Total submissions: 5
Submitter | RCV | SCV | Clinical significance | Condition | Last evaluated | Review status | Method | Comment |
---|---|---|---|---|---|---|---|---|
Evidence- |
RCV000239167 | SCV000300192 | pathogenic | Breast-ovarian cancer, familial, susceptibility to, 1 | 2016-09-08 | reviewed by expert panel | curation | Variant allele predicted to encode a truncated non-functional protein. |
Quest Diagnostics Nichols Institute San Juan Capistrano | RCV000239167 | SCV000296433 | likely pathogenic | Breast-ovarian cancer, familial, susceptibility to, 1 | 2016-03-05 | criteria provided, single submitter | clinical testing | |
Consortium of Investigators of Modifiers of BRCA1/2 |
RCV000239167 | SCV000326120 | pathogenic | Breast-ovarian cancer, familial, susceptibility to, 1 | 2015-10-02 | criteria provided, single submitter | clinical testing | |
Labcorp Genetics |
RCV000539566 | SCV000636005 | pathogenic | Hereditary breast ovarian cancer syndrome | 2024-10-08 | criteria provided, single submitter | clinical testing | This sequence change creates a premature translational stop signal (p.Thr1684Tyrfs*10) in the BRCA1 gene. It is expected to result in an absent or disrupted protein product. Loss-of-function variants in BRCA1 are known to be pathogenic (PMID: 20104584). This variant is not present in population databases (gnomAD no frequency). This premature translational stop signal has been observed in individual(s) with BRCA1-related conditions (PMID: 21520333). ClinVar contains an entry for this variant (Variation ID: 252385). RNA analysis performed to evaluate the impact of this premature translational stop signal on mRNA splicing indicates it does not significantly alter splicing (internal data). For these reasons, this variant has been classified as Pathogenic. |
Ambry Genetics | RCV000565393 | SCV000661123 | pathogenic | Hereditary cancer-predisposing syndrome | 2021-08-09 | criteria provided, single submitter | clinical testing | The c.5050_5051delAC pathogenic mutation, located in coding exon 15 of the BRCA1 gene, results from a deletion of two nucleotides at nucleotide positions 5050 to 5051, causing a translational frameshift with a predicted alternate stop codon (p.T1684Yfs*10). This alteration was identified in a large, worldwide study of BRCA1/2 mutation positive families (Rebbeck TR et al. Hum Mutat, 2018 05;39:593-620). In addition to the clinical data presented in the literature, 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. |