Total submissions: 4
Submitter | RCV | SCV | Clinical significance | Condition | Last evaluated | Review status | Method | Comment |
---|---|---|---|---|---|---|---|---|
Consortium of Investigators of Modifiers of BRCA1/2 |
RCV000111705 | SCV000326415 | pathogenic | Breast-ovarian cancer, familial, susceptibility to, 1 | 2015-10-02 | criteria provided, single submitter | clinical testing | |
Ambry Genetics | RCV000509617 | SCV000607774 | pathogenic | Hereditary cancer-predisposing syndrome | 2019-10-09 | criteria provided, single submitter | clinical testing | The c.80+1G>C intronic variant results from a G to C substitution one nucleotide after coding exon 1 of the BRCA1 gene. This nucleotide position is highly conserved in available vertebrate species. Using the BDGP and ESEfinder splice site prediction tools, this alteration is predicted to abolish the native splice donor site; however, direct evidence is unavailable. Similar alterations at this splice donor site through +5 have been shown to cause skipping of coding exon 1 (also known as Exon 2) with resulting loss of the start codon (Ambry internal data; Steffensen AY et al. Eur J Hum Genet. 2014 Dec;22(12):1362-8). One study found that this nucleotide substitution is non-functional in a high throughput genome editing haploid cell survival assay (Findlay GM et al. Nature, 2018 10;562:217-222). In addition to the clinical data presented in the literature, 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 disease-causing mutation. |
Breast Cancer Information Core |
RCV000111705 | SCV000144208 | pathogenic | Breast-ovarian cancer, familial, susceptibility to, 1 | 2004-11-25 | no assertion criteria provided | clinical testing | |
Brotman Baty Institute, |
RCV000111705 | SCV001243697 | not provided | Breast-ovarian cancer, familial, susceptibility to, 1 | no assertion provided | in vitro |