Total submissions: 5
Submitter | RCV | SCV | Clinical significance | Condition | Last evaluated | Review status | Method | Comment |
---|---|---|---|---|---|---|---|---|
Labcorp Genetics |
RCV000206320 | SCV000259524 | pathogenic | Ataxia-telangiectasia syndrome | 2022-10-20 | 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: 219578). This variant has not been reported in the literature in individuals affected with ATM-related conditions. This variant is not present in population databases (gnomAD no frequency). This sequence change creates a premature translational stop signal (p.Leu262*) in the ATM gene. It is expected to result in an absent or disrupted protein product. Loss-of-function variants in ATM are known to be pathogenic (PMID: 23807571, 25614872). |
Counsyl | RCV000206320 | SCV000793316 | likely pathogenic | Ataxia-telangiectasia syndrome | 2017-08-10 | criteria provided, single submitter | clinical testing | |
Revvity Omics, |
RCV000206320 | SCV003818707 | likely pathogenic | Ataxia-telangiectasia syndrome | 2021-12-22 | criteria provided, single submitter | clinical testing | |
Baylor Genetics | RCV003462368 | SCV004216221 | pathogenic | Familial cancer of breast | 2023-12-22 | criteria provided, single submitter | clinical testing | |
Myriad Genetics, |
RCV003462368 | SCV004933694 | pathogenic | Familial cancer of breast | 2024-01-11 | 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. |