Total submissions: 2
Submitter | RCV | SCV | Clinical significance | Condition | Last evaluated | Review status | Method | Comment |
---|---|---|---|---|---|---|---|---|
Women's Health and Genetics/Laboratory Corporation of America, |
RCV000549585 | SCV000697525 | pathogenic | Von Hippel-Lindau syndrome | 2016-02-04 | criteria provided, single submitter | clinical testing | |
Labcorp Genetics |
RCV001388392 | SCV001589362 | pathogenic | Chuvash polycythemia; Von Hippel-Lindau syndrome | 2020-05-03 | criteria provided, single submitter | clinical testing | This sequence change results in a premature translational stop signal in the VHL gene (p.Tyr175*). While this is not anticipated to result in nonsense mediated decay, it is expected to disrupt the last 39 amino acids of the VHL protein. For these reasons, this variant has been classified as Pathogenic. This variant disrupts the C-terminus of the elongin C binding domain (PMID: 14987375), which is required for protein stability and tumor suppressive activity (PMID: 9447969, 10900011). Other variants that disrupt this region (p.Tyr185*) have been determined to be pathogenic (PMID: 23298237, 7987306). This suggests that variants that disrupt this region of the protein are likely to be causative of disease. This variant has been observed in individuals with von Hippel-Lindau (VHL) syndrome (PMID: 9829912, 12202531, 15300849, 27527340). It has also been observed to segregate with disease in related individuals. ClinVar contains an entry for this variant (Variation ID: 182974). This variant is not present in population databases (ExAC no frequency). |