tissue (buccal swab or peripheral blood) and RNA sequencing (RNA-seq) of tumor tissue. This assay was optimized for fresh or frozen specimens. When sample adequacy was a concern, we also utilized a directed cancer gene panel assay which sequenced 467 cancer-associated genes and was optimized for use with formalin fixed paraffin embedded (FFPE) material (Columbia Comprehensive Cancer Panel, CCCP). If a constitutionally encoded disease was suspected (e.g. familial hemophagocytic lymphohistiocytosis), we performed constitutional WES from the patient and both parents (trio) when available.
    1. VHL Variants

      This report studied the prevalence of germline variants in Japanese PPGL patients. Of the 370 PPGL original Japanese probands, this cohort consisted of 15 patients with pheochromocytoma and/or paragangliomas with germline VHL varaints. Blood samples were used to examine 7 genes: MAX, SDHB, SDHC, SDHD, TMEM127, VHL, and RET, using Sanger sequencing. Of these 15 VHL patients: 10 had bilateral PCC, 4 had PCC with abdominal/thoracic PGL, and one had metastatic PPGL. The variant R167Q (c.500G>A) was one of the 15 found in a patient with PPGL. Their family history or further manifestations were not detailed.

    1. Arg161Gln

      GroupID: 8

      DiseaseAssertion: Neuroendocrine neoplasm (pheochromocytoma or paraganglioma)

      GroupSize: 3

      GroupNumberMales: N/A

      GroupNumberFemales: N/A

      GroupEthnicity: Ethnicity unknown

      GroupAgeRange: N/A

      GroupInfo: This mutation (p.R161Q (c.482G>A)) was found in 3 patients, 1 with a family history and/or a syndromic presentation, and 2 patients with an apparently sporadic presentation.

      GroupPresentingHPOs: HP:0100634 (Neuroendocrine neoplasm)

      GroupHPOFreeText: Patients with a pheochromocytoma or a functional paraganglioma were recruited from several different French clinical centers participating in several clinical research networks (Cortico et Medullosurrènale: les Tumeurs Endocrines, Paragan-Glioma Network, Groupe des Tumeurs Endocrines)

      GroupNotHPOs: N/A

      GroupNotHPOFreeText: N/A

      GroupPreviousTesting: N/A

      PreviouslyPublished: N/A

      SupplementalData: N/A

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

      CaseProblemVariantFreeText: N/A

      LegacyVariant: 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. RNSH06 VHL VHL 0.79 

      PatientID: RNSH06

      KindredID: 1

      Case: Sex Unknown, 34Y0M, Ethnicity Unknown

      DiseaseAssertion: pheochromocytoma

      FamilyInfo: N/A

      CasePresentingHPOs: HP:0006748 (adrenal pheochromocytoma)

      CaseHPOFreeText: Presented with bilateral adrenal pheochromocytoma

      CaseNotHPOs: N/A

      CaseNotHPOFreeText: N/A

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

      PreviouslyPublished: N/A

      SupplementalData: Yes

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

      LegacyVariant: Given as ENSP00000256474.2 p.Arg161*

      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. Genomic DNA was extracted from peripheral blood using a QIAamp DNA Blood Mini Kit (QIAGEN, Hilden, Germany). Three coding exons and their flanking intronic regions were amplified by polymerase chain reaction (PCR) using previously described primers [5]. Direct sequencing was performed to screen missense and splicing mutations. Large exon deletions were screened using a multiplex ligation-dependent probe amplification kit (P016-C2; MRC Holland, Amsterdam, the Netherlands) and confirmed by real-time quantitative PCR with primers described by Ebenazer et al. [6]. The reaction conditions and primers used for amplification were as previously described [7].

      ArticleReferenceSequence: NM_000551.3

      GenotypingMethod: Direct sequencing performed to screen missense and splicing mutations. Large exon deletions were screened using a multiplex ligation-dependent probe amplification kit (P016-C2; MRC Holland, Amsterdam, the Netherlands) and confirmed by real-time quantitative PCR with primers previously described.

      SamplingMethod: peripheral blood

    1. 5330Y33Y49YNYYYc.499C>TExon 3p.Arg167TrpMissense

      PatientID: 5

      KindredID: 3

      Case: Sex Unknown, 49Y0M, Brazilian (Latino/Admixed American)

      DiseaseAssertion: VHL

      FamilyInfo: None

      CasePresentingHPOs: HP:0002668, HP:0002666; HP:0030405; HP:0005584; HP:0010797; HP:0001737; HP:0009711 (Paraganglioma, pheochromocytoma, pancreatic endocrine tumor, renal cell carcinoma, hemangioblastoma, pancreatic cyst, retinal capillary hemangioma)

      CaseHPOFreeText: The patient developed PPGL at 33Y of age, and a PNET at 49Y. They were also recorded with all of the above manifestations

      CaseNotHPOs: HP:0000107 (renal cyst)

      CaseNotHPOFreeText: N/A

      CasePreviousTesting: N/A

      PreviouslyPublished: N/A

      SupplementalData: N/A

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

      CaseProblemVariantFreeText: N/A

      LegacyVariant: N/A

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

      CAID: N/A

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

      VariantEvidence: N/A

      MutationType: missense_variant;transition

      CivicName: R167W (c.499C>T)

      MultipleGeneVariants: N/A

    1. 17 (22%) had frameshift variants

      PatientID: 45

      KindredID: 45

      Case: Sex Unknown, Age Unknown, Ethnicity Unknown

      DiseaseAssertion: VHL

      FamilyInfo: N/A

      CasePresentingHPOs: HP:0006770 (hemangioblastoma)

      CaseHPOFreeText: N/A

      CaseNotHPOs: HP:0010797; HP:0100634; HP:0030405; HP:0009711; HP:0030421 (clear cell renal cell carcinoma; Neuroendocrine neoplasm, pancreatic neuroendocrine neoplasm, retinal capillary hemangioma, Epididymal neoplasm)

      CaseNotHPOFreeText: N/A

      CasePreviousTesting: N/A

      PreviouslyPublished: N/A

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

      Variant: p.L140Qfs*3 (c.419_420delTC)

      LegacyVariant: N/A

      CaseProblemVariantFreeText: N/A

      ClinVarID: 223207 https://www.ncbi.nlm.nih.gov/clinvar/variation/223207/

      CAID: N/A

      gnomAD: N/A

      VariantEvidence: N/A

      MutationType: minus_2_frameshift_variant

      CivicName: L140fs*3 (c.419_420delTC)

      MultipleGeneVariants: N/A

    2. missense variants

      PatientID: 48

      KindredID: 48

      Case: Sex Unknown, Age Unknown, Ethnicity Unknown

      DiseaseAssertion: VHL

      FamilyInfo: N/A

      CasePresentingHPOs: HP:0100634 (neuroendocrine neoplasm)

      CaseHPOFreeText: N/A

      CaseNotHPOs: HP:0010797; HP:0006770; HP:0030405; HP:0009711; HP:0030421 (hemangioblastoma; clear cell renal cell carcinoma, pancreatic neuroendocrine neoplasm, retinal capillary hemangioma, Epididymal neoplasm)

      CaseNotHPOFreeText: N/A

      CasePreviousTesting: N/A

      PreviouslyPublished: N/A

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

      Variant: p.S65A (c.193T>G)

      LegacyVariant: N/A

      CaseProblemVariantFreeText: N/A

      ClinVarID: 223160 https://www.ncbi.nlm.nih.gov/clinvar/variation/223160

      CAID: N/A

      gnomAD: N/A

      VariantEvidence: N/A

      MutationType: missense_variant; transversion

      CivicName: S65A (c.193T>G)

      MultipleGeneVariants: N/A

    1. (c. 340 + 1G > A)

      The male proband, age 29, underwent surgery for cervical hemangioblastoma (C2-C3) 2 years prior. He was genetically confirmed for Type 1 VHL syndrome although the method for genetic sequencing and analysis is not specified. Noncontrast CT of the abdomen revealed a lesion in the left adrenal gland, later confirmed by immunohistochemistry to be an adrenocortical adenoma. In bilateral kidneys, there were multiple lesions (morphological features were compatible with the clear cell type of RCC) along with nonenhancing cystic areas (renal cysts). Pancreas also showed multiple cysts. The patient underwent genetic analysis revealing a heterozygous 5' VHL splice site variation of exon 1 (c.340+1G>A). The author does not provide family genetic data. The proband’s sister presented Type 1 VHL features such as cerebral hemangiomas, RCC on the left kidney, bilateral renal cysts and pancreatic serous neoplasm. All other members of the family do not present VHL features.

    1. 570 C>G 119 Phe>Leu Missense 

      PatientID: 1695

      KindredID: 1695

      Case: Sex Unknown, 38Y0M, Ethnicity Unknown

      DiseaseAssertion: VHL

      FamilyInfo: N/A

      CohortInfo: 44 patients with renal cell carcinoma who had known industrial exposure to trichloroethylene (TRI).

      CasePresentingHPOs: HP:0005584 (Renal cell carcinoma)

      CaseHPOFreeText: The patient had TRI exposure at age 27 and was diagnosed with renal cell carcinoma at age 38.

      CaseNotHPOs: N/A

      CaseNotHPOFreeText: N/A

      CasePreviousTesting: N/A

      PreviouslyPublished: N/A

      SupplementalData: N/A

      Variant: p.F119L(c.357C>G)

      LegacyVariant: p.F119L(c.570C>G)

      CaseProblemVariantFreeText: N/A

      ClinVarID: 625240 https://www.ncbi.nlm.nih.gov/clinvar/variation/625240/?new_evidence=false

      CAID: N/A

      gnomAD: N/A

      VariantEvidence: The patient had LOH.

      MutationType: missense_variant;transversion

      CivicName: C162Y(c.486C>G) and L188V(c.562C>G) and P81S(c.241C>T) and F119L(c.357C>G)

      MultipleGeneVariants: Germline, VHL, c.241C>T (p.Pro81Ser), Somatic, VHL, c.486C>G (Cys162Trp) Somatic, VHL, c.562C>G (Leu188Val)

    1. GroupID: 183

      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. Likely previously published in PMID 32179488 (Kindred 14) but correspondence to a patient in this group is not confirmed.

      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: Stated as being previously reported in PMID 7728151 (2 families reported with this mutation) and/or 8956040 (7 families reported with this mutation). Likel

      SupplementalData: N/A

      Variant: p.F76del (c.227_229del)

      LegacyVariant: c.439_441delTTC

      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: NM_000551.3:c.226_228delTTC automaps to NM_000551.3:c.227_229delTCT due to redundancy

      MutationType: deletion; inframe_deletion

      CivicName: F76del (c.227_229del)

      MultipleGeneVariants: N/A

    2. GroupID: 76

      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.R107P (c.320G>C)

      LegacyVariant: c.533G>C

      CaseProblemVariantFreeText: N/A

      ClinVarID: 36900, https://www.ncbi.nlm.nih.gov/clinvar/variation/36900/

      CAID: N/A

      gnomAD: N/A

      VariantEvidence: N/A

      MutationType: missense_variant;transversion

      CivicName: R107P (c.320G>C)

      MultipleGeneVariants: N/A

    3. GroupID: 102

      DiseaseAssertion: VHL

      GroupSize: N/A

      GroupNumberMales: N/A

      GroupNumberFemales: N/A

      GroupEthnicity: N/A

      GroupAgeRange: N/A

      GroupInfo: VHL family found to have the c.712C>T (R167W) germline variant of the VHL gene. The number of family members included in this study is not specified.

      GroupPresentingHPOs: HP:0002666 (Pheochromocytoma)

      GroupHPOFreeText: Number of family affected members is not specified.

      GroupNotHPOs: N/A

      GroupNotHPOFreeText: N/A

      GroupPreviousTesting: 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: N/A

      MutationType: missense_variant;transition

      CivicName: R167W (c.499C>T)

      MultipleGeneVariants: N/A

    4. 93 families examined at the Clinical Center of the National Institutes of Health (Bethesda, MD) underwent genetic testing for germline mutations of the VHL gene. Whole blood was extracted and genomic DNA was amplified by PCR and products were sequences using a cycle sequencing kit with dye-labeled terminators and automatically sequenced. This mutation was found in VHL type 1 family (lineage 11). The variant was reported as c.488_490del18bp (AF010238.1) and was mapped to G93_Y98del (c.277_294del/c.275_292del) (NM_000551.3).

    1. VHL-12c.326delTp.Ile109 fsStop at codon 158this studyyesA1Multiple+––+–

      PatientID: VHL-12

      KindredID: 12

      Case: Sex Unknown, Age Unknown, Italian

      DiseaseAssertion: VHL

      FamilyInfo: Family history of VHL. No further details provided.

      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:0005584; HP:0010797; HP:0009711 (Renal cell carcinoma, Hemangioblastoma, Retinal capillary hemangioma)

      CaseHPOFreeText: Multiple CNS hemangioblastomas. Clinical classification: A1.

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

      CaseNotHPOFreeText: N/A

      CasePreviousTesting: N/A

      PreviouslyPublished: N/A

      SupplementalData: N/A

      Variant: p.I109Tfs*50 (c.326del)

      LegacyVariant: N/A

      CaseProblemVariantFreeText: N/A

      ClinVarID: N/A

      CAID: CA658820709, https://reg.clinicalgenome.org/redmine/projects/registry/genboree_registry/allele?hgvsOrDescriptor=NM_000551.3%3Ac.326del

      gnomAD: N/A

      VariantEvidence: N/A

      MutationType: minus_1_frameshift_variant; deletion

      CivicName: I109TfsX50 (c.326del)

      MultipleGeneVariants: N/A

    1. Case 3The 16-year-old presented with no audiovestibular symptoms. Peripheral hearing assessment and screening MRI of brain/spine were normal. Vestibular assessment highlighted covert saccades in the left posterior semicircular canal on vHIT with normal gain. SHIMP showed significant asymmetry (38%) with a weaker right side (Figure 4).

      PatientID: N/A (Case 3)

      KindredID: 1

      Case: Sex Unknown, 16Y0M, Ethnicity Unknown

      DiseaseAssertion: VHL

      FamilyInfo: Patient’s two younger 9Y0M twin siblings possessed the same VHL variant and had abnormal vestibular assessments.

      CasePresentingHPOs: HP:0001756 (Vestibular hypofunction)

      CaseHPOFreeText: Following a genetic VHL diagnosis, patient presented with no audiovestibular symptoms. Vestibular assessment highlighted covert saccades in the left posterior semicircular canal on vHIT. Patient also showed signidicant assymmetry with weakness on the right side.

      CaseNotHPOs: HP:0009713; HP:0006880 (spinal hemangioblastoma; cerebellar hemangioblastoma)

      CaseNotHPOFreeText: peripheral hearing assessment and screening MRI of brain/spine were normal.

      CasePreviousTesting: N/A

      PreviouslyPublished: N/A

      SupplementalData: N/A

      Variant: Exon 1-3 Deletion

      LegacyVariant: N/A

      CaseProblemVariantFreeText: N/A

      ClinVarID: N/A

      CAID: N/A

      gnomAD: N/A

      VariantEvidence: N/A

      MutationType: deletion

      CivicName: Exon 1-3 Deletion

      MultipleGeneVariants: N/A

    1. p.Val170Gly

      17 patients with genetic variants in SDHB, VHL, EPAS1, or RET with pheochromocytoma were identified retroactively for this study. 5 pathogenic germline variants were confirmed in patients with clinical criteria of von Hippel Lindau syndrome. Next generation sequencing (NGS) re-confirmed these germline mutations. One of which was a p.V170G (c.509T>G) mutation in patient 5, an 11Y male with pheochromocytoma. No further manifestation details were provided, nor was family information.

    1. 6 F c.464−?_642 +? Bilateral Positive (CNS, retinal) Positive 

      PatientID: 6

      KindredID: 6

      Case: F, Age Unknown, Ethnicity Unknown

      DiseaseAssertion: VHL

      FamilyInfo: N/A

      CasePresentingHPOs: HP:0000107; HP:0005584; HP:0010797; HP:0001737; HP:0009711 (Renal cyst, Renal cell carcinoma, Hemangioblastoma, Pancreatic cysts, Retinal capillary hemangioma)

      CaseHPOFreeText: Bilateral RCC add renal cysts, CNS hemangioblastoma, positive for pancreatic cysts, retinal hemangioblastoma.

      CaseNotHPOs: N/A

      CaseNotHPOFreeText: N/A

      CasePreviousTesting: N/A

      PreviouslyPublished: N/A

      SupplementalData: Table 1

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

      LegacyVariant: N/A

      CaseProblemVariantFreeText: N/A

      ClinVarID: N/A

      CAID: N/A

      gnomAD: N/A

      VariantEvidence: The variant was noted as “c.464-?_642+?” by the authors; this was assumed to be a deletion. This study found coexpression of Epo and EpoR in 11 RCCs and in 10 benign renal cysts in a spectrum of VHL renal disease suggesting that Epo/EpoR coexpression is present in both benign and malignant stages of renal neoplasia. Six benign cysts stained for Epo but not EpoR. The researchers detected loss of heterozygosity of a wild-type VHL allele in different RCCs with microsatellite markers, D3S1110 and D3S2452, flanking the VHL gene

      MutationType: exon_loss_variant

      CivicName: Exon 3 Deletion

      MultipleGeneVariants: N/A

    2. Immunohistochemistry. Immunohistochemistry was done on formalin-fixed, paraffin-embedded tissue sections of RCC, renal cysts, and adjacent normal kidneys. Tissue sections were first soaked in xylene and then washed in decreasing concentrations of ethanol. For antigen retrieval, sections were treated with DAKO target retrieval solution and incubated at95°C for 20 to 30 minutes. Sections were cooled at room temperature, washed thrice in PBS, and then quenched for 20 minutes in a solution of 3 mL H2O2 and 180 mL methanol. After three washes in PBS, sections were drenched in 10% horse serum for 1hour. The primary antibody was diluted in 2% horse serum, and the sections were incubated in a humidified chamber at 4°C overnight. Primary antibodies used were rabbit polyclonal anti-human Epo (1:100) and sheep polyclonal anti-human EpoR (1:200). Sections were then incubated with secondary antibody and avidin-biotin complex for one hour each. 3,3′-Diaminobenzidine was used for visualization, followed by counterstaining with hematoxylin. The sections were dehydrated with graded ethanol washes and xylene wash and mounted. The presence and intensity of antibody expression were examined in RCC, renal cysts, and normal kidney. Microdissection and DNA Analysis. Formalin-fixed, paraffin-embedded tissue from 11 RCCs, and normal kidney in eight patients was used for loss of heterozygosity analysis. Unstained 5-μm tumor tissue sections on glass slides were deparaffinized with xylene, rinsed in 100% to 80% ethanol, briefly stained with H&E, and rinsed in 10% glycerol in Tris-EDTA buffer. Microdissection was done under direct light microscopic visualization using a 30-gauge needle. Control samples were obtained from the matched normal kidney tissue on the same histologic slide. Procured cells were immediately resuspended in 30 μL buffer containing Tris-EDTA-HCl (pH8.0), 10 mmol/L EDTA (pH 8.0), 1% Tween 20, and 0.1mg/mL proteinase K and were incubated at 37°C overnight. The mixture was boiled for 15 minutes to inactivate proteinase K and 2 μL of the DNA solution were used for PCR amplification using markers D3S2452 and D3S1110 (Research Genetics, Huntsville, AL) flanking the VHL gene. 32P-labeled amplified DNA was mixed with an equal volume of formamide loading dye (95% formamide, 20 mmol/L EDTA, 0.05% bromphenol blue, and 0.05% xylene cyanol). Samples were then denatured for 5 minutes at 95°, loaded onto a 6% acrylamide gel, electrophoresed at 1,800 V for 90 minutes, and transferred to Whatman paper for autoradiography. Total RNA Isolation and Epo/EpoR Reverse Transcription–PCR. Frozen RCC and normal kidney tissue from three patients with VHL were sectioned at 10 μm and microdissected under a light microscope to procure tumor and normal cells. Total RNA was extracted using TRIZOL reagent (InvitrogenCarlsbad, CA) according to manufacturer's instructions. During the RNA precipitation step nucleic acid carrier (Novagen, San Diego, CA) was added. A first-strand cDNA from total RNA was synthesized as follows. To avoid amplification of possible contaminating genome DNA, total RNA was treated with RNase-free DNase I (0.2 unit, total volume 10 μL, Invitrogen) at room temperature for 15 minutes, denatured at 65°C for 10 minutes, and subsequently reverse transcribed by SuperScript II (Invitrogen) with 0.5 μg of oligodeoxythymidylic acid primer in a volume of20 μL. The PCR amplification was done following cycling parameters: initial denaturing for 1 minute at 95°C, 15 seconds at 95°C, and 30 seconds at 68°C for 35 cycles. Reaction mixture contained 4 μL of the cDNA template, 1.0 unit of Advantage-2 DNA polymerase (Clontech, San Jose, CA), 1×PCR buffer, 200 μmol/L of each dNTP, and 200 nmol/L of each primer. The sequences of oligonucleotides used for reverse transcription–PCR were as follows: for Epo, 5′-TCTATGCCTGGAAGAGGATGGAGGTCG-3′; for EpoR, 5′-CACAAGGGTAACTTCCAGCTGTGGCTGTA-3′ and 5′-CATTTGTCCAGCACCAGATAGGTATCCTGG-3′. The PCR products were separated in 2.0% agarose gel and stained with ethidium bromide. Western Blot Analysis. Frozen RCC tissue from three patients with VHL was used for Western blot analysis for Epo and EpoR. One frozen hemangioblastoma from a patient with VHL was used as a positive control for Western blot analysis for both Epo and EpoR. For Western blotting, 20 μL of cell lysate were separated by electrophoresis on 4% to 12% gradient Bis-Tris gels (Invitrogen). Proteins were electrotransferred onto polyvinylidene difluoride membrane (Novex, San Diego, CA). Blots were blocked in PBS/0.05% Tween 20 containing 5% fetal bovine serum and incubated with anti-Epo (1:100, Oncogene, Cambridge, MA) and anti-EpoR (1:100, Calbiochem, San Diego, CA) antibodies, respectively. Antibody binding was detected with horseradish peroxidase–conjugated secondary antibodies (Amersham Biosciences UK Ltd., Little Chalfont, United Kingdom). Enhanced chemiluminescence reagent (Pierce, Rockford, IL) was used for visualization. RESULTS Immunohistochemistry analysis of clear cell epithelium in VHL-associated RCC showed coexpression of Epo and EpoR in the cytoplasm of all 11 tumors Figs. 1 and 2. Coexpression of Epo and EpoR was also detected in cells of 10 of 16 renal cysts (Figs. 1D and 2D). Six renal cysts stained positively for Epo but not for EpoR. Fig. 1View largeDownload slidePositive cytoplasmic immunohistochemistry staining for Epo is detected in cells of solid RCC (A), cystic RCC (B), microscopic RCC arising in a cyst, (C), and benign cyst (D).Fig. 1View largeDownload slidePositive cytoplasmic immunohistochemistry staining for Epo is detected in cells of solid RCC (A), cystic RCC (B), microscopic RCC arising in a cyst, (C), and benign cyst (D). Fig. 2View largeDownload slidePositive cytoplasmic immunohistochemistry staining for EpoR is detected in cells of solid RCC (A), cystic RCC (B), microscopic RCC arising in a cyst, (C) and benign complex cyst (D).Fig. 2View largeDownload slidePositive cytoplasmic immunohistochemistry staining for EpoR is detected in cells of solid RCC (A), cystic RCC (B), microscopic RCC arising in a cyst, (C) and benign complex cyst (D). All patients had known germ line VHL mutations. In addition, we detected loss of heterozygosity of a wild-type VHL allele in different RCCs with microsatellite markers, D3S1110 and D3S2452, flanking the VHL gene (Fig. 3A). Fig. 3View largeDownload slideA, representative four VHL-associated RCCs (T1-4) show marked allelic imbalance (loss of heterozygosity) after amplification with VHL gene flanking primers D3S1110 and D3S2452. Matched adjacent normal kidney (N1-4) shows preservation of both alleles of the VHL gene. B, expression of Epo and EpoR mRNA in VHL-associated RCC abnormal kidney by reverse transcription–PCR. Lane 1, molecular weight marker; lane 2, normal VHL kidney; lane 3, VHL-associated RCC. Epo mRNA is expressed in RCC. Normal kidney shows low intensity of Epo mRNA expression. EpoR mRNA is expressed in VHL-associated RCC but not in normal kidney. C, Western blot analysis for Epo and EpoR expression in VHL-associated RCC. Epo and Epo-R proteins are expressed in three VHL-associated RCCs (lanes 1-3) and in VHL-associated hemangioblastoma (lane 4) used as positive control. Adrenal gland tissue is used as negative control (lane 5).Fig. 3View largeDownload slideA, representative four VHL-associated RCCs (T1-4) show marked allelic imbalance (loss of heterozygosity) after amplification with VHL gene flanking primers D3S1110 and D3S2452. Matched adjacent normal kidney (N1-4) shows preservation of both alleles of the VHL gene. B, expression of Epo and EpoR mRNA in VHL-associated RCC abnormal kidney by reverse transcription–PCR. Lane 1, molecular weight marker; lane 2, normal VHL kidney; lane 3, VHL-associated RCC. Epo mRNA is expressed in RCC. Normal kidney shows low intensity of Epo mRNA expression. EpoR mRNA is expressed in VHL-associated RCC but not in normal kidney. C, Western blot analysis for Epo and EpoR expression in VHL-associated RCC. Epo and Epo-R proteins are expressed in three VHL-associated RCCs (lanes 1-3) and in VHL-associated hemangioblastoma (lane 4) used as positive control. Adrenal gland tissue is used as negative control (lane 5). Reverse transcription–PCR consistently revealed the presence of Epo mRNA in VHL-associated RCC (Fig. 3B). In normal VHL kidney, Epo mRNA was expressed in low levels. EpoR mRNA was consistently detected by reverse transcription–PCR analysis in RCC but not in normal kidney of patients with VHL (Fig. 3B). Coexpression of Epo and EpoR in VHL renal tumors was further confirmed by demonstrating both Epo and EpoR protein expression in VHL-associated RCC using Western blot analysis (Fig. 3C). VHL-associated hemangioblastoma was used as positive control and showed coexpression of both Epo and EpoR.

      ArticleReferenceSequence: Genbank submission (NM_000551) and Ensemble Genome Browser (www.ensembl.org).

      GenotypingMethod: All germline mutations were previously found. Tumor samples: Total RNA was extracted using TRIZOL reagent, reverse transcription–PCR, frozen tumor tissues were used for Western blot analysis for Epo and EpoR.

      SamplingMethod: tissue resection

    1. 1228Fnt 694 C to T, Arg to stop, exon 3

      PatientID: 12

      KindredID: 6004

      Case: F, 28Y0M, Ethnicity Unknown

      DiseaseAssertion: VHL

      FamilyInfo: N/A

      CasePresentingHPOs: HP:0030405 (pancreatic endocrine tumour)

      CaseHPOFreeText: She presented with one pathologic pancreatic endocrine tumour.

      CaseNotHPOs: N/A

      CaseNotHPOFreeText: N/A

      CasePreviousTesting: N/A

      PreviouslyPublished: N/A

      SupplementalData: N/A

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

      LegacyVariant: p.R161* (c.694C>T)

      CaseProblemVariantFreeText: N/A

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

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

      gnomAD: N/A

      VariantEvidence: N/A

      MutationType: stop_gained

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

      MultipleGeneVariants: N/A

    1. A previous study of 26 Japanese, VHL families was extended to 41 additional families. Germline mutations were detected in 55 of 77 Japanese families using SSCP, direct sequencing, and Southern Blot analysis of peripheral blood samples. The N78H (c.232A>C) germline mutation was found in a VHL type 1 patient with hemangioblastomas of the central nervous system and retinal angioma (family ID 1). This individual was previously reported in PMID 8634692.

    2. A previous study of 26 Japanese, VHL families was extended to 41 additional families. Germline mutations were detected in 55 of 77 Japanese families using SSCP, direct sequencing, and Southern Blot analysis of peripheral blood samples. The C77Sfs*82 (c.230del) germline mutation was found in a VHL type 1 patient with hemangioblastomas of the central nervous system and renal cell carcinoma (family ID 16). This individual was previously reported in PMID 8634692.

    3. A previous study of 26 Japanese, VHL families was extended to 41 additional families. Germline mutations were detected in 55 of 77 Japanese families using SSCP, direct sequencing, and Southern Blot analysis of peripheral blood samples. The N131S (c.392A>G) missense mutation was found in 1 VHL type 2 family with both family members having retinal angiomas and pheochromocytomas (family ID 87). 1/2 individuals had hemangioblastomas of the central nervous system and 1/2 had pancreatic cysts or tumor (unspecified).

