Total submissions: 3
Submitter | RCV | SCV | Clinical significance | Condition | Last evaluated | Review status | Method | Comment |
---|---|---|---|---|---|---|---|---|
Counsyl | RCV000409497 | SCV000486473 | likely pathogenic | Ataxia-telangiectasia syndrome | 2016-06-07 | criteria provided, single submitter | clinical testing | |
Color Diagnostics, |
RCV000583031 | SCV000687397 | pathogenic | Hereditary cancer-predisposing syndrome | 2020-05-13 | criteria provided, single submitter | clinical testing | This variant deletes 2 nucleotides in exon 17 of the ATM gene, creating a frameshift and premature translation stop signal. This variant is expected to result in an absent or non-functional protein product. To our knowledge, this variant has not been reported in individuals affected with hereditary cancer in the literature. This variant has not been identified in the general population by the Genome Aggregation Database (gnomAD). Loss of ATM function is a known mechanism of disease (clinicalgenome.org). Based on the available evidence, this variant is classified as Pathogenic. |
Labcorp Genetics |
RCV000409497 | SCV004250190 | pathogenic | Ataxia-telangiectasia syndrome | 2023-12-15 | criteria provided, single submitter | clinical testing | This sequence change creates a premature translational stop signal (p.Ala869Glufs*14) 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: 371020). For these reasons, this variant has been classified as Pathogenic. |