Total submissions: 3
Submitter | RCV | SCV | Clinical significance | Condition | Last evaluated | Review status | Method | Comment |
---|---|---|---|---|---|---|---|---|
Gene |
RCV000521866 | SCV000617332 | pathogenic | not provided | 2020-03-06 | 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 2016); This variant is associated with the following publications: (PMID: 24206555, 25525159, 20685668, 22449158, 20649969, 16264375) |
Myriad Genetics, |
RCV004561492 | SCV004043997 | pathogenic | Familial adenomatous polyposis 1 | 2023-05-01 | criteria provided, single submitter | clinical testing | This variant is considered pathogenic. This variant creates a termination codon and is predicted to result in premature protein truncation. |
Labcorp Genetics |
RCV004561492 | SCV004293610 | pathogenic | Familial adenomatous polyposis 1 | 2023-10-29 | criteria provided, single submitter | clinical testing | This sequence change creates a premature translational stop signal (p.Trp421*) in the APC gene. It is expected to result in an absent or disrupted protein product. Loss-of-function variants in APC are known to be pathogenic (PMID: 17963004, 20685668). This variant is not present in population databases (gnomAD no frequency). This premature translational stop signal has been observed in individual(s) with clinical features of familial adenomatous polyposis (PMID: 20685668). ClinVar contains an entry for this variant (Variation ID: 449331). For these reasons, this variant has been classified as Pathogenic. |