    1. c712C→T, R167W

      PatientID: None

      KindredID: 4

      Case: Sex Unknown, Age Unknown, Ethnicity Unknown

      DiseaseAssertion: pheochromocytoma

      FamilyInfo: None - isolated bilateral pheochromocytoma

      CasePresentingHPOs: HP:0002666 (pheochromocytoma)

      CaseHPOFreeText: N/A

      CaseNotHPOs: N/A

      CaseNotHPOFreeText: N/A

      CasePreviousTesting: RET

      PreviouslyPublished: N/A

      SupplementalData: N/A

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

      LegacyVariant: p.R167W (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: N/A

      MutationType: missense_variant;transition

      CivicName: R167W (c.499C>T)

      MultipleGeneVariants: N/A

    1. Approximately 1 year after IV:6 was diagnosed with VHL, her father (III:4) developed hematuria. Evaluation and subsequent treatment confirmed disease consistent with VHL, including clear-cell renal-cell carcinoma, renal cysts, pancreatic cysts, and multiple hemangioblastomas of the cerebellum and lower brainstem (fig. 2D). Southern blot analysis and DNA sequencing of the VHL gene in the father's PBLs were negative (fig. 4A) by the initial genetic testing

      PatientID: III-4

      KindredID: 2

      Case: F, 48Y0M, Ethnicity Unknown

      DiseaseAssertion: VHL

      FamilyInfo: The patient’s 23Y daughter was diagnosed with VHL disease and spinal cord hemangioblastomas at 15Y. At 20Y, she had multiple cystic lesions in the right kidney, a solid lesion of the left kidney, multiple pancreatic cysts, and a small peripheral retinal angioma. She was also found to carry the same NM_000551.3:c.227_229del mutation the patient carried. The patient’s daughter’s mother was unaffected. Of the patient’s three other daughters and two brothers, one underwent clinical examination and two underwent genetic testing of unclear nature, and were found to be unaffected. The remaining two children of the patient were not evaluated.

      CasePresentingHPOs: HP:0006880; HP:0001737; HP:0000107; HP:0006770 (Cerebellar hemangioblastoma, pancreatic cyst, renal cyst, clear cell renal cell carcinoma)

      CaseHPOFreeText: The age 48Y patient originally presented with hematuria at age 39Y, and further investigation found clear-cell renal-cell carcinoma, renal cysts, pancreatic cysts, and multiple hemangioblastomas of the cerebellum and lower brainstem. Initial southern blot analysis and DNA sequencing of the VHL gene in the patient’s peripheral blood lymphocytes were negative; however, application of additional methods directed specifically at the region of the mutation found in the patient’s daughter (IV-6) discovered that approximately one-seventh of the patient’s peripheral blood lymphocytes carried the same VHL mutation the patient’s daughter carried, suggesting mosaic VHL disease.

      CaseNotHPOs: N/A

      CaseNotHPOFreeText: N/A

      CasePreviousTesting: N/A

      PreviouslyPublished: N/A

      SupplementalData: N/A

      Variant: p.F76del(c.226_228delTTC)

      LegacyVariant: p.F76del(c.439_441delTTC)

      ClinVarID: N/A

      CAID: CA357012

      gnomAD: N/A

      VariantEvidence: Southern blot analysis and DNA sequencing of the VHL gene in the father's PBLs were negative (fig. 4A) by the initial genetic testing, on the basis of standard methods that identified VHL mutations in 99 of 99 (Stolle et al. 1998) and in a subsequent total of 131 of 131 (Glenn et al. 1999) affected individuals. However, genetic testing of the daughter's (IV:6) PBLs by direct sequencing revealed a 3-bp deletion (TTC) at nucleotides 439–441 (fig. 4B). After identification of the mutation in IV:6, the father's DNA was again analyzed, by application of additional methods directed specifically at the region of the 3-bp deletion

      MutationType: inframe_deletion

      CivicName: F76del(c.226_228delTTC)

      MultipleGeneVariants: N/A

    1. PatientID: 53 (Cousin)

      KindredID: 18

      Case: F, 57Y0M, Ethnicity Unknown

      DiseaseAssertion: Assumed VHL

      FamilyInfo: 11 members of this family tested positive for the c.712C>T/c.499C>T germline variant of the VHL gene. 14 members of this family were assumed to carry this variant due to family history/personal medical history. Members of this family range from asymptomatic to multi-organ involvement (pheochromocytoma, pancreatic and renal cysts/tumors and hemangioblastomas). The family was previously reported in PMID 3942913.

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

      CaseHPOFreeText: This patient presented with CNS hemangioblastoma (23Y) and retinal angioma (14Y).

      CaseNotHPOs: HP:0005584; HP:0000077; HP:0001732; HP:0002666 (Renal cell carcinoma, Abnormality of the kidney, Abnormality of the pancreas, Pheochromocytoma)

      CaseNotHPOFreeText: N/A

      CasePreviousTesting: N/A

      PreviouslyPublished: 3942913 (some members of this family are previously reported (phenotypes only) but unable to match patients across papers with confidence)

      SupplementalData: Supplementary Table 1.

      Variant: N/A

      LegacyVariant: N/A

      CaseProblemVariantFreeText: N/A

      ClinVarID: N/A

      CAID: N/A

      gnomAD: N/A

      VariantEvidence: Authors state that the c.712C>T germline familial variant of the VHL gene in this patient is “inferred from the family”. No genetic testing was done on this patient to confirm this. Being that this familial variant is out of bound with respect to the NM_000551.3 reference sequence, it was concluded that this variant is noted in the Latif et al. (1993) reference and was translated to c.499C>T (NM_000551.3).

      MutationType: N/A

      CivicName: N/A

      MultipleGeneVariants: N/A

    2. PatientID: 1 (Proband)

      KindredID: 13

      Case: F, 15Y0M, Ethnicity Unknown

      DiseaseAssertion: Asymptomatic

      FamilyInfo: 5 members of this family were found to harbour the deletion of one VHL allele. The sister (ID 2) and uncle (ID 5) were all asymptomatic. The father (ID 3) presented with CNS hemangioblastoma (34Y). The Grandmother (ID 9) presented with CNS hemangioblastoma (57Y).

      CasePresentingHPOs: N/A

      CaseHPOFreeText: N/A

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

      CaseNotHPOFreeText: N/A

      CasePreviousTesting: N/A

      PreviouslyPublished: N/A

      SupplementalData: Supplementary Table 1.

      Variant: Complete Deletion

      LegacyVariant: N/A

      CaseProblemVariantFreeText: N/A

      ClinVarID: N/A

      CAID: N/A

      gnomAD: N/A

      VariantEvidence: Reported as “del one vHL allele”.

      MutationType: deletion

      CivicName: Null (del one VHL allele)

      MultipleGeneVariants: N/A

    1. PatientID: None (Twin)

      KindredID: A-V6

      Case: Sex Unknown, 30Y0M, Korean

      DiseaseAssertion: VHL

      FamilyInfo: 2 affected individuals (twin brothers) in this family.

      CasePresentingHPOs: HP:0002666 (Pheochromocytoma)

      CaseHPOFreeText: Bilateral pheochromocytoma. Died of VHL.

      CaseNotHPOs: N/A

      CaseNotHPOFreeText: N/A

      CasePreviousTesting: N/A

      PreviouslyPublished: 25078357

      SupplementalData: N/A

      Variant: N/A

      LegacyVariant: N/A

      CaseProblemVariantFreeText: N/A

      ClinVarID: N/A

      CAID: N/A

      gnomAD: N/A

      VariantEvidence: Family and medical history make it likely that this patient had the p.R167W (c.499C>T) germline variant of VHL (as did this patient's twin brother) but this was not genetically confirmed. The variant is reported in Table 1 as c.499G>T which was assumed to be a typo and was corrected to c.499C>T.

      MutationType: N/A

      CivicName: N/A

      MultipleGeneVariants: N/A

    1. 500G→A Ts Exon 3 167 CGG R R167Q

      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, the missense mutation (c.500G>A (p.Arg167Gln)) was found in 10 patients total - 3 of which are stated to have retinal HBs and 7 are said to not. Other manifestations are possible but not clear. This is possibly previously published in PMID: 15300849

    1. Through PCR purification and Sanger sequencing of peripheral blood (using an alcohol precipitation method), 121 consecutive, unrelated, index PCC/PGL patients underwent genetic testing for five PCC/PGL susceptibility genes (RET, VHL, SDHB, SDHD and SDHC), and were evaluated for clinical diagnosis of neurofibromatosis type1. Two unrelated probands were genetically confirmed with a non-familial mutation at c.500G>A of the VHL gene. The first was a female who presented with sympathic paraganglioma at 11Y and bilateral pheochromocytoma at 22Y. The second was a 13 year old female who presented with bilateral pheochromocytoma. Family histories are unknown.

    1. A 26-year-old male with history of hemicranial intermittent severe headache with vomiting, sweating, and palpitations since 6 years. Patient also had intermittent abdominal pain with no focal neurological deficits or seizures. He consulted a neurosurgeon for these complaints and MRI brain was done that showed cerebellar hemangioblastoma. Patient underwent surgery for same. Patient was lost to follow up after the surgery and then after 4 years consulted our institute for persistence of similar complaints. Patient was evaluated keeping syndromic association in mind because of strong family history of cerebellar hemangioblastoma.On examination patient was found to be hypertensive with postural fall. On hormonal evaluation he was found to have high levels of 24 h urinary normetanephrines. CECT abdomen [Figure 2a] showed enlarged right adrenal gland heterogeneous (red), pancreatic head solid mass situated posteriorly (blue), and cyst in pancreatic tail (green). In order to rule out other NET and tumor in contralateral adrenal functional imaging was done. FDG PET scan showed avid uptake in right adrenal and pancreatic head. Hence, a clinical diagnosis of Vhl was made. With adequate alpha blockade patient was planned for right adrenalectomy and pancreatic surgery. Open transperitoneal anterior adrenalectomy with IOUSG and bidigital palpation of pancreas—tumor located posteriorly, close to main pancreatic duct as enucleation not possible hence decision was taken for pancreaticoduodenectomy [Figure 2b]. Postoperative course was uneventful. Postoperative urinary normetanephrines were normal on 10th day. Histopathology showed right adrenal PCC and pancreatic NET with uncertain malignant potential. Mutation analysis revealed positive mutation in exon 3 of VHL gene at 167th position of amino acid Arg (arginine) is replaced by Gln (glutamine) happens due to CGG-CAG a single nucleotide change.

      PatientID: 4

      KindredID: 4

      Case: M, 30Y0M, Ethnicity Unknown

      DiseaseAssertion: VHL

      FamilyInfo: Strong family history of cerebellar hemangioblastoma.

      CasePresentingHPOs: HP:0006880, HP:0030405, HP:0002666, HP:0001737 (cerebellar hemangioblastoma, pancreatic endocrine tumour, pheochromocytoma, pancreatic cysts)

      CaseHPOFreeText: At age 26 was diagnosed with cerebellar hemangioblastoma. Four years later, he was found to have pancreatic endocrine tumour, pheochromocytoma, and pancreatic cysts.

      CaseNotHPOs: HP:0005584 (Renal cell carcinoma)

      CaseNotHPOFreeText: N/A

      CasePreviousTesting: N/A

      PreviouslyPublished: N/A

      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. probands

      PatientID: 2

      KindredID: 2

      Case: Sex Unknown, 33Y0M, Chinese

      DiseaseAssertion: VHL

      FamilyInfo: Patient had no family history of VHL disease. Although, patient’s daughter possesses the same mutation.

      CohortInfo: 16 Chinese patients clinically diagnosed with VHL disease.

      CasePresentingHPOs: HP:0009711; HP:0005584; HP:0001732; HP:0002666 (retinal capillary hemangioma; renal cell carcinoma; abnormality of the pancreas; pheochromocytoma)

      CaseHPOFreeText: The patient presented with retinal capillary hemangioma at age 12, as well as renal cell carcinoma, abnormality of the pancreas, and pheochromocytoma at age 33.

      CaseNotHPOs: HP:0030424, HP:0030393, HP:0010797 (epididymal cyst, endolymphatic sac tumor, hemangioblastoma)

      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

    2. two large deletions

      PatientID: N/A

      KindredID: 13

      Case: F, 32Y0M, Chinese

      DiseaseAssertion: VHL

      FamilyInfo: Patient had family history of VHL disease. The patient's sibling presented with a hemangioblastoma, renal cell carcinoma and multiple pancreatic cysts or tumors at age 23 and then retinal hemangioma at age 24. He/she possessed the same mutation as the patient. The patient's mother presented with hemangioblastoma at age 43; but died prior to diagnosis and genetic testing.

      CohortInfo: 16 Chinese patients clinically diagnosed with VHL disease.

      CasePresentingHPOs: HP:0010797; HP:0005584; HP:0001732 (hemangioblastoma; renal cell carcinoma; abnormality of the pancreas)

      CaseHPOFreeText: The patient presented with a hemangioblastoma, renal cell carcinoma and multiple pancreatic cysts or tumors at age 30.

      CaseNotHPOs: HP:0002666, HP:0030393, HP:0030424; HP:0009711 (pheochromocytoma, endolymphatic sac tumor, epididymal cyst, retinal capillary hemangioma; )

      CaseNotHPOFreeText: N/A

      CasePreviousTesting: N/A

      PreviouslyPublished: N/A

      SupplementalData: N/A

      Variant: Exon 3 Deletion

      LegacyVariant: N/A

      CaseProblemVariantFreeText: N/A

      ClinVarID: N/A

      CAID: N/A

      gnomAD: N/A

      VariantEvidence: N/A

      MutationType: deletion

      CivicName: Exon 3 Deletion

      MultipleGeneVariants: N/A

    1. Eight patients with VHL disease type 2 were selected from the group of familial VHL patients with known VHL germline mutations followed on a clinical protocol at the Urologic Oncology Branch, National Cancer Institute, National Institutes of Health (NIH). Patient 6 was found with a c.334T>C/p.Tyr112His mutation in the VHL gene (legacy notation c.547T>C converted to NM_000551.3). Patient 6 was a male diagnosed with VHL type 2A, a right adrenal pheochromocytoma (41Y) and retinal angioma and no metastasis. His last follow-up was 4 years after the initial diagnosis. Suspected to be previously published, since the papers states that reported VHL patients were selected from the group of familial VHL patients with known VHL germline mutations followed on a clinical protocol at the Urologic Oncology Branch, National Cancer Institute, National Institutes of Health (NIH).

    1. PMID: 21461997

      PatientID: 1

      KindredID: 1

      Case: M, 19Y6M, Ethnicity Unknown

      DiseaseAssertion: assumed VHL

      FamilyInfo: The mother of the patient was negative for the VHL mutation; the father was not tested. The family history was negative for VHL syndrome and PCCs

      CasePresentingHPOs: HP:0006748; HP:0009711 (adrenal pheochromocytoma, retinal capillary hemangioma)

      CaseHPOFreeText: scans at 13Y revealed bilateral adrenal masses (left, 4 cm×3.5 cm×5 cm; right, 5 cm×4 cm×4.5 cm) and retinal capillary hemangioma. A bilateral resection of the adrenal glands was performed and histological examination of the tissues confirmed pheochromocytoma.

      CaseNotHPOs: N/A

      CaseNotHPOFreeText: asymptomatic at 13Y but went to hospital for hypertension. The patient remains in complete remission (CR) 79 months after diagnosis.

