Total submissions: 2
Submitter | RCV | SCV | Clinical significance | Condition | Last evaluated | Review status | Method | Comment |
---|---|---|---|---|---|---|---|---|
Ambry Genetics | RCV000561824 | SCV000661586 | pathogenic | Hereditary cancer-predisposing syndrome | 2017-03-20 | criteria provided, single submitter | clinical testing | The c.308delG pathogenic mutation, located in coding exon 3 of the BRIP1 gene, results from a deletion of one nucleotide at nucleotide position 308, causing a translational frameshift with a predicted alternate stop codon (p.G103Efs*54). This alteration is expected to result in loss of function by premature protein truncation or nonsense-mediated mRNA decay. As such, this alteration is interpreted as a disease-causing mutation. |
Labcorp Genetics |
RCV001858090 | SCV002229833 | pathogenic | Familial cancer of breast; Fanconi anemia complementation group J | 2022-02-19 | criteria provided, single submitter | clinical testing | For these reasons, this variant has been classified as Pathogenic. ClinVar contains an entry for this variant (Variation ID: 479468). This variant has not been reported in the literature in individuals affected with BRIP1-related conditions. This variant is not present in population databases (gnomAD no frequency). This sequence change creates a premature translational stop signal (p.Gly103Glufs*54) in the BRIP1 gene. It is expected to result in an absent or disrupted protein product. Loss-of-function variants in BRIP1 are known to be pathogenic (PMID: 16116423, 17033622, 21964575). |