Total submissions: 3
Submitter | RCV | SCV | Clinical significance | Condition | Last evaluated | Review status | Method | Comment |
---|---|---|---|---|---|---|---|---|
Eurofins Ntd Llc |
RCV000404768 | SCV000342952 | pathogenic | not provided | 2016-06-30 | criteria provided, single submitter | clinical testing | |
Genomic Diagnostic Laboratory, |
RCV000767266 | SCV000897817 | pathogenic | Von Hippel-Lindau syndrome | 2018-08-01 | criteria provided, single submitter | clinical testing | |
Labcorp Genetics |
RCV001859684 | SCV002238994 | pathogenic | Chuvash polycythemia; Von Hippel-Lindau syndrome | 2024-01-13 | criteria provided, single submitter | clinical testing | This sequence change creates a premature translational stop signal (p.Gln132*) in the VHL gene. It is expected to result in an absent or disrupted protein product. Loss-of-function variants in VHL are known to be pathogenic (PMID: 8956040, 12202531). This variant is not present in population databases (gnomAD no frequency). This premature translational stop signal has been observed in individual(s) with von Hippel-Lindau syndrome (PMID: 8707293). This variant is also known as c.607C>T. ClinVar contains an entry for this variant (Variation ID: 288749). Algorithms developed to predict the effect of sequence changes on RNA splicing suggest that this variant may disrupt the consensus splice site. For these reasons, this variant has been classified as Pathogenic. |