Total submissions: 2
Submitter | RCV | SCV | Clinical significance | Condition | Last evaluated | Review status | Method | Comment |
---|---|---|---|---|---|---|---|---|
Labcorp Genetics |
RCV004565730 | SCV003525888 | pathogenic | Familial adenomatous polyposis 1 | 2022-06-15 | criteria provided, single submitter | clinical testing | This sequence change affects an acceptor splice site in intron 4 of the APC gene. RNA analysis indicates that disruption of this splice site induces altered splicing and may result in an absent or disrupted protein product. This variant is not present in population databases (gnomAD no frequency). Disruption of this splice site has been observed in individuals with familial adenomatous polyposis (PMID: 10598803, 15459959). It has also been observed to segregate with disease in related individuals. Studies have shown that disruption of this splice site results in skipping of exon 5 (also known as exon 4) and introduces a premature termination codon (PMID: 15459959). The resulting mRNA is expected to undergo nonsense-mediated decay. For these reasons, this variant has been classified as Pathogenic. |
Quest Diagnostics Nichols Institute San Juan Capistrano | RCV003477054 | SCV004219371 | pathogenic | not provided | 2022-12-22 | criteria provided, single submitter | clinical testing | This variant disrupts a canonical splice-acceptor site and interferes with normal APC mRNA splicing. This variant has not been reported in large, multi-ethnic general populations (http://gnomad.broadinstitute.org). In the published literature, the variant has been reported in individuals with familial adenomatous polyposis (FAP) (PMID: 15459959 (2004)). Functional analysis demonstrates that this variant causes exon 4 skipping (PMID: 15459959 (2004)). Based on the available information, this variant is classified as pathogenic. |