      CasePreviousTesting: SDHB, SDHC, SDHC, RET,

      PreviouslyPublished: N/A

      SupplementalData: N/A

      Variant: p.H125P (c.374A>C)

      LegacyVariant: N/A

      CaseProblemVariantFreeText: N/A

      ClinVarID: 223201 https://www.ncbi.nlm.nih.gov/clinvar/variation/223201/

      CAID: N/A

      gnomAD: N/A

      VariantEvidence: N/A

      MutationType: missense_variant;transversion

      CivicName: H125P (c.374A>C)

      MultipleGeneVariants: N/A

    1. daughter

      PatientID: None

      KindredID: 1

      Case: F, 0Y0M, Ethnicity Unknown

      DiseaseAssertion: Asymptomatic

      FamilyInfo: The patient’s mother had bilateral adrenal pheochromocytoma at 27Y, and was found to have bilateral small lesions suspicious for inactive retinal angiomas upon further investigation. The patient’s grandfather had a right adrenal pheochromocytoma at 48Y, and was found to have left epididymal cysts and bilateral renal cysts upon further investigation. Genetic testing found that the patient’s mother and grandfather both carried the same NM_000551.3:c.277G>A mutation that the patient was found to carry. The patient's mother’s paternal grandmother had also died at 42Y as a result of a stroke, and the patient’s mother’s paternal grandmother’s brother had died at 57Y as a result of a stroke. There is no genetic information available about them. The patient’s aunt did not carry the mutation.

      CasePresentingHPOs: N/A

      CaseHPOFreeText: N/A

      CaseNotHPOs: N/A

      CaseNotHPOFreeText: N/A

      CasePreviousTesting: N/A

      PreviouslyPublished: N/A

      SupplementalData: N/A

      Variant: p.G93S (c.277G>A)

      LegacyVariant: N/A

      ClinVarID: 2237, https://www.ncbi.nlm.nih.gov/clinvar/variation/2237/

      gnomAD: N/A

      VariantEvidence: N/A

      MutationType: missense_variant;transition

      CivicName: G93S(c.277G>A)

      MultipleGeneVariants: N/A

    1. Another sister of the patient (II-2) carried the mutated VHL gene. However, no VHL-associated lesions were detected, therefore II-2 was considered to be a mutation carrier.

      PatientID:II-2

      KindredID: 2

      Case: F, Sex Unknown, Chinese

      DiseaseAssertion:Asymptomatic

      FamilyInfo: The mother of the patient (I-2) was deceased, and the cause was unknown. The mother exhibited a brain tumor and coronary heart disease whilst alive. Multiple nodules were detected in the thyroid gland of the patient's eldest sister (II-1), but were not treated. The patient's brother (II-3) also had the mutation but was asymptomatic. See Figure 2 for pedigree.

      CasePresentingHPOs: N/A

      CaseHPOFreeText: MRI of the brain of the patient's brother (II-3) indicated a nodule in the left cerebellar tonsil with a size of ~9.0×10.5 mm, which indicated the presence of a hemangioblastoma, astrocytoma or ependymoma. However, the diagnosis could not be confirmed.

      CaseNotHPOs: N/A

      CaseNotHPOFreeText: N/A

      CasePreviousTesting: N/A

      PreviouslyPublished: N/A

      SupplementalData: N/A

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

      CaseProblemVariantFreeText: N/A

      LegacyVariant: N/A

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

      CAID: N/A

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

      VariantEvidence: N/A

      MutationType: missense_variant;transition

      CivicName: R167W (c.499C>T)

      MultipleGeneVariants: N/A

    1. PatientID: None

      KindredID: 1

      Case: Sex Unknown, Age Unknown, Ethnicity Unknown

      DiseaseAssertion: Adrenal pheochromocytoma

      FamilyInfo: The proband was part of a cohort of apparently sporadic cases of pheochromocytoma/ paraganglioma, implying this individual had no family history of VHL disease or pheochromocytoma.

      CasePresentingHPOs: HP:0006748 (Adrenal Pheochromocytoma)

      CaseHPOFreeText: N/A

      CaseNotHPOs: HP:0002668 (Paraganglioma)

      CaseNotHPOFreeText: N/A

      CasePreviousTesting: RET, SDHB, SDHC, and SDHD

      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?dataset=gnomad_r2_1

      VariantEvidence: N/A

      MutationType: missense_variant;transition

      CivicName: P25L (c.74C>T)

      MultipleGeneVariants: N/A

    1. Abstract

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

      GenotypingMethod: Exons 1, 2, and 3 of VHL gene were amplified by PCR. Exons 10, 11, 13, 14, 15, and 16 RET proto-oncogene were also examined by PCR and direct DNA sequencing

      SamplingMethod: peripheral blood leukocytes

    1. 475 T/AW88R

      42 CNS hemangioblastoma 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 were analyzed for VHL mutations. One patient of 17 presenting with VHL germline mutations presented with the W88R (c.262T>A) mutation (stated as c.475T>A in the paper which used the Latif sequence as reference). Single strand conformation polymorphism and southern blotting for variant identification in the DNA found in blood samples. The patient was established as having VHL disease by standard of Neumann at al., 1987. The patient presented with a cerebellum tumor and a spinal T7/8 tumor.

    1. 5

      PatientID: II-3

      KindredID: I

      Case: M, Age Unknown, Chinese

      DiseaseAssertion: VHL

      FamilyInfo: In the patient’s 12 member Chinese family, 7 members were found to carry the NM_000551.3:c.114delC mutation. Five had manifestations of CNS hemangioblastoma, and three of the five were deceased. The other two members found to carry the mutation were asymptomatic, although the paper states that this is likely due to their young age.

      CasePresentingHPOs: HP:0010797 (Hemangioblastoma)

      CaseHPOFreeText: The patient is deceased. The paper implies that the mutation was confirmed through stored tumour tissue.

      CaseNotHPOs: N/A

      CaseNotHPOFreeText: N/A

      CasePreviousTesting: N/A

      PreviouslyPublished: N/A

      SupplementalData: N/A

      Variant: p.G39Afs*28(c.114delC)

      LegacyVariant: p.G39Afs*28(c.327delC)

      ClinVarID: N/A

      CAID: CA2573047816, https://reg.clinicalgenome.org/redmine/projects/registry/genboree_registry/by_canonicalid?canonicalid=CA2573047816

      gnomAD: N/A

      VariantEvidence: N/A

      MutationType: minus_1_frameshift_variant

      CivicName: G39Afs(c.114delC)

      MultipleGeneVariants: N/A

    1. Medical files and histopathology reports of patients who had been operated on before were also reviewed.

      PatientID: IV-18

      KindredID: 1

      Case: F, 17Y0M, Iranian

      DiseaseAssertion: assumed VHL

      FamilyInfo: Familial history was positive. See Fig 1. A total of 43 members of the kindred, 24 males and 19 females, aged 2-77 years were reached for evaluation. It is stated in the paper that all affected subjects (13) were positive for the same mutation (c.500G>A). Additionally, gene sequencing revealed that 4 asymptomatic members of the kindred also harbored the pathogenic mutation. Phenotypes include pheochromocytoma, hemangioblastoma, and retinal HB.

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

      CaseHPOFreeText: Patient had a bilateral PCC and retinal HB at 14Y which was surgically removed at the time. Histopathology was benign, and there was no case of relapse or metastatic dissemination.

      CaseNotHPOs: HP:0000077 (abnormality of the kidney)

      CaseNotHPOFreeText: There was no case of kidney tumors among the kindred.

      CasePreviousTesting: N/A

      PreviouslyPublished: N/A

      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. Patients presenting with juxtapapillary capillary retinal angioma in Germany were queried for the presence of VHL mutations. Peripheral blood samples were obtained, exons of the VHL gene were amplified with polymerase chain reaction (PCR), and products were separated by single-stranded conformation polymorphism (SSCP) for the detection of intragenic mutations. Aberrant bands were sequenced to identify mutations. Southern blotting was performed to detect large deletions if the SSCP failed to show a band shift. This patient (patient ID 8) was found to have a c.344A>G mutation (stated as c.557A>G in the paper which used the Latif sequence as reference). The patient was diagnosed at 5 years of age with juxtapapillary capillary retinal angioma and had a history of epidydimal cystadenoma and CNS hemangioblastoma. On follow-up, over the subsequent 3.7 years, the patient experienced renal cell carcinoma, pheochromocytoma, and additional CNS hemangioblastoma. There is indication, but no description, of a positive family history of VHL disease.

    1. P25L,

      Tissue specimens of apparent sporadic pheochromocytoma were retrieved from the archives of the Department of Pathology of the Erasmus MC (Rotterdam), the Radboud University Nijmegen Medical Center, and the University Hospital Zurich (Switzerland). Mutation analysis was performed using SSCP analysis and BigDye® Terminator V3.1 cycle sequencing kit (Applied Biosystems, Foster City, CA). 136 VHL cases and six germline VHL mutations were found. A c.74C>T, p.Pro25Leu mutation (stated as c.287C>T in the paper which used the Latif sequence as reference) was found in one 38Y female patient with benign adrenal pheochromocytoma. No other phenotypes, patient demographics, or family history was described.

    1. Case 2The patient’s daughter is a 36-year-old woman diagnosed with VHLD (C.500G > A, p.Arg167Glu) in 2008 with retinal and cerebellar hemangioblastomas, pheochromocytoma, pancreatic neuroendocrine tumor, and recurrent renal cell carcinoma. The patient’s pedigree was significant for multiple cancers in prior generations (Fig. 2). In 2012, surveillance MRI showed few hyperintense subcortical lesions and a prominent C3 lesion without contrast enhancement. MRI in 2019 showed an increase in subcortical and periventricular lesions on T2 weighted images, as well as substantial accumulation of multifocal cervical and thoracic spinal cord lesions.Fig. 2Pedigree of the patients’ family structure. Half-grey symbols: Cancer. Half-black symbols: Multiple Sclerosis. Checkerboard or half-checkerboard symbols: VHLD. Known cancer types and other notable medical conditions are provided as text under each symbol. The patients from each case are labeled as “Pt 1″ and “Pt 2″Full size imageIn April 2020, she developed an episode of numbness and burning/tingling in her arms and legs for which she was treated with corticosteroids. MRI showed new white matter lesions in the brain and enhancement of the dorsal cervical spine (Fig. 3). Numbness of the hands and feet worsened over the next month. MS mimicker labs including myelin oligodendrocyte glycoprotein or aquaporin 4 antibodies, vitamin B12 and TSH levels were normal. She also developed painful loss of vision in left eye in November 2020, and repeat MRI showed subtle asymmetric contrast enhancement of the left optic nerve consistent with optic neuritis, reinforcing MS diagnosis. Plans were made to initiate Tecfidera and further monitoring is pending follow-up.

      PatientID: 2

      KindredID: 1

      Case: F, 36Y0M, Ethnicity Unknown

      DiseaseAssertion: VHL

      FamilyInfo: Patient’s 51Y0M mother also carried the same VHL mutation and had relapsing-remitting multiple sclerosis (MS) in the background of VHL disease. She was diagnosed with hemangioblastomas in the spinal cord and cerebellum, renal cell carcinoma, pancreatic neoplasm and a left ovarian dermoid cyst. She also exhibited vision loss in 1993 and then developed left lower extremity muscle weak in 2007. The limb weakness worsened in 2012 and decreased vision for 2 months, which raised a diagnosis of MS. Since then, treatment with corticosteroids showed partial response of symptoms and Copaxone was then initiated for treating MS. Their family history was significant for multiple cancers in prior generations. Her three sons were also affected by VHL disease, but no mention of genetic testing in these individuals. (see Fig.2 for Pedigree).

      CasePresentingHPOs: HP:0006880; HP:0009711; HP:0002666; HP:0030405; HP:0005584; HP:0000572 (Cerebellar Hemangioblastoma; Retinal capilllary Hemangioma; Pheochromocytoma; Pancreatic neuroendocrine tumor; Renal Cell Carcinoma, vision loss)

      CaseHPOFreeText: Patient daughter also carried the same VHL mutation and had relapsing-remitting multiple sclerosis (MS) in the background of VHL disease. She had retinal and cerebellar hemangioblastomas, pheochromocytoma, pancreatic neuroendocrine tumor, and recurrent renal cell carcinoma. She exhibited numbness in her limbs and developed vision loss.

      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

      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. PatientID: 2

      KindredID: 54

      Case: Sex, Age, Ethnicity Unknown

      DiseaseAssertion: VHL

      FamilyInfo: another member of the family (54/1) was detected with an HB and the same mutation

      CasePresentingHPOs: HP:0006880 (hemangioblastoma)

      CaseHPOFreeText: one RCC tumor was detected in this patient

      CaseNotHPOs: N/A

      CaseNotHPOFreeText: N/A

      CasePreviousTesting: N/A

      PreviouslyPublished: N/A

      SupplementalData: N/A

      Variant: p.R177Dfs*25 (c.528delG)

      CaseProblemVariantFreeText: N/A

      LegacyVariant: p.176 FS (c.741delG)

      ClinVarID: N/A

      CAID: CA432423454 http://reg.clinicalgenome.org/redmine/projects/registry/genboree_registry/allele?hgvsOrDescriptor=NM_000551.3%3Ac.528delG

      gnomAD: N/A

      VariantEvidence: LOH detected.

      MutationType: minus_1_frameshift_variant

      CivicName: R177fs (c.528delG)

      MultipleGeneVariants: N/A

    1. L158VExon 36/2

      Seven Hungarian families (35 members) with VHL and 37 unrelated patients with apparently sporadic pheochromocytoma had their VHL gene molecularly analyzed. Peripheral blood samples were isolated, amplified by PCR, and subsequently underwent direct sequencing using either SequiTherm Excel II DNA Sequencing Kit-LC (Epicentre Technologies, Madison, WI, USA) and an automated Li-COR IR2 sequencer (Li-COR Inc., Lincoln, NE, USA) or the Big Dye Terminator Cycle Sequencing kit v3.1 (Applied Biosystems, Foster City, CA, USA), and run on an automated sequencer 310 Genetic Analyzer from Applied Biosystems. The L158V (c.472C>G) mutation was found in 1 family (ID A) and molecularly confirmed in 2 family members (proband and son). The proband was a woman who had multiple (occipital, parietal, and cerebellar) hemangioblastomas, renal cysts, and retinal hemangiomas. Her son presented with retinal hemangiomas.

    1. PatientID: 6

      KindredID: A (III-13)

      Case: F, 30Y0M, Ethnicity Unknown

      DiseaseAssertion: VHL

      FamilyInfo: The patient's mother (II:7) carried the VHL mutation and presented with hemangioblastoma, renal cell carcinoma, pheochromocytoma, and renal cysts. The patient had two brothers who both carried the mutation, one (III:12) presented with renal cell carcinoma, the other (III:11) with hemangioblastoma, renal cell carcinoma, renal cyst, and retinal capillary hemangioma. The patient also had one asymptomatic sister (III:10) who did not undergo genetic testing. On the mother's side of the family there was extensive history of VHL disease. Refer to Figure 1 for family pedigree and information regarding extended family members.

