Total submissions: 4
Submitter | RCV | SCV | Clinical significance | Condition | Last evaluated | Review status | Method | Comment |
---|---|---|---|---|---|---|---|---|
Institute of Medical Genetics and Applied Genomics, |
RCV001268810 | SCV001447998 | pathogenic | not provided | 2020-10-23 | criteria provided, single submitter | clinical testing | |
Labcorp Genetics |
RCV004562120 | SCV003525739 | pathogenic | Familial adenomatous polyposis 1 | 2022-04-15 | criteria provided, single submitter | clinical testing | For these reasons, this variant has been classified as Pathogenic. This variant is also known as 1866 TAC-TAG; Tyr-Stop. This premature translational stop signal has been observed in individual(s) with familial adenomatous polyposis (PMID: 11247896, 33654310). This variant is not present in population databases (gnomAD no frequency). This sequence change creates a premature translational stop signal (p.Tyr622Glyfs*7) 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). |
Myriad Genetics, |
RCV004562120 | SCV004044709 | pathogenic | Familial adenomatous polyposis 1 | 2023-05-03 | criteria provided, single submitter | clinical testing | This variant is considered pathogenic. This variant creates a frameshift predicted to result in premature protein truncation. |
Gene |
RCV001268810 | SCV005201641 | pathogenic | not provided | 2023-09-21 | criteria provided, single submitter | clinical testing | Frameshift 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 at significant frequency in large population cohorts (gnomAD); Also known as 1863delTTAC; This variant is associated with the following publications: (PMID: 33654310, 35968980, 11247896) |