Total submissions: 4
Submitter | RCV | SCV | Clinical significance | Condition | Last evaluated | Review status | Method | Comment |
---|---|---|---|---|---|---|---|---|
Labcorp Genetics |
RCV002833587 | SCV003214122 | pathogenic | Ataxia-telangiectasia syndrome | 2024-12-04 | criteria provided, single submitter | clinical testing | This sequence change creates a premature translational stop signal (p.Trp2769Glyfs*37) 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). This variant is not present in population databases (gnomAD no frequency). This variant has not been reported in the literature in individuals affected with ATM-related conditions. ClinVar contains an entry for this variant (Variation ID: 2008065). For these reasons, this variant has been classified as Pathogenic. |
Baylor Genetics | RCV003464607 | SCV004213960 | likely pathogenic | Familial cancer of breast | 2021-11-11 | criteria provided, single submitter | clinical testing | |
Ambry Genetics | RCV004064928 | SCV005020530 | pathogenic | Hereditary cancer-predisposing syndrome | 2024-02-28 | criteria provided, single submitter | clinical testing | The c.8305delT pathogenic mutation, located in coding exon 56 of the ATM gene, results from a deletion of one nucleotide at nucleotide position 8305, causing a translational frameshift with a predicted alternate stop codon (p.W2769Gfs*37). This alteration is expected to result in loss of function by premature protein truncation or nonsense-mediated mRNA decay. This variant is considered to be rare based on population cohorts in the Genome Aggregation Database (gnomAD). As such, this alteration is interpreted as a disease-causing mutation. |
Fulgent Genetics, |
RCV005045006 | SCV005680927 | likely pathogenic | Familial cancer of breast; Ataxia-telangiectasia syndrome | 2024-01-23 | criteria provided, single submitter | clinical testing |