Total submissions: 3
Submitter | RCV | SCV | Clinical significance | Condition | Last evaluated | Review status | Method | Comment |
---|---|---|---|---|---|---|---|---|
Mendelics | RCV002249280 | SCV002518536 | pathogenic | Familial cancer of breast | 2022-05-04 | criteria provided, single submitter | clinical testing | |
Ambry Genetics | RCV002325713 | SCV002606672 | pathogenic | Hereditary cancer-predisposing syndrome | 2020-08-20 | criteria provided, single submitter | clinical testing | The p.Q1116* pathogenic mutation (also known as c.3346C>T), located in coding exon 22 of the ATM gene, results from a C to T substitution at nucleotide position 3346. This changes the amino acid from a glutamine to a stop codon within coding exon 22. 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. |
Labcorp Genetics |
RCV003500691 | SCV004332079 | pathogenic | Ataxia-telangiectasia syndrome | 2023-10-13 | criteria provided, single submitter | clinical testing | This sequence change creates a premature translational stop signal (p.Gln1116*) 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: 1685553). For these reasons, this variant has been classified as Pathogenic. |