Total submissions: 4
Submitter | RCV | SCV | Clinical significance | Condition | Last evaluated | Review status | Method | Comment |
---|---|---|---|---|---|---|---|---|
Centre for Mendelian Genomics, |
RCV000415316 | SCV000492866 | pathogenic | Adenomatous colonic polyposis | 2014-06-17 | criteria provided, single submitter | clinical testing | |
Department of Molecular Diagnostics, |
RCV000755040 | SCV000882860 | pathogenic | Familial adenomatous polyposis 1 | 2018-10-24 | criteria provided, single submitter | clinical testing | |
Clinical Genetics and Genomics, |
RCV001269921 | SCV001450282 | pathogenic | not provided | 2015-06-30 | criteria provided, single submitter | clinical testing | |
Ambry Genetics | RCV004943831 | SCV005467190 | pathogenic | Hereditary cancer-predisposing syndrome | 2024-09-25 | criteria provided, single submitter | clinical testing | The c.4901delC pathogenic mutation, located in coding exon 15 of the APC gene, results from a deletion of one nucleotide at nucleotide position 4901, causing a translational frameshift with a predicted alternate stop codon (p.P1634Rfs*16). This alteration occurs at the 3' terminus of theAPC gene, is not expected to trigger nonsense-mediated mRNA decay, and impacts the last 43% of the protein. However, premature stop codons are typically deleterious in nature and a significant portion of the protein is affected (Ambry internal data). This variant has been observed in at least one individual with a personal and/or family history that is consistent with APC-associated disease (Ambry internal data). This variant is considered to be rare based on population cohorts in the Genome Aggregation Database (gnomAD). Based on the supporting evidence, this variant is interpreted as a disease-causing mutation. |