Total submissions: 3
Submitter | RCV | SCV | Clinical significance | Condition | Last evaluated | Review status | Method | Comment |
---|---|---|---|---|---|---|---|---|
Consortium of Investigators of Modifiers of BRCA1/2 |
RCV000258303 | SCV000327384 | pathogenic | Breast-ovarian cancer, familial, susceptibility to, 2 | 2015-10-02 | criteria provided, single submitter | clinical testing | |
Gene |
RCV000486311 | SCV000569285 | pathogenic | not provided | 2018-05-29 | criteria provided, single submitter | clinical testing | This variant is denoted BRCA2 c.631+2T>A or IVS7+2T>A and consists of a T>A nucleotide substitution at the +2 position of intron 7 of the BRCA2 gene. Using alternate nomenclature, this variant would be defined as BRCA2 859+2T>A. This variant destroys a canonical splice donor site and is predicted to cause abnormal gene splicing, leading to either an abnormal message that is subject to nonsense-mediated mRNA decay or to an abnormal protein product. While BRCA2 c.631+2T>A has not, to our knowledge, been reported in the literature, another variant at the same position, BRCA2 c.631+2T>G, has been observed in individuals with hereditary breast and/or ovarian cancer syndrome, with functional studies revealing impacts on splicing and protein expression (Pyne 2000, Biswas 2011, Wong-Brown 2015). Based on the current evidence, we consider BRCA2 c.631+2T>A to be pathogenic. |
Counsyl | RCV000258303 | SCV000785355 | likely pathogenic | Breast-ovarian cancer, familial, susceptibility to, 2 | 2017-07-11 | criteria provided, single submitter | clinical testing |