      CohortInfo: 10 VHL patients with renal cell carcinoma and a definite VHL family history.

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

      CaseHPOFreeText: Diagnosed with hemangioblastoma at age 20. At 24, she was diagnosed with renal cell carcinoma. She underwent nephron-sparing surgery of the left side and one RCC measuring 2 cm in diameter was removed.

      CaseNotHPOs: HP:0002666, HP:0000107 (pheochromocytoma, renal cyst)

      CaseNotHPOFreeText: N/A

      CasePreviousTesting: N/A

      PreviouslyPublished: N/A

      SupplementalData: N/A

      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

    2. PatientID: 9

      KindredID: C

      Case: Sex Unknown, 35Y0M, Ethnicity Unknown

      DiseaseAssertion: VHL

      FamilyInfo: Positive VHL family history.

      CohortInfo: 10 VHL patients with renal cell carcinoma and a definite VHL family history.

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

      CaseHPOFreeText: The patient had a hemangioblastoma diagnosed at age 29. The patient was diagnosed with renal cell carcinoma at age 31. A nephron-sparing surgery was performed on the left side. He was found to have one lesion with a diameter of 2 cm.

      CaseNotHPOs: N/A

      CaseNotHPOFreeText: N/A

      CasePreviousTesting: N/A

      PreviouslyPublished: N/A

      SupplementalData: N/A

      Variant: Exon 1-2 loss (c.1-?_463+?del)

      CaseProblemVariantFreeText: N/A

      LegacyVariant: N/A

      ClinVar: N/A

      CAID: N/A

      gnomAD: N/A

      VariantEvidence: N/A

      MutationType: exon_loss_variant

      CivicName: Exon 1-2 Deletion

      MultipleGeneVariants: N/A

    1. GroupID: 50

      DiseaseAssertion: VHL

      GroupSize:3

      GroupNumberMales: N/A

      GroupNumberFemales: N/A

      GroupEthnicity: French

      GroupAgeRange: N/A

      GroupInfo: 3 members of this family presented with the c.499C>T germline variant of the VHL gene. Member 6338 had no renal involvement. Members 6340 and 6339 had mild renal disease. 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 (Renal neoplasm)

      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: Paper states that this family is previously reported in PMID 12202531 and/or 9829912, where 15 individuals and 3 families 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 reported individuals/families could alternatively correspond to family 23 or 1.

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

      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

    2. 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.Q203Gfs*52 (c.607_608del) germline variant of the VHL gene was detected in a family (ID 399). Member 10025 had no renal involvement. Member 10024 had unknown renal involvement. Member 8840 presented with mild renal disease. The variant was reported as c.604_605del which was mapped to c.607_608del. The paper states that this family is previously reported in PMID 12202531.

    3. GroupID: 96

      DiseaseAssertion: VHL

      GroupSize: 3

      GroupNumberMales: N/A

      GroupNumberFemales: N/A

      GroupEthnicity: French

      GroupAgeRange: N/A

      GroupInfo: 3 members of this family are reported as carrying the c.211_212insT germline variant of the VHL gene. Members 5997 and 5993 have unknown renal involvement. Member 5999 presented with mild renal disease. 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 (Renal neoplasm)

      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: 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.

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

      Variant: p.P71Lfs*61 (c.211_212insT)

      LegacyVariant: N/A

      CaseProblemVariantFreeText: N/A

      ClinVarID: N/A

      CAID: CA2501268513, https://reg.clinicalgenome.org/redmine/projects/registry/genboree_registry/allele?hgvsOrDescriptor=NM_000551.3%3Ac.211_212insT

      gnomAD: N/A

      VariantEvidence: N/A

      MutationType: plus_1_frameshift_variant; insertion

      CivicName: P71Lfs*61 (c.211_212insT)

      MultipleGeneVariants: N/A

    4. PatientID: 2288

      KindredID: 65

      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: 12202531

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

      Variant: p.E46* (c.136G>T)

      LegacyVariant: N/A

      CaseProblemVariantFreeText: N/A

      ClinVarID: N/A

      CAID: CA351748085, https://reg.clinicalgenome.org/redmine/projects/registry/genboree_registry/allele?hgvsOrDescriptor=NM_000551.3%3Ac.136G%3ET

      gnomAD: N/A

      VariantEvidence: N/A

      MutationType: missense_variant;transversion; stop_gained

      CivicName: E46* (c.136G>T)

      MultipleGeneVariants: N/A

    5. PatientID: 1968

      KindredID: 224

      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: 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]). Individual RCC phenotype is noted as positive.

      CaseNotHPOs: N/A

      CaseNotHPOFreeText: N/A

      CasePreviousTesting: N/A

      PreviouslyPublished: 12202531

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

      Variant: p.H115Y (c.343C>T)

      LegacyVariant: N/A

      CaseProblemVariantFreeText: N/A

      ClinVarID: N/A

      CAID: CA16621930, https://reg.clinicalgenome.org/redmine/projects/registry/genboree_registry/allele?hgvsOrDescriptor=NM_000551.3%3Ac.343C%3ET

      gnomAD: N/A

      VariantEvidence: N/A

      MutationType: missense_variant;transition

      CivicName: H115Y (c.343C>T)

      MultipleGeneVariants: N/A

    1. the P86L missense heterozygous germline mutation was identified in exon 1

      A retrospective study of 14 patients (6 female and 8 male; mean age, 43.5 yr) with no family history and no other clinical manifestations of VHL disease and were operated for symptomatic CNS hemangioblastoma between 1993-2002 at the Casa Sollievo della Sofferenza Hospital in Italy was conducted. Peripheral blood was used through PCR and dHPLC for molecular genetic analysis. Germline mutations of the VHL gene were identified in 2 of the 14 patients. Patient #1 (40Y, male) and found with P86L mutation in the VHL gene and cerebellar hemangioblastoma. Genetic analysis on close family members was negative for the mutation. Four years after diagnosis (32Y0M) they developed a retinal hemangioblastoma (36Y0M).

    1. Sequence analysis of the AIP gene (NM_003977.2), MEN type 1 gene (MEN1; NM_130799.2), cyclin-dependent kinase inhibitor 1B gene (CDKN1B; coding region NM_004064.3, upstream open reading frame NM_004064.2) was performed using Sanger sequencing and multiplex ligation-dependent probe amplification (MLPA), as previously described (10,–12). Genes implicated in pheo/PGL [MYC associated factor X (MAX; NM_002382.3), rearranged during transfection tyrosine kinase receptor gene (RET; NM_020975.4), succinate dehydrogenase subunit A (SDHA; NM_004168.2), succinate dehydrogenase complex assembly factor 2 (SDHAF2; NM_017841.2), succinate dehydrogenase subunit B (SDHB; NM_003000.2), succinate dehydrogenase subunit C (SDHC; NM_003001.3), succinate dehydrogenase subunit D (SDHD; NM_003002.2), transmembrane protein 127 (TMEM127; NM_017849.3), and von Hippel-Lindau gene (VHL; NM_000551.3)] were analyzed using a combination of next-generation sequencing, Sanger sequencing and MLPA, as previously described (13, 14). In addition, fumarate hydratase (NM_000143) was studied in a subset of patients. Tissue DNA analysis with PCR and sequencing was carried out according to standard protocols (Applied Biosystems). The sequences were analyzed using Mutation Surveyor (version 4.0.6; Softgenetics). In silico analysis of variants was performed using the Polyphen2 (http//:genetics.bwh.harvard.edu) and ALAMUT 2.2.0 (http://www.interactive-biosoftware.com/) softwares.

      ArticleReferenceSequence: NM_000551.3 (Standard)

      GenotypingMethod: Combination of next-generation sequencing, Sanger sequencing and MLPA.

      SamplingMethod: peripheral blood

    1. 1 (50)

      GroupID: 35b

      Case: Sex Unknown, Age Unknown, Ethnicity Unknown

      DiseaseAssertion: VHL

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

      CasePresentingHPOs: N/A

      CaseHPOFreeText: This was 1 of 2 patients discussed with this mutation. The individual did NOT have retinal hemangiomas; Other VHL manifestations were discussed but not per- variant.

      CaseNotHPOs: HP:0009711 (retinal capillary hemangioma)

      CaseNotHPOFreeText: N/A

      CasePreviousTesting: N/A

      PreviouslyPublished: N/A

      SupplementalData: Yes - Supplementary Table S1

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

      LegacyVariant: N/A

      CaseProblemVariantFreeText: N/A

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

      CAID: N/A

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

      VariantEvidence: N/A

      MutationType: missense_variant; transition

      CivicName: F136S (c.407T>C)

      MultipleGeneVariants: N/A

    1. Von Hippel-Lindau (VHL) syndrome is an autosomal dominant genetic disorder caused by germline mutation of the VHL gene. It is associated with multiple neoplasias including hemangioblastoma, clear cell renal cell carcinoma, pheochromocytoma, and neuroendocrine tumors. Ovarian tumors are extremely rare in this syndrome. We describe the case of a 16-yr-old girl with a previous diagnosis of bilateral pheochromocytoma and several pancreatic neuroendocrine tumors in VHL syndrome context. Follow-up abdominal-pelvic magnetic resonance imaging revealed a 33 mm, well-circumscribed nodule in the right ovary. The patient was submitted to laparoscopic right salpingo-oophorectomy. Microscopically, the tumor consisted of polygonal cells with abundant microvacuolized clear cytoplasm arranged in a solid pattern. The neoplastic cells were immunohistochemically positive for inhibin and calretinin. A diagnosis of ovarian steroid cell tumor was made. Only 4 cases with this association have been reported to date. Of the previously described cases, only one concerns a child; the others were all adult women. All of them had a previous diagnosis of VHL syndrome and presented with secondary amenorrhea and/or hirsutism due to testosterone-secreting ovarian steroid cell tumors. Although extremely rare, the association between VHL syndrome and ovarian steroid cell tumor has been reported, and our case suggests there is a link between the 2 entities.

      PatientID: 1

      KindredID: 1

      Case: F, 17Y0M, Ethnicity Unknown

      DiseaseAssertion: assumed VHL

      FamilyInfo: N/A - no family history of VHL disease. Authors indicate probably a de novo mutation, however no testing on family members was completed.

      CasePresentingHPOs: HP:0006748; HP:0030405; HP:0100615 (pheochromocytoma, pancreatic endocrine tumor, ovarian neoplasm)

      CaseHPOFreeText: hospitalized in 2011 (11Y old) due to a hypertensive crisis with end-organ damage (bilateral papilledema and left ventricular hypertrophy). MRI showed 2 heterogenous nodular lesions where the largest was in the right adrenal gland (65x51x39mm) and the other in the left adrenal gland (36x28x25mm). A bilateral adrenalectomy diagnosed both tumors as pheochromocytomas of the adrenal gland. Lymph node metastasis was detected in the adipose tissue surrounding the left adrenal gland. 2 years later (at age 13Y) a PET/CT scan showed a nodular lesion in the tail of the pancreas (11mm) and a nodule in between the inferior vena cava and the portal vein (13mm) and both were later diagnosed as neuroendocrine tumors the former in the pancreas and the latter in the perihaptic ectopic pancreatic tissue. At 14Y, more pancreatic lesions were found. At 16Y, an MRI found a nodule int he right ovary (33mm) which was later diagnosed as a benign ovarian steroid cell tumor

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

      CaseNotHPOFreeText: Table 1 indicates this was did not have the above manifestations

      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. nt 452 G/A 80 Ser→Asn S80N Missense 1

      PatientID: 9

      GroupID/ KindredID: 9

      Case: Sex Unknown, Age Unknown, Ethnicity Unknown

      DiseaseAssertion: hemangioblastoma

      FamilyInfo: N/A

      CasePresentingHPOs: HP:0010797 (hemangioblastoma)

      CaseHPOFreeText: other phenotypes unknown

      CaseNotHPOs: N/A

      CaseNotHPOFreeText: N/A

      CasePreviousTesting: N/A

      PreviouslyPublished: N/A

      SupplementalData: N/A

      Variant: p.S80N (c.239G>A)

      LegacyVariant: p.S80N (c.452G>A)

      CaseProblemVariantFreeText: N/A

      ClinVarID: 1070179 https://www.ncbi.nlm.nih.gov/clinvar/variation/1070179/

      CAID: CA70046108 http://reg.clinicalgenome.org/redmine/projects/registry/genboree_registry/allele?hgvsOrDescriptor=NM_000551.3%3Ac.239G%3EA

      gnomAD: N/A

      VariantEvidence: N/A

      MutationType: missense_variant; transition

      CivicName: S80N (c.239G>A)

      MultipleGeneVariants: N/A

    1. W117C (20) 

      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. Two patients were listed with this missense mutation, c.351G>T.

    1. Three novel mutations in the von Hippel-Lindau tumour suppressor gene in Italian patients Paola Mandich, Corresponding Author Institute of Biology and Genetics, University of Genoa, Genoa, ItalyInstitute of Biology and Genetics, University of Genoa, Viale Benedetto XV, 6-16132, Genoa Italy; Fax: +39 10 3538978Search for more papers by this authorMariapina Montera, Institute of Biology and Genetics, University of Genoa, Genoa, ItalySearch for more papers by this authorEmilia Bellone, Institute of Biology and Genetics, University of Genoa, Genoa, ItalySearch for more papers by this authorAlessandra Trojani, Institute of Biology and Genetics, University of Genoa, Genoa, ItalySearch for more papers by this authorSalvatore Daniele, Department of Medical Surgery, University of Perugia, Perugia, ItalySearch for more papers by this authorFranco Ajmar, Institute of Biology and Genetics, University of Genoa, Genoa, ItalySearch for more papers by this author

      PMID: 9452106

      Gene: VHL

      StandardizedReferenceSequence: NM_000551.3

    1. 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: 5

      KindredID: 1

      Case: M, 57Y0M, 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:0000107; HP:0006748; HP:0009713; HP:0009711; HP:0006880; HP:0030405; HP:0001737 (renal cysts, adrenal pheochromocytoma, spinal hemangioblastoma, retinal hemangioblastoma, cerebellar hemangioblastoma, pancreatic endocrine tumor, pancreatic cysts)

      CaseHPOFreeText: Patient presented with his initial VHL-related clinical manifestations at 16Y0M. He was found to have renal and pancreatic cysts, adrenal pheochromocytoma, spinal hemangioblastoma, retinal hemangioblastoma, cerebellar hemangioblastoma, and pancreatic endocrine tumor (see table 1). Patient also had bone metastasis. He was diagnosed with VHL subtype 2A at age 49Y0M and passed away at age 57Y0M.

      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

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

      PatientID: 21

      KindredID: C

      Case: Sex Unknown, 29Y0M, Mexican (Latino/Admixed American)

      DiseaseAssertion: asymptomatic

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

      CasePresentingHPOs: N/A

      CaseHPOFreeText: Patient was asymptomatic at the time.

      CaseNotHPOs: N/A

      CaseNotHPOFreeText: N/A

      CasePreviousTesting: N/A

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

      SupplementalData: N/A

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

      LegacyVariant: c.1012_1013insA

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

      ClinVarID: N/A

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

      gnomAD: N/A

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

      MutationType: plus_1_frameshift_variant; duplication

      CivicName: T100Nfs*32 (c.298dupA)

      MultipleGeneVariants: N/A

    1. frameshift mutations (4/16)

      A retrospective cohort study was conducted at a public children’s hospital (Buenos Aires, Argentina). Eligible patients were all index cases with clinical diagnosis or clinical suspicion of type 1 VHL referred for genetic testing from 2003 to 2015. Universal primer quantitative fluorescent multiplex polymerase chain reaction (UPQFM-PCR) and multiplex ligation-dependent probe amplification (MLPA) analysis was completed using peripheral blood leukocytes. This patient (ID #10) was diagnosed with VHL with genetic testing confirming this VHL mutation Q73Pfs*59 (c.217dupC) when they were 29Y. They presented with CNS hemangioblastoma at 29Y, clear cell renal cell carcinoma at 30Y and renal cysts at 30Y. The family history of the patient was unknown.

    2. nonsense mutations (6/16)

      PatientID: 3

      KindredID: 3

      Case: 27Y0M, Sex Unknown, Argentinian

      DiseaseAssertion: VHL

      FamilyInfo: No family history

      CasePresentingHPOs: HP:0010797; HP:0006770; HP:0001737; HP:0000107; HP:0030424 (hemangioblastoma; clear cell renal cell carcinoma; pancreatic cysts; renal cyst; epididymal cyst)

      CaseHPOFreeText: Aged 20Y at diagnosis (genetic testing); fulfils type 1 VHL clinical diagnosis. CNS angiomas diagnosed at 20, 25, and 26Y, pancreatic, renal, and epididymal cysts diagnosed at 25Y, ccRCC diagnosed at 27Y. (See Table 1 & 2).

      CaseNotHPOs: N/A

      CaseNotHPOFreeText: N/A

      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. A 45-year old Japanese woman was referred to our hospital for the management of a pancreatic tumor and multiple liver tumors. At 17 years of age, she underwent surgical resection of a cerebellar hemangioblastoma and was diagnosed with VHL following a genetic examination. Genome sequencing revealed a nonsense mutation c.394C>T(p.Gln132X) in exon 2. There was no evidence of a family history of VHL. She experienced multiple recurrent cerebellar hemangioblastoma and underwent three additional surgical operations. She also had a history of surgery of retinal hemangioblastoma and adrenalectomy for pheochromocytoma at age of 26 and 30 age years of age, respectively.

      A 45-year old Japanese woman presented with a pancreatic tumor, multiple liver tumors and pancreatic cyst lesions. The examination of percutaneous liver tumor biopsy specimen led to a diagnosis of pancreatic neuroendocrine tumor (NET)-G3. She passed away 13 months after her diagnosis. Her previous medical history included surgical resection of a cerebellar hemangioblastoma at 17 years of age. She also experienced multiple recurrent cerebellar hemangioblastoma and underwent three additional surgical operations. She also had a history of surgery of retinal hemangioblastoma and adrenalectomy for pheochromocytoma at age of 26 and 30 age years of age, respectively. Genome sequencing revealed a nonsense mutation c.394C>T(p.Gln132*) in exon 2 of the VHL gene. There was no evidence of a family history of VHL. AMCG evidence codes: PP4 because the patients phenotype is highly specific for a mutation in the VHL gene.

    1. M45orangeMale45delA, fsArg1762nd R (1 prior L, 1 subs L)Former- 12 pack years24.06 (5*)Yes

      PatientID: None

      KindredID: 1

      Case: M, 45Y0M, Ethnicity Unknown

      DiseaseAssertion: Clear Cell Renal Cell Carcinoma

      FamilyInfo: N/A

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

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

      CaseHPOFreeText: One of the samples from this patient had few variants and clustered with the normal samples. Further inspection showed these samples were cyst-like rather than tumours, so they were excluded from further analysis. This suggests that the patient had renal cysts alongside ccRCC at age 45.

      CaseNotHPOs: N/A

      CaseNotHPOFreeText: N/A

      CasePreviousTesting: N/A

      PreviouslyPublished: N/A

      SupplementalData: N/A

      Variant: p.R176fsGfs*26 (c.526del)

      LegacyVariant:N/A

      CaseProblemVariantFreeText: N/A

      ClinVarID: 625257 https://www.ncbi.nlm.nih.gov/clinvar/variation/625257/

      CAID: N/A

      gnomAD: N/A

      VariantEvidence: N/A

      MutationType: minus_1_frameshift_variant

      CivicName:R176fs (c.526del)

      MultipleGeneVariants: N/A

    1. NM_000551:c.A269T:p.N90I

      ArticleReferenceSequence: NM_000551

      GenotypingMethod: Sanger sequencing of the VHL gene was performed using peripheral blood samples from 6 family members to initially identify any germline VHL variants. The CH tumor tissue from the proband, the RCCC tumor tissue and CH tumor tissue from his father's elder brother, and the RCCC tumor tissue from his uncle, as well as three peripheral blood samples were subjected to WES to identify somatic gene variants. After detecting novel gene variants, Sanger sequencing was applied for subsequent validation. Immunohistochemical staining for the HIF‐1 and phospho‐S6 ribosomal proteins was performed to assess the expression levels of key proteins.

      SamplingMethod: Peripheral blood, cerebellar tumour, renal tumour

    1. Western blots were done with 50 5-μm sections (approximately 10 mg) cut from five frozen phaeochromocytoma tissue samples from patients with germline mutations in SDHB (EX3del), SDHD (p.Asp92Tyr), RET (p.Cys634Arg), VHL (c.191G>C; p.Arg64Pro), and NF1 (clinically determined). Immunohistochemical staining was done on all tissue samples. Peripheral samples were isolated and direct, in-house, or commercial (Baseclear, Leiden, Netherlands) sequencing of PCR products. There were 29 samples with germline VHL mutations but it is not specified if all 29 of these patients had the R64P mutation. 21 of these patients presented with pheochromocytoma and 5 presented with paragangliomas.

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

      GroupID/ KindredID: VHL 17

      DiseaseAssertion: assumed VHL

      GroupSize: 3

      GroupNumberMales: N/A

      GroupNumberFemales: N/A

      GroupEthnicity: German

      GroupAgeRange: N/A

      FamilyInfo: 3 affected members belong to this VHL type 2A family. One representative affected member was analyzed with this mutation, and VHL was diagnosed clinically in this index person. It is unclear as to whether the additional patients had this precise mutation, although assumed.

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

      GroupHPOFreeText: 2 individuals had Pheos, 1 had a retinal capillary hemangiomas, and 1 had a CNS hemangioblastoma.

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

      GroupNotHPOFreeText: No patients had the above tumors

      GroupPreviousTesting: N/A

      PreviouslyPublished: 11134110, 9681856, 11850829

      SupplementalData: N/A

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

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

      CaseProblemVariantFreeText: N/A

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

      CAID: N/A

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

      VariantEvidence: N/A

      MutationType: missense_variant;transition

      CivicName: Y98H (c.292T>C)

      MultipleGeneVariants: N/A

    1. in seven of the asymptomatic family members.

      PatientID: IV-7

      KindredID: 1

      Case: F, Age Unknown, Turkish

      DiseaseAssertion: asymptomatic

      FamilyInfo: 17 family members from three generations were examined with the c.445G>T mutation and diagnosed with VHL type 2B. 11 individuals had clinical manifestations and 6 were asymptomatic carriers. One additional member (II-9) had passed before testing however were likely a carrier of the mutation. This patient’s father, grandmother and more, had the mutation. See Fig. 1 for full family pedigree.

      CasePresentingHPOs: N/A

      CaseHPOFreeText: None - described as a carrier of the p.A149S mutation, with no clinical manifestations. Their asymptomatic work up could have been due to the individual's young age

      CaseNotHPOs: N/A

      CaseNotHPOFreeText: N/A

      CasePreviousTesting: 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

    1. In family 9 in our series, we identified a VHL germline mutation(470 C>T, Pro86Leu) in a 53 years old woman (proband 9) with asynchronous bilateral renal clear cell carcinomas, multiple renal cysts and pancreatic cysts and with no positive family history, in her younger brother with a single phenotype (pancreatic cysts),and in her niece with no detectable VHL lesions. It is of interest that we find the same mutation in another unrelated VHL family (family 10) in which affected patients have severe phenotypes including multiple CNS haemangioblastoma, retinal angiomas, bilateral RCCs and pancreatic cysts. Compared with the family 10, it is very likely that the affected members in the family 9 will develop CNS haemangioblastoma and retinal angiomas in the future.

      PatientID: II-3

      KindredID: 9

      Case: M, Age Unknown, Chinese

      DiseaseAssertion: assumed VHL

      FamilyInfo: Older sister was examined to have asynchronous bilateral renal clear cell carcinomas, multiple renal cysts and pancreatic cysts. III-1, III-2, IV-1, IV-2, IV-3 all tested for the VHL gene but found to be normal. daughter was detected with the same mutation but with no detectable VHL lesions. [see Fig. 2].

      CasePresentingHPOs: HP:0001737 (pancreatic cysts)

      CaseHPOFreeText: patient had a single phenotype of Pancreatic cysts

      CaseNotHPOs: HP:0002666; HP:0010797; HP:0009711; HP:0006770 (pheochromocytoma, hemangioblastoma, retinal capillary hemangioma, renal cell carcinoma)

      CaseNotHPOFreeText: N/A

      CasePreviousTesting: N/A

      PreviouslyPublished: N/A

      SupplementalData: N/A

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

      CaseProblemVariantFreeText: N/A

      LegacyVariant: p.P86L (c.470C>T)

      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. Case Presentation: A 37 year old Caucasian male with past medical history of HTN who presented with complaints of episodic spells of excessive sweating, mood swing, hypertension, abdominal pain. He also had significant family history in grandmother who had adrenalctomy and his son diagnosed with Hypertension. His urine studies were negative for metanephrines and normetanephrines. CT scan showed 5.5 cm tumor on right adrenal gland and underwent successful right adrenalectomy. Pathology revealed pheochromocytoma. He was followed with biochemical test which were normal. Due to his diagnosis of pheochromocytoma at early age, genetic testing was ordered. Genetic testing showed positive for VHL gene mutation, with variant of p.Glu32Gly, Heterozygous, autosomal dominant considered to be unknown significance by the laboratory. This mutation has not been previously reported in HGMD database, nor in the Broad ExAc dataset indicating it is rare and not well-characterized. He later underwent MRI with contrast of brain, spine, abdomen and pelvis which showed no evidence of other tumors.

      PatientID: N/A (case)

      KindredID: 1

      Case: M, 37Y0M, Ethnicity Unknown

      DiseaseAssertion: adrenal pheochromocytoma

      FamilyInfo: He had significant family history with his grandmother who had an adrenalctomy, and his son diagnosed with Hypertension. No genetic testing was described for them

      CasePresentingHPOs: HP:0006748 (adrenal pheochromocytoma)

      CaseHPOFreeText: 37Y Caucasian male had a medical history of HTN and complained of excessive sweating, mood swing, hypertension, abdominal pain. CT scan showed 5.5 cm tumor on right adrenal gland and underwent successful right adrenalectomy. Pathology revealed pheochromocytoma.

      CaseNotHPOs: N/A

      CaseNotHPOFreeText: He underwent MRI with contrast of brain, spine, abdomen and pelvis which showed no evidence of other tumors.

      CasePreviousTesting: N/A

      PreviouslyPublished: N/A

      SupplementalData: N/A

      Variant: p.E32G (c.95A>G)

      LegacyVariant: N/A

      CaseProblemVariantFreeText: N/A

      ClinVarID: 186635 https://www.ncbi.nlm.nih.gov/clinvar/variation/186635/

      CAID: N/A

      gnomAD: 0.00002749 https://gnomad.broadinstitute.org/variant/3-10183626-A-G

      VariantEvidence: N/A

      MutationType: missense_variant;transition

      CivicName: N/A

      MultipleGeneVariants: N/A

    1. p.P2P (c.6C>G)

      The authors evaluated a family of five VHL c.6C>G (p.Pro2Pro) carriers. Five members of one family were investigated and their blood samples were taken and sequencing using sanger sequencing of exons and exon-intron boundaries. The proband (age 31), presented with renal cell carcinoma at age 29 and had an additional VHL mutation (p.P81S). The proband had one son who was asymptomatic and only carried the p.P2P mutation. The proband's two brothers, mother, and maternal grandmother were all found to carry the other VHL mutation (p.P81S). The proband’s paternal uncle died from metastasizing renal cell carcinoma at 46 years of age, and the proband’s father died from urosepsis in relation to bladder cancer in situ at the age of 56. Neither of these men were able to undergo genetic testing.

    1. 430 C/T

      A retrospective study described polyglobulia in 19 patients precise germline VHL mutations and with hemangioblastomas. 10 other patients followed with VHL mutations without an exact location. Patient 22 was a 28Y male. They had a hemangioblastoma tumor 1.0cm3 in size, and an unspecified tumor cyst. The mutation p.Q73* (c.217C>T) was described in the paper as c.430C>T due to a difference in transcript reference. No family information was provided.

    1. VHLD-associated E-HB

      A 40-year old Caucasian female from Slovenia was found to have a missense germline mutation in VHL, c.452T>A (p.Ile151Asn). The patient's extraneuraxial hemangioblastoma tissue was also tested for somatic mutations in the VHL gene. A somatic c.500G>A (p.R167Q) was found. PCR amplification was performed searching for point mutation in the entire VHL coding sequence and promoter region, including exon-intron boundaries. Amplification was performed in a Gene Amp PCR System 9700 (Perkin Elmer). When mutations were detected in DNA from tumor samples, it was searched for in the corresponding peripheral blood DNA in order to identify germline mutations. 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. There was no known family history of VHL disease, but the patient had a family history of (unspecified) "brain tumors". AMCG evidence codes: ’PP4’ because the patients phenotype is highly specific for a mutation in the VHL gene.

    1. (ACT>ATT; Thr157Ile)

      An Italian 45Y0M female patient presented with adrenal phechromocytoma at age 22, which was removed via surgery. Two years later, she underwent a pancreaticduodenectomy to remove a pancreatic neuroendocrine tumour. After 21 years without symptoms, metastases of the original pancreatic neuroendocrine tumour was detected and three neuroendocrine tumours with the same immunohistochemical characteristics were removed. Genetic testing confirmed the presence of a T157I (c.470C>T) missense mutation in VHL. Genetic analysis was performed on the patients relatives, including her daughter. Her 55Y0M brother had the same mutation but no clinical signs of VHL disease. No other family information was provided.

    1. H125P

      DNA samples of 20 members from the Chinese family with non-syndromic PCCs and 41 patients with apparently sporadic pheochromocytoma were analyzed by polymerase chain reaction and direct sequencing, confirmed by Taqman probe. Five probands were genetically confirmed with a familial missense mutation at c.374A>C of the VHL gene. The first was an 18 year old Chinese female patient (Proband 1) who presented with recurrent headaches, palpitations, sweating and blurred vision for five months as well as unilateral, multiple pheochromocytomas. The patient has a sister (Carrier 1) and a nephew (Carrier 2) confirmed with the same mutation. The proband's sister presented with bilateral pheochromocytoma and the proband's nephew is asymptomatic. The second was a Chinese male patient (Proband 2) who first presented at 8 years old with bilateral pheochromocytoma. The patient has a son (Carrier 3) confirmed with the same mutation who is asymptomatic. The third was a 17 year old Chinese male patient (Proband 3) who presented with bilateral pheochromocytoma. The patient has a father (Carrier 4), brother (Carrier 5), nephew (Carrier 6), and niece (Carrier 7) all confirmed with the same mutation who are asymptomatic. The fourth was a 16 year old Chinese female patient (Proband 4) who presented with bilateral pheochromocytoma. Family history is unknown. The fifth was a 16 year old Chinese male patient (Proband 5) who presented with bilateral pheochromocytoma. All of these patients are stated as being from the same Chinese family. Probands were those initially evaluated.

    1. 14 Chinese patients from 10 families were diagnosed with Von Hippel-Lindau disease based on clinical criteria. Genetic testing using single-strand conformation polymorphism (SSCP) was conducted and aberrant bands were purified and sequenced. Patient 1 and 2 from family I were found to harbour a c.194C>G mutation in the VHL gene (stated as c.407C>G in the paper which used the Latif sequence as reference). Patient 1 and 2 both presented with retinal capillary hemangioma and hemangioblastoma.

    1. A deletion wasfound in one family (F)

      KindredID: F

      GroupSize: 8

      DiseaseAssertion: VHL

      GroupNumberMales: N/A

      GroupNumberFemales: N/A

      GroupEthnicity: N/A

      GroupAgeRange: N/A

      GroupInfo: In family F, 8 patients were diagnosed with VHL disease. A deletion in the VHL gene was found in this family that confirmed their diagnosis of VHL disease. However, the specific deletion is not reported and no information regarding genotyping methodology is given.

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

      GroupHPOFreeText: In family F, eight individuals are affected with clinical type 1 VHL disease. Phenotypic information is only reported for 2/8 patients, who suffer from cerebellar hemangioblastomas and retinal angiomas. In one of these patients (unspecified whom) the retinal angiomas caused an exudative retinal detachment

      GroupNotHPOs: N/A

      GroupNotHPOFreeText: N/A

      GroupPreviousTesting: N/A

      PreviouslyPublished: N/A

      SupplementalData: N/A

      Variant: deletion Note: specific cDNA change not reported

      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. recognized in a large family that originated in Newfoundland but has some members who live in New Brunswick and Ontario. A collaborative investigation was begun in 1982 to document the number of affected members and the extent of their disease and to improve management of the disease. The condition has been documented in 38 members of the family, 28 living and 10 dead. The most common manifestations are retinal angioma (present in 60% of the gene carriers) and pheochromocytoma (present in 53%). Of the 28 living affected members 14 had been identified before the study began. Only 3 of the 14 patients in whom the disease was subsequently diagnosed presented with symptoms; in the remaining 11 the condition was detected by routine screening. Overall the mean age at the time of diagnosis was 23 years; in the 21 affected members of the fourth generation it was 18 years.

      PatientID: III-2

      KindredID: 1

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

      DiseaseAssertion: Assumed VHL

      FamilyInfo: 38 family members had been affected at the date of 1986, and 10 had passed away. Pheochromocytoma, cerebellar, spinal and retinal hemangioblastomas, and various cysts were clinical manifestations of VHL seen throughout the family. This male (III-2) appears to have inherited this disease from his mother and appears not to have passed it onto his kin thereafter. See Fig. 1 for family pedigree.

      CasePresentingHPOs: HP:0009711 (retinal capillary hemangioma)

      CaseHPOFreeText: Patient had retinal hemangiomas described as “probable”. No further details were provided.

      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: Although never given at the time of this publication, the germline mutation is confirmed in this family in later publications (PMID 7987306; 29437867) for this specific family. It is only here assumed this member had the VHL mutation.

      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

    1. A 42-year-old man came to the emergency department with progressive dyspnea on exertion for 1 month. His medical conditions included type 1 diabetes mellitus (DM), age onset of 25 years old. The chest X-ray revealed a left homogeneous density compatible with pleural effusion. Thoracocentesis was subsequently performed and pleural fluid profile was consistent with metastatic effusion. Computed tomography of the chest and abdomen showed multiple bilateral pulmonary nodules accompanied with significant left pleural effusion and mediastinal lymphadenopathy. A 7.6-cm left renal mass (large arrow) with invasion to the left renal vein and a few small hypodense cysts at the right kidney were also showed along with a 3.4-cm cystic mass at the pancreatic head (small arrow) and diffuse pancreatic cysts with calcification (asterisk) (Figure A). Clear cell renal cell carcinoma was confirmed by renal biopsy. He received palliative treatment with pazopanib. After a meticulous review, he had a history of bilateral scrotal masses that had been diagnosed as benign cysts and underwent cyst removal. Review of ultrasonography of the right testis showed a thick wall cyst with papillary projection (asterisk) and some calcifications (Figure B). In addition, a solid mass with multiple tiny cysts resembling ductal ectasia of the rete testis was also found (Figure B). The similar sonographic findings were found at the left testis.

      PatientID: N/A

      KindredID: 1

      Case: M, 42Y0M, Ethnicity Unknown

      DiseaseAssertion: Assumed VHL

      FamilyInfo: Family history revealed an intracranial tumor in his brother, father, and grandfather.

      CasePresentingHPOs: HP:0006770; HP:0009715 (Clear cell renal cell carcinoma; Papillary cystadenoma of the epididymis)

      CaseHPOFreeText: Patient came to the emergency department at 42Y0M with progressive dyspnea on exertion for 1 month. X-ray revealed pleural effusion, thus thoracocentesis was performed. CT scan revealed a mass consistent with clear cell renal cell carcinoma, confirmed by a renal biopsy. He received palliative treatment with pazopanib. He previously had bilateral scrotal masses that were identified as benign cysts and surgically removed. Ultrasonogrophy of both testes revealed bilateral papillary cystadenomas of the epididymis (PCEs). Patient was previously diagnosed with diabetes mellitus (DM) at age 25. It was noted that the cause of insulin-dependent DM may be from chronic pancreatitis, rather than type 1 DM.

      CaseNotHPOs: N/A

      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

    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 3158 was found with c.180delG mutation in the VHL gene (legacy notation c.393delG converted to NM_000551.3): 1/4 had pheochromocytoma, 3/4 had renal cell carcinoma, 4/4 had CNS hemangioblastoma, 2/4 had retinal angiomas, 2/4 had cysts and pancreatic neuroendocrine tumor was present in the family (number of PNET cases not described).

    1. Twelve (75%) of 16 gene carriers were found to have ocular hemangioblastomas(Figure 1 and Figure 2), and 7 of these had bilateral disease (Table 1). The mean number of angiomas was 3.3. However, 1 individual had 22 angiomas, most of which were in an area of previous exudative retinal detachment (see the "Comment" section) (Table 2). Exclusion of this individual resulted in a mean number of angiomas of 2.1. Six eyes had optic disc angiomas (Figure 2). Six of the 19 eyes with ocular hemangioblastomas had visual acuity less than 20/40. Two patients had no light perception in one or both eyes. The average age at diagnosis of ocular angiomatosis was 37 years.

      PatientID: 7

      KindredID: 1

      Case: Sex Unknown, 42Y0M, Ethnicity Unknown

      DiseaseAssertion: VHL

      FamilyInfo: Significant family history. Pedigree follows 8 generations (see Figure 3). Family immigrated to Iowa, US, from Baden-Baden, Germany, in 1832; Likely sharing a common ancestor to the traced lineage of the Black Forest region of Germany.

      CasePresentingHPOs:; HP:0009711 (retinal capillary hemangioma)

      CaseHPOFreeText: 41Y at first ocular angioma (retinal capillary hemangioma).

      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.Y98H (c.292T>C)

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

      CaseProblemVariantFreeText: N/A

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

      CAID: N/A

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

      VariantEvidence: N/A

      MutationType: missense_variant;transition

      CivicName: Y98H (c.292T>C)

      MultipleGeneVariants: N/A

    1. 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: 11

      KindredID: 11

      Case: F, 28Y0M, Ethnicity unknown

      DiseaseAssertion: pancreatic endocrine tumor

      FamilyInfo: None

      CasePresentingHPOs: HP:0030405 (pancreatic endocrine tumor)

      CaseHPOFreeText: See Table 1 for more information

      CaseNotHPOs: N/A

      CaseNotHPOFreeText: N/A

      CasePreviousTesting: N/A

      PreviouslyPublished: N/A

      SupplementalData: N/A

      Variant: c.463+1G>A

      CaseProblemVariantFreeText: N/A

      LegacyVariant: N/A

      ClinVarID: 526679 https://www.ncbi.nlm.nih.gov/clinvar/variation/526679/

      CAID: CA16621909 http://reg.clinicalgenome.org/redmine/projects/registry/genboree_registry/allele?hgvsOrDescriptor=NM_000551.3%3Ac.463%2B1G%3EA

      gnomAD: N/A

      VariantEvidence: N/A

      MutationType: splice_site_variant

      CivicName: c.463+1G>A

      MultipleGeneVariants: N/A

    1. PatientID: None

      KindredID: 215

      Case: Age unknown, Sex unknown, Ethnicity unknown

      DiseaseAssertion: assumed VHL

      FamilyInfo: Paper states familial VHL

      CasePresentingHPOs: HP:0005584 (renal cell carcinoma)

      CaseHPOFreeText: N/A

      CaseNotHPOs: N/A

      CaseNotHPOFreeText: N/A

      CasePreviousTesting: N/A

      PreviouslyPublished: N/A

      SupplementalData: Yes (Specifically Supp. Table S2)

      Variant: Exon 1-2 Deletion (c.1-?_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 1-2 Deletion

      MultipleGeneVariants: N/A

    1. Patients from a single kindred with a VHL germline deletion were studied (Fig 1).

      An unspecified germline deletion in the VHL gene were found in three members of the same kindred and were demonstrated by FISH analysis. No VHL-associated visceral malignancies were found in any of the patients. The proband inherited the deletion from her father and paternal grandmother and passed the mutation to her daughter. However, no phenotypic data was provided for these familials. The proband presented with 2 cerebellar hemangioblastomas, both operated on at the age of 57. The proband's sister was found to have this deletion and presented with a C6 hemangioblastoma and a TH2 hemangioblastoma. The cervical spinal level was operated on at age 33 and the thoracic spinal level at age 34. Lastly the proband's niece also had the VHL deletion and presented with a brainstem hemangioblastomas that was operated on at the age of 57. The nature of the familial germline deletion not specified in further detail. All 5 hemangioblastoma tumors were analyzed for somatic mutations, and found (second hit in each tumor). The somatic mutations are as follows: p.K159E (c.475A>G); p.N131Y (c.391A>T); p.L89R (c.266T>G); p.E16D (c.48G>T) OR, c.8678 (p.Lys159Glu); c.5442A>T (p.Asn131Tyr); c.980T>G (p.Leu89Arg); c.762G>T (p.Glu16Asp); and an unspecified c.903_904insT; via Latif et al.’s (1993) old transcript) - used in paper. ACMG evidence codes: 'PP1' since there is cosegregation with disease in multiple affected family members, 'PP4' since the patient presents phenotypes highly specific for a disease with a single genetic etiology.

    1. c.499 C > T R167W 

      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 with a germline missense mutation (c.499C>T; p.Arg167Trp) in the VHL gene was diagnosed at age 43 with brainstem hemangioblastoma. The patient has positive family history for VHL disease.

    2. Polymerase chain reaction (PCR) amplification of DNA from both PB and tumor tissue was performed for the entire VHL coding sequence and the promoter region, including exon-intron boundaries. The set of primers is original (Table 2). Amplifications were performed in a Gene Amp PCR System 9700 (Perkin Elmer, Foster City, CA) in a final reaction volume of 25 µL, containing 100 ng of genomic DNA template, 0.25 nmol/L dNTPs, 20 pmol of each primer, and 1 U HotMaster Taq polymerase (Eppendorf, Milan, Italy) in 10 × PCR Reaction Buffer. Polymerase chain reaction cycling conditions consisted of an initial denaturation step at 94°C for 2 minutes, followed by 35 cycles with denaturation at 94°C for 30 seconds, annealing at the specific temperature for 30 seconds, elongation step at 72°C for 30 seconds, and a final elongation step at 72°C for 10 minutes. Polymerase chain reaction products were purified using GFX PCR DNA and Gel Band Purification Kit (GE Healthcare, Buckinghamshire, UK) and sequenced. Sequencing reactions were performed in 10 µL of final volume using 3.2 pmol of primer, 4 to 6 ng of DNA template, and 1 µL of 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). Once mutations in the DNA from the tumor samples had been detected, we searched for the same mutations in the corresponding PB to identify germline mutations.

      ArticleReferenceSequence: NM_000551.2

      GenotypingMethod: PCR was used to purify products and subsequently 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).

      SamplingMethod: tissue resection and peripheral blood

    1. MATERIALS AND METHODS

      ArticleReferenceSequence: Not specified – Assumption: variants assumed to have been documented by the author under reference sequence NM_000551.3 (variant for patient 2 has been documented by the authors under the reference sequence AF010238.1 (Latif et al.) and has been annotated after lift-over under NM_000551.3)

      GenotypingMethod: N/A

      SamplingMethod: N/A

    1. patients with VHL disease (Figs. 1 and 2, and Table 1)

      PatientID: 3

      KindredID: 2

      Case: F, 69Y0M, Arab

      DiseaseAssertion: VHL

      FamilyInfo: No family history of VHL disease was described for this patient. Immediate family members were recommended to genetically test for the relevant variant or monitor for VHL-related symptoms.

      CasePresentingHPOs: HP:0006770; HP:0006880; HP:0009713; HP:0000107; HP:0001737 (clear cell renal cell carcinoma; cerebellar hemangioblastoma; spinal hemangioblastoma; renal cyst; pancreatic cysts)

      CaseHPOFreeText: At 63Y, Patient 3 had a left radical nephrectomy for renal cell carcinoma. She also had multiple pancreatic and right renal cysts. At 67Y, Patient 3 exhibited cerebellar and spinal hemangioblastomas, renal cell carcinoma, and cysts in kidneys and pancreas. She was diagnosed with VHL disease. Two years later, had a right radical nephrectomy for renal cell carcinoma. Her entire pancreas was covered with cysts (see table 1).

      CaseNotHPOs: HP:0002088; HP:0001392; HP:0005264; HP:0001743 (abnormal lung morphology; abnormality of the liver; abnormality of the gallbladder; abnormality of the spleen)

      CaseNotHPOFreeText: No lesions were observed in the lungs, liver, gallbladder, and spleen.

      CasePreviousTesting: N/A

      PreviouslyPublished: N/A

      SupplementalData:  N/A

      Variant: p.I151T (c.452T>C)

      LegacyVariant: N/A

      CaseProblemVariantFreeText: N/A

      ClinVarID: 428803, www.ncbi.nlm.nih.gov/clinvar/variation/428803/

      CAID: N/A

      gnomAD: N/A

      VariantEvidence: N/A

      MutationType: missense_variant; transition

      CivicName: I151T (c.452T>C)

      MultipleGeneVariants: N/A

    1. PatientID: V-39

      KindredID: 2

      Case: F, Age Unknown, German

      DiseaseAssertion: VHL (Asymptomatic)

      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: N/A

      CaseHPOFreeText: N/A

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

      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. We used a multi-array and Meso-Scale Discovery (MSD) technology to detect and quantify the levels of phosphorylated and non-phosphorylated intracellular kinase proteins of the PI3K-AKT-mTOR pathway. In all tumor regions, there was evidence of either S6K or 4EPB1 phosphorylation, consistent with pathway activation, relative to normal kidney from each side (Figure 5). In particular, S6K was phosphorylated in the tumor regions harboring the L2427P MTOR mutation. Additionally, immunohistochemical analysis of the mTOR substrates S6K and 4E-BP1 in all tumor regions revealed enhanced staining of either or both substrates relative to normal kidney in a pattern consistent with the proteomic data (Additional file 1: Table S3; Additional file 7). This is in contrast to absent staining of S6K and 4E-BP1 in MTOR wild-type tumor regions in a ccRCC previously reported [11]. We conclude that all tumors displayed functional convergence of mTOR pathway activation, despite distinct evolutionary somatic routes. Tumor four (harboring the FAT domain mutation) demonstrated markedly elevated phosphorylation of AKT, to a similar extent as induced in tumor three (harboring the kinase domain mutation). However, in tumor four there was increased phosphorylation of 4E-BP1 but not of S6K. Absent S6K phosphorylation would appear to be consistent with the lack of an activating mutation in mTOR in this region described earlier. There is evidence indicating that 4E-BP1 is regulated independently of S6K and it remains unclear whether the effect of AKT signaling on 4E-BP1 is wholly integrated by mTOR, or alternative kinases [30,31].
    1. 41 non-related patients with retinal angiomatosis presenting in the Benjamin Franklin University Eye Clinic between 1988 to 1999 Germany were evaluated for the presence of other VHL lesions. VHL disease was diagnosed clinically in 33 patients based on the presence of other severe VHL lesions (spinal hemangioblastoma 45% prevalence, cerebellar hemangioblastoma 42% prevalence, renal cysts 39% prevalence, pancreatic cyst 39% prevalence, renal carcinoma 18% prevalence, PCC 18% prevalence). Blood samples were taken and analyzed by PCR and single-strand conformational polymorphism (SSCP). VHL germline mutations were identified in 27 out of 29 VHL families screened with molecular genetics. This patient (group 8) with VHL-related retinal angiomatosis was found to have germline missense (c. 233A>G) mutation in the VHL gene. It should be noted that this VHL mutation was stated as c.446A>G in the paper which used the Latif sequence as reference. No other affected family members were described for this patient. Other VHL lesions harbored by the patients were not specified.

    1. VHL promoter variants

      A female 27 year old presented with two right renal masses and several pancreatic cysts at 22Y, as well as a family history of ccRCC. Next generation sequencing and exon level copy number analysis for VHL was performed. VHL gene was found to have 45% mRNA expression levels and western blotting showed 23% protein expression. A heterozygous germline VHL 5' UTR (c.-77_-32del) 45 base pair deletion (including the promoter) was found. The proband was also not found to possess BAP1, CDC73, FH, FLCN, MET, MLH1, MSH2, MSH6, PMS2, PTEN, SDHB, SDHC, SDHD, SMARCB1, TP53,

      TSC1, TSC2, or WT1 mutations. The proband's father, age 45, presented a 2.8cm renal mass and pancreatic cysts. A right nephrectomy was consistent with ccRCC. No evidence of hemangioblastomas was found with brain and spine MRI. The proband’s uncle, age 38, underwent a partial nephrectomy consistent with ccRCC. Segregation analysis returned positive for the variant in both father and uncle.

    1. In our study, group 5 represented the c.262T > C p.Trp88Arg mutation that included 21 patients from 2 families (Figure 4 and Table 3). Variability was observed in the mean age at onset for CHB and RCC, which were 41.1 ± 9.1 (range = 29–62) and 37.4 ± 12.9 (range = 23–65), respectively.

      PatientID: 13

      KindredID: 1 (group ID 5)

      Case: M, 39Y0M, Chinese

      DiseaseAssertion: assumed VHL

      CohortInfo: Clinical characteristics of 258 patients from 80 unrelated Chinese families were reported in this study. Grouped by the 21 mutations found, 2 families with 21 members total were described, and phenotypic information was given for this group.

      FamilyInfo: In family 1, 17 members were described. The first generation describes 5 members with the VHL mutation, each passing on the gene to further generations. Patient 13’s mother and sister had this familial mutation. His son had not been yet tested at the time of the study. See Fig 4 for family pedigree; Table 3 for details.

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

      CaseHPOFreeText: He had hemangioblastoma at 39Y and RCC at 37Y

      CaseNotHPOs: N/A

      CaseNotHPOFreeText: N/A

      CasePreviousTesting: N/A

      PreviouslyPublished: N/A

      SupplementalData: N/A

      Variant: p.W88R (c.262T>C)

      LegacyVariant: N/A

      CaseProblemVariantFreeText: N/A

      ClinVarID: 496053 https://www.ncbi.nlm.nih.gov/clinvar/variation/496053/

      CAID: N/A

      gnomAD: N/A

      VariantEvidence: N/A

      MutationType: missense_variant;transition

      CivicName: W88R (c.262T>C)

      MultipleGeneVariants: N/A

    2. only three VHL lesions (CHB, RCC, and PCT) presented in the c.194C > G p.Ser65Trp mutational subgroup

      GroupID: 1B

      DiseaseAssertion: assumed VHL

      GroupSize: 7

      GroupNumberMales: N/A

      GroupNumberFemales: N/A

      GroupEthnicity: Chinese

      GroupAgeRange: 17-61Y

      GroupInfo: Clinical characteristics of 258 patients from 80 unrelated Chinese families were reported in this study. Grouped by the 21 mutations found, it is unclear how many distinct families are reported in group 1B. 7 individuals were described. Phenotypic information was given for each mutation.

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

      GroupHPOFreeText: 5 of the 7 members presented with CNS hemangioblastoma (mean age of 30.2Y), 4/7 had renal cell carcinoma (mean age of 36.3Y), and pancreatic cysts in 3/7 members (means age of 32.3Y)

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

      GroupNotHPOFreeText: No patients were given with retinal capillary hemangioma, pheochromocytoma, or genital system tumors (epididymis or broad ligament).

      GroupPreviousTesting: N/A

      PreviouslyPublished: 29330336; 28388566

      SupplementalData: N/A

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

      LegacyVariant: N/A

      CaseProblemVariantFreeText: N/A

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

      CAID: N/A

      gnomAD: N/A

      VariantEvidence: N/A

      MutationType: missense_variant; transversion

      CivicName: S65W (c.194C>G)

      MultipleGeneVariants: N/A

    1. 709 G-->T transversion present in all affected subjects and in four presymptomatic children.

      A Jewish-Kurdish family of 25 individuals has 11 members as likely carriers of this missense mutation (V166F (c.496G>T)). It was reported in the paper under "c.709G>T" due to a difference in the use of an older transcript. All but 2 were diagnosed specifically with the mutation, however two members were said to have died of complications of the disease, and although genotype was not established prior, it is assumed that they carried the same VHL mutation. In the family, seven family members have clinical manifestations of VHL disease. All seven family members had pheochromocytomas. Patient II4 had retinal angiomas and renal cysts and patient II7 developed a cerebellar hemangioblastoma at 25 yr after his initial diagnosis of pheochromocytoma, leading to the clinical diagnosis of VHL in the kindred. Four members were under the age of 5 without any manifestations yet (likely pre-symptomatic). This (member) was published in a future publication: PMID: 33471715. As of this publication, several asymptomatic carriers developed a neuroendocrine tumor, 7 new children were born where 3 of them carry the mutation. In addition, 2 patients died, one of which was due to metastatic PNEN-related liver failure. Cosegregation with disease in multiple affected family members in a gene definitively known to cause the disease (ACMG code: PP1).

    1. PMID: 7977367

      PatientID: N/A

      KindredID: 769-P (cell line)

      Case: Sex Unknown, Age Unknown, Ethnicity Unknown

      DiseaseAssertion: Renal cell carcinoma

      FamilyInfo: N/A

      CasePresentingHPOs: HP:0005584 (renal cell carcinoma)

      CaseHPOFreeText: Described as sporadic RCC from cell line 769-P

      CaseNotHPOs: N/A

      CaseNotHPOFreeText: N/A

      CasePreviousTesting: N/A

      PreviouslyPublished: N/A

      SupplementalData: N/A

      Variant: p.I180N (c.539T>A)

      LegacyVariant: p.I251N (c.752T>A)

      CaseProblemVariantFreeText: N/A

      ClinVarID: N/A

      CAID: CA351756277 https://reg.clinicalgenome.org/redmine/projects/registry/genboree_registry/allele?hgvsOrDescriptor=NM_000551.3%3Ac.539T%3EA

      gnomAD: N/A

      VariantEvidence:N/A

      MutationType: missense_variant; transversion

      CivicName: I180N (c.539T>A)

      MultipleGeneVariants: N/A

    1. 36 VHL-related pheochromocytomas (from 21 patients) and 10 VHL-related CNS hemangioblastomas (from 6 patients) were studied using comparative genomic hybridization (CGH) to detect genetic imbalances. The study identified selective loss of chromosome 11 in pheochromocytomas associated with VHL. Patient XIX with VHL-associated pheochromocytoma was found with a germline missense mutation (c.482G>A) in the VHL gene. (stated as c.695G>A in the paper which used the Latif sequence as reference) in the VHL gene. All patients have familial VHL.

    1. 9 Yes Yes Yes Yes Yes

      PatientID: 9

      KindredID: 6

      Case: F, 32Y0M, Ethnicity Unknown

      DiseaseAssertion: VHL

      FamilyInfo: Three total family members presented with this germline variant in VHL. No phenotypes were reported for patients 6 and 7 of this family.

      CohortInfo: A retrospective analysis of case notes of 17 patients was performed for this study. Initially, 23 consecutive patients with VHL disease followed by the Department of Endocrinology at St Bartholomew's Hospital since 1988 were reviewed.

      CasePresentingHPOs: HP:0001732; HP:0000077; HP:0002666; HP:0009711; HP:0010797; HP:0002017; HP:0001082 (Abnormality of the pancreas, Abnormality of the kidney, Pheochromocytoma, Retinal capillary hemangioma, Hemangioblastoma, Nausea and vomiting, Cholecystitis)

      CaseHPOFreeText: This patient developed upper abdominal pain, nausea and vomiting, which was attributed to gallstone cholecystitis based on ultrasound findings. Her symptoms settled on conventional treatment for cholecystitis.

      CaseNotHPOs: N/A

      CaseNotHPOFreeText: N/A

      CasePreviousTesting: N/A

      PreviouslyPublished: N/A

      SupplementalData: N/A

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

      LegacyVariant: c.677T>A

      CaseProblemVariantFreeText: N/A

      ClinVarID: N/A

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

      gnomAD: N/A

      VariantEvidence: Reported as: T677A, assumed to be in Legacy reference sequence (AF010238.1) and mapped to c.464T>A according to NM_000551.3 reference sequence.

      MutationType: missense_variant;transversion

      CivicName: V155E (c.464T>A)

      MultipleGeneVariants: N/A

    1. VHL (c.263G>T; p.W88L)

      A case report revealed a 57Y female caucasian patient presenting with metastatic clear cell renal cell carcinoma, with signs of liver spread, and pelvic and lumbar spinal cord bone metastases. WES (whole-exome sequencing) and Sanger sequencing were performed on peripheral blood, tumor tissue (primary tumor obtained before treatment, in the skull metastasis resected 7 years after temsirolimus treatment initiation). VHL (c.263G>T; p.W88L) and MTOR (c.5920T>C; p.Y1974H) variants were not explicitly stated to be germline in the text but were not present in Supplementary eTable 1 where variants present in tumor/metastasis and absent in blood are listed. The variants affecting genes frequently mutated in ccRCC were detected in all tumor samples analyzed: VHL, BAP1 (c.1359dup; p.E454Rfs*15), and MTOR.

    1. PatientID: VI-1

      KindredID: 1

      Case: F, Age Unknown, Ethnicity Unknown

      DiseaseAssertion: Assumed VHL

      FamilyInfo: 13 affected individuals in this family were found. The p.Tyr112Asn (c.334T>A) mutation of the VHL gene cosegregated with the disease in all five tested affected individuals from the family (V-5, VI-1, VI-2, VI-3, and VII-1). 7/13 have had renal cell carcinoma. Other manifestations of the disease in this family include renal cysts, retinal angioma, and CNS hemangioblastoma. There was one case of pheochromocytoma (VII-1). No other pheochromocytomas or related neuroendocrine tumors of the pancreas or adrenal gland have been diagnosed or recognized retrospectively by review of medical records and recall of relatives. The mutation was also found in three asymptomatic relatives (VII-2, VII-3, and VII-4).

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

      CaseHPOFreeText: CNS hemangioblastoma and RCC. Age of onset not provided.

      CaseNotHPOs: N/A

      CaseNotHPOFreeText: N/A

      CasePreviousTesting: N/A

      PreviouslyPublished: N/A

      SupplementalData: N/A

      Variant: p.Y112N (c.334T>A)

      LegacyVariant: T547A

      CaseProblemVariantFreeText: N/A

      ClinVarID: 2228, https://www.ncbi.nlm.nih.gov/clinvar/variation/2228/

      CAID: N/A

      gnomAD: N/A

      VariantEvidence: Variant is inferred in this patient from clinical findings and family history.

      MutationType: missense_variant;transversion

      CivicName: Y112N (c.334T>A)

      MultipleGeneVariants: N/A