Total submissions: 3
Submitter | RCV | SCV | Clinical significance | Condition | Last evaluated | Review status | Method | Comment |
---|---|---|---|---|---|---|---|---|
Ambry Genetics | RCV002453122 | SCV002739897 | pathogenic | Hereditary cancer-predisposing syndrome | 2021-03-09 | criteria provided, single submitter | clinical testing | The c.265dupA pathogenic mutation, located in coding exon 3 of the FANCC gene, results from a duplication of A at nucleotide position 265, causing a translational frameshift with a predicted alternate stop codon (p.I89Nfs*11). This allele was reported in one heterozygous individual in population-based cohorts in the Genome Aggregation Database (gnomAD). 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 |
RCV003523136 | SCV004337973 | pathogenic | Fanconi anemia | 2023-06-01 | 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: 1794430). This variant has not been reported in the literature in individuals affected with FANCC-related conditions. This variant is present in population databases (rs751757203, gnomAD 0.0009%). This sequence change creates a premature translational stop signal (p.Ile89Asnfