Total submissions: 3
Submitter | RCV | SCV | Clinical significance | Condition | Last evaluated | Review status | Method | Comment |
---|---|---|---|---|---|---|---|---|
Baylor Genetics | RCV001004551 | SCV001163630 | likely pathogenic | Fanconi anemia complementation group C | criteria provided, single submitter | clinical testing | ||
Ambry Genetics | RCV002454254 | SCV002616322 | pathogenic | Hereditary cancer-predisposing syndrome | 2020-02-14 | criteria provided, single submitter | clinical testing | The c.362_363delTA pathogenic mutation, located in coding exon 4 of the FANCC gene, results from a deletion of two nucleotides at nucleotide positions 362 to 363, causing a translational frameshift with a predicted alternate stop codon (p.I121Tfs*7). 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 |
RCV003769405 | SCV004666282 | pathogenic | Fanconi anemia | 2022-12-22 | criteria provided, single submitter | clinical testing | This sequence change creates a premature translational stop signal (p.Ile121Thrfs*7) in the FANCC gene. It is expected to result in an absent or disrupted protein product. Loss-of-function variants in FANCC are known to be pathogenic (PMID: 17924555). For these reasons, this variant has been classified as Pathogenic. ClinVar contains an entry for this variant (Variation ID: 813471). This variant has not been reported in the literature in individuals affected with FANCC-related conditions. This variant is not present in population databases (gnomAD no frequency). |