Total submissions: 4
Submitter | RCV | SCV | Clinical significance | Condition | Last evaluated | Review status | Method | Comment |
---|---|---|---|---|---|---|---|---|
Labcorp Genetics |
RCV000690554 | SCV000818242 | pathogenic | Fanconi anemia complementation group O | 2023-09-20 | 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: 569830). This variant has not been reported in the literature in individuals affected with RAD51C-related conditions. This variant is not present in population databases (gnomAD no frequency). This sequence change creates a premature translational stop signal (p.Glu67*) in the RAD51C gene. It is expected to result in an absent or disrupted protein product. Loss-of-function variants in RAD51C are known to be pathogenic (PMID: 20400964, 21990120, 24800917, 29278735). |
Ambry Genetics | RCV002422492 | SCV002717718 | pathogenic | Hereditary cancer-predisposing syndrome | 2017-04-14 | criteria provided, single submitter | clinical testing | The p.E67* pathogenic mutation (also known as c.199G>T), located in coding exon 2 of the RAD51C gene, results from a G to T substitution at nucleotide position 199. This changes the amino acid from a glutamic acid to a stop codon within coding exon 2. 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. |
Myriad Genetics, |
RCV004025057 | SCV004931503 | pathogenic | Breast-ovarian cancer, familial, susceptibility to, 3 | 2024-01-02 | criteria provided, single submitter | clinical testing | This variant is considered pathogenic. This variant creates a termination codon and is predicted to result in premature protein truncation. |
German Consortium for Hereditary Breast and Ovarian Cancer, |
RCV000785445 | SCV000924017 | pathogenic | Ovarian neoplasm | 2018-12-01 | no assertion criteria provided | research |