Total submissions: 2
Submitter | RCV | SCV | Clinical significance | Condition | Last evaluated | Review status | Method | Comment |
---|---|---|---|---|---|---|---|---|
Gene |
RCV000255777 | SCV000322571 | likely pathogenic | not provided | 2017-03-10 | criteria provided, single submitter | clinical testing | This apparently mosaic deletion of two nucleotides is denoted APC c.508_509delGA at the cDNA leveland p.Asp170Ter (D170X) at the protein level. The normal sequence, with the bases that are deleted in braces, isAATA{GA}TAGT. The deletion creates a nonsense variant, which changes an Aspartic Acid to a premature stop codon.Although this variant has not been previously reported to our knowledge, it is predicted to cause loss of normal proteinfunction through either protein truncation or nonsense-mediated mRNA decay, and is considered likely pathogenic. |
Labcorp Genetics |
RCV004563294 | SCV000822771 | pathogenic | Familial adenomatous polyposis 1 | 2018-03-05 | criteria provided, single submitter | clinical testing | For these reasons, this variant has been classified as Pathogenic. Loss-of-function variants in APC are known to be pathogenic (PMID: 17963004, 20685668). This variant has been reported in an individual affected with familial adenomatous polyposis and papillary thyroid carcinoma (PMID: 27623068). ClinVar contains an entry for this variant (Variation ID: 265581). This variant is not present in population databases (ExAC no frequency). This sequence change creates a premature translational stop signal (p.Asp170*) in the APC gene. It is expected to result in an absent or disrupted protein product. |