Total submissions: 3
Submitter | RCV | SCV | Clinical significance | Condition | Last evaluated | Review status | Method | Comment |
---|---|---|---|---|---|---|---|---|
Gene |
RCV000579176 | SCV000680526 | pathogenic | not provided | 2019-11-04 | criteria provided, single submitter | clinical testing | Nonsense variant predicted to result in protein truncation or nonsense mediated decay in a gene for which loss-of-function is a known mechanism of disease; Not observed in large population cohorts (Lek et al., 2016); This variant is associated with the following publications: (PMID: 25525159, 29637653, 26633542, 10814714) |
Labcorp Genetics |
RCV000692634 | SCV000820467 | pathogenic | Wilms tumor 1 | 2022-03-12 | criteria provided, single submitter | clinical testing | For these reasons, this variant has been classified as Pathogenic. ClinVar contains an entry for this variant (Variation ID: 11689). This premature translational stop signal has been observed in individual(s) with Simpson-Golabi-Behmel syndrome (PMID: 10814714). This variant is not present in population databases (gnomAD no frequency). This sequence change creates a premature translational stop signal (p.Arg199*) in the GPC3 gene. It is expected to result in an absent or disrupted protein product. Loss-of-function variants in GPC3 are known to be pathogenic (PMID: 10402475, 12713262, 17603795). |
OMIM | RCV000012455 | SCV000032689 | pathogenic | Simpson-Golabi-Behmel syndrome type 1 | 2000-05-22 | no assertion criteria provided | literature only |