Total submissions: 3
Submitter | RCV | SCV | Clinical significance | Condition | Last evaluated | Review status | Method | Comment |
---|---|---|---|---|---|---|---|---|
Labcorp Genetics |
RCV001057098 | SCV001221574 | pathogenic | not provided | 2023-06-13 | criteria provided, single submitter | clinical testing | For these reasons, this variant has been classified as Pathogenic. ClinVar contains an entry for this variant (Variation ID: 852483). This premature translational stop signal has been observed in individual(s) with breast cancer (PMID: 32051609). This variant is not present in population databases (gnomAD no frequency). This sequence change creates a premature translational stop signal (p.Arg360Valfs*8) in the CTNNA1 gene. It is expected to result in an absent or disrupted protein product. Loss-of-function variants in CTNNA1 are known to be pathogenic (PMID: 32051609, 34425242). |
Myriad Genetics, |
RCV004031799 | SCV004930938 | pathogenic | Hereditary diffuse gastric adenocarcinoma | 2024-02-21 | criteria provided, single submitter | clinical testing | This variant is considered pathogenic. This variant creates a frameshift predicted to result in premature protein truncation. |
Ambry Genetics | RCV004609600 | SCV005103483 | uncertain significance | Hereditary cancer-predisposing syndrome | 2024-05-07 | criteria provided, single submitter | clinical testing | The c.1078_1081delAGAA variant, located in coding exon 7 of the CTNNA1 gene, results from a deletion of 4 nucleotides at nucleotide positions 1078 to 1081, causing a translational frameshift with a predicted alternate stop codon (p.R360Vfs*8). This alteration is expected to result in loss of function by premature protein truncation or nonsense-mediated mRNA decay. The evidence for this gene-disease relationship is limited; therefore, the clinical significance of this alteration is unclear. |