Total submissions: 3
Submitter | RCV | SCV | Clinical significance | Condition | Last evaluated | Review status | Method | Comment |
---|---|---|---|---|---|---|---|---|
Labcorp Genetics |
RCV001975157 | SCV002243339 | pathogenic | Ataxia-telangiectasia syndrome | 2021-02-11 | criteria provided, single submitter | clinical testing | For these reasons, this variant has been classified as Pathogenic. This variant has not been reported in the literature in individuals with ATM-related conditions. This variant is not present in population databases (ExAC no frequency). This sequence change creates a premature translational stop signal (p.Phe1445Leufs*5) 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). |
Ambry Genetics | RCV002331535 | SCV002633125 | pathogenic | Hereditary cancer-predisposing syndrome | 2019-10-04 | criteria provided, single submitter | clinical testing | The c.4335_4338delTGTT pathogenic mutation, located in coding exon 28 of the ATM gene, results from a deletion of 4 nucleotides at nucleotide positions 4335 to 4338, causing a translational frameshift with a predicted alternate stop codon (p.F1445Lfs*5). This alteration is expected to result in loss of function by premature protein truncation or nonsense-mediated mRNA decay. As such, this alteration is interpreted as a disease-causing mutation. |
Myriad Genetics, |
RCV004044395 | SCV004933707 | pathogenic | Familial cancer of breast | 2024-01-24 | criteria provided, single submitter | clinical testing | This variant is considered pathogenic. This variant creates a frameshift predicted to result in premature protein truncation. |