Total submissions: 4
Submitter | RCV | SCV | Clinical significance | Condition | Last evaluated | Review status | Method | Comment |
---|---|---|---|---|---|---|---|---|
University of Washington Department of Laboratory Medicine, |
RCV000210089 | SCV000266009 | pathogenic | Colorectal cancer, susceptibility to | 2015-11-20 | criteria provided, single submitter | clinical testing | |
Myriad Genetics, |
RCV004563140 | SCV004043245 | pathogenic | Familial adenomatous polyposis 1 | 2023-04-26 | criteria provided, single submitter | clinical testing | This variant is considered pathogenic. This variant creates a termination codon and is predicted to result in premature protein truncation. |
Ambry Genetics | RCV004649098 | SCV005141832 | pathogenic | Hereditary cancer-predisposing syndrome | 2024-03-28 | criteria provided, single submitter | clinical testing | The p.Q188* pathogenic mutation (also known as c.562C>T), located in coding exon 5 of the APC gene, results from a C to T substitution at nucleotide position 562. This changes the amino acid from a glutamine to a stop codon within coding exon 5. This alteration has been reported in multiple individuals with colonic polyposis (Ambry internal data; Moisio AL et al. Gut, 2002 Jun;50:845-50; Lagarde A et al. J Med Genet, 2010 Oct;47:721-2; Shirts BH et al. Genet Med, 2016 Oct;18:974-81). This variant is considered to be rare based on population cohorts in the Genome Aggregation Database (gnomAD). In addition to the clinical data presented in the literature, 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. |
Department of Pathology and Laboratory Medicine, |
RCV000501976 | SCV000591040 | uncertain significance | not provided | no assertion criteria provided | clinical testing |