Total submissions: 2
Submitter | RCV | SCV | Clinical significance | Condition | Last evaluated | Review status | Method | Comment |
---|---|---|---|---|---|---|---|---|
Labcorp Genetics |
RCV002932695 | SCV003260385 | pathogenic | Ataxia-telangiectasia syndrome | 2023-05-22 | criteria provided, single submitter | clinical testing | For these reasons, this variant has been classified as Pathogenic. Studies have shown that this variant results in activation of a cryptic splice site and introduces a premature termination codon (Invitae). The resulting mRNA is expected to undergo nonsense-mediated decay. ClinVar contains an entry for this variant (Variation ID: 2052386). 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 falls in intron 57 of the ATM gene. It does not directly change the encoded amino acid sequence of the ATM protein. RNA analysis indicates that this variant induces altered splicing and may result in an absent or disrupted protein product. |
Ambry Genetics | RCV003170579 | SCV003858411 | uncertain significance | Hereditary cancer-predisposing syndrome | 2022-01-19 | criteria provided, single submitter | clinical testing | The c.8418+704G>T intronic alteration consists of a G to T substitution 04 nucleotides after coding exon 56 in the ATM gene. Based on insufficient or conflicting evidence, the clinical significance of this alteration remains unclear. |