Total submissions: 2
Submitter | RCV | SCV | Clinical significance | Condition | Last evaluated | Review status | Method | Comment |
---|---|---|---|---|---|---|---|---|
Labcorp Genetics |
RCV001207027 | SCV001378364 | pathogenic | Fanconi anemia complementation group O | 2019-08-16 | criteria provided, single submitter | clinical testing | This variant is not present in population databases (ExAC no frequency). This sequence change creates a premature translational stop signal (p.Gly189*) in the RAD51C gene. It is expected to result in an absent or disrupted protein product. This variant has not been reported in the literature in individuals with RAD51C-related conditions. For these reasons, this variant has been classified as Pathogenic. Loss-of-function variants in RAD51C are known to be pathogenic (PMID: 20400964, 21990120, 24800917). Algorithms developed to predict the effect of sequence changes on RNA splicing suggest that this variant may create or strengthen a splice site, but this prediction has not been confirmed by published transcriptional studies. |
Ambry Genetics | RCV002348676 | SCV002652380 | pathogenic | Hereditary cancer-predisposing syndrome | 2018-08-03 | criteria provided, single submitter | clinical testing | The p.G189* pathogenic mutation (also known as c.565G>T), located in coding exon 3 of the RAD51C gene, results from a G to T substitution at nucleotide position 565. This changes the amino acid from a glycine to a stop codon within coding exon 3. 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. |