Total submissions: 5
Submitter | RCV | SCV | Clinical significance | Condition | Last evaluated | Review status | Method | Comment |
---|---|---|---|---|---|---|---|---|
Evidence- |
RCV000661851 | SCV000784176 | pathogenic | Breast-ovarian cancer, familial, susceptibility to, 2 | 2017-12-15 | reviewed by expert panel | curation | Variant allele predicted to encode a truncated non-functional protein. |
Gene |
RCV000487145 | SCV000571655 | pathogenic | not provided | 2016-09-15 | criteria provided, single submitter | clinical testing | This variant is denoted BRCA2 c.5110A>T at the cDNA level and p.Arg1704Ter (R1704X) at the protein level. The substitution creates a nonsense variant, which changes an Arginine to a premature stop codon (AGA>TGA), and is predicted to cause loss of normal protein function through either protein truncation or nonsense-mediated mRNA decay. Although this variant has not, to our knowledge, been reported in the literature, it is considered pathogenic. |
Labcorp Genetics |
RCV001382436 | SCV001581207 | pathogenic | Hereditary breast ovarian cancer syndrome | 2024-06-12 | criteria provided, single submitter | clinical testing | This sequence change creates a premature translational stop signal (p.Arg1704*) in the BRCA2 gene. It is expected to result in an absent or disrupted protein product. Loss-of-function variants in BRCA2 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 ovarian cancer (PMID: 30322717). ClinVar contains an entry for this variant (Variation ID: 422242). For these reasons, this variant has been classified as Pathogenic. |
Ambry Genetics | RCV002350070 | SCV002645539 | pathogenic | Hereditary cancer-predisposing syndrome | 2023-11-22 | criteria provided, single submitter | clinical testing | The p.R1704* pathogenic mutation (also known as c.5110A>T), located in coding exon 10 of the BRCA2 gene, results from an A to T substitution at nucleotide position 5110. This changes the amino acid from an arginine to a stop codon within coding exon 10. This variant was identified in a cohort of 4439 women with ovarian cancer undergoing multigene panel testing at one laboratory (Carter NJ et al. Gynecol Oncol, 2018 12;151:481-488). 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. |
Revvity Omics, |
RCV000487145 | SCV003821052 | likely pathogenic | not provided | 2022-02-08 | criteria provided, single submitter | clinical testing |