Total submissions: 3
Submitter | RCV | SCV | Clinical significance | Condition | Last evaluated | Review status | Method | Comment |
---|---|---|---|---|---|---|---|---|
Ambry Genetics | RCV001018402 | SCV001179636 | pathogenic | Hereditary cancer-predisposing syndrome | 2019-08-21 | criteria provided, single submitter | clinical testing | The c.3064dupA pathogenic mutation, located in coding exon 9 of the BRCA1 gene, results from a duplication of A at nucleotide position 3064, causing a translational frameshift with a predicted alternate stop codon (p.T1022Nfs*6). This variant was identified in 1/2733 women aged 40 years or younger at first diagnosis of invasive breast cancer (Copson ER et al. Lancet Oncol., 2018 02;19:169-180). 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. |
Labcorp Genetics |
RCV000496552 | SCV003260942 | pathogenic | Hereditary breast ovarian cancer syndrome | 2021-12-21 | criteria provided, single submitter | clinical testing | For these reasons, this variant has been classified as Pathogenic. Algorithms developed to predict the effect of sequence changes on RNA splicing suggest that this variant may create or strengthen a splice site. ClinVar contains an entry for this variant (Variation ID: 431240). This variant has not been reported in the literature in individuals affected with BRCA1-related conditions. This variant is not present in population databases (gnomAD no frequency). This sequence change creates a premature translational stop signal (p.Thr1022Asnfs*6) 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). |
Research Molecular Genetics Laboratory, |
RCV000496552 | SCV000587278 | pathogenic | Hereditary breast ovarian cancer syndrome | 2014-01-31 | no assertion criteria provided | research |