Total submissions: 3
Submitter | RCV | SCV | Clinical significance | Condition | Last evaluated | Review status | Method | Comment |
---|---|---|---|---|---|---|---|---|
Ambry Genetics | RCV000166762 | SCV000217575 | likely pathogenic | Hereditary cancer-predisposing syndrome | 2019-08-06 | criteria provided, single submitter | clinical testing | The c.2493-1G>C intronic variant, results from a G to C one nucleotide upstream from coding exon 17 of the BRIP1 gene. This nucleotide position is highly conserved in available vertebrate species. In one study, this alteration was observed in 1/3236 cases with invasive epithelial ovarian cancer and 0/3431 controls (Ramus SJ et al. J. Natl. Cancer Inst. 2015 Nov;107:). Using the BDGP and ESEfinder splice site prediction tools, this alteration is predicted to abolish the native acceptor splice site; however, direct evidence is unavailable. Alterations that disrupt the canonical splice site are expected to cause aberrant splicing, resulting in an abnormal protein or a transcript that is subject to nonsense-mediated mRNA decay. As such, this alteration is classified as likely pathogenic. |
Myriad Genetics, |
RCV003335166 | SCV004043041 | likely pathogenic | Familial cancer of breast | 2023-06-07 | criteria provided, single submitter | clinical testing | This variant is considered likely pathogenic. This variant occurs within a consensus splice junction and is predicted to result in abnormal mRNA splicing of either an out-of-frame exon or an in-frame exon necessary for protein stability and/or normal function. |
Laboratory for Genotyping Development, |
RCV003162712 | SCV002758227 | pathogenic | Gastric cancer | 2021-07-01 | no assertion criteria provided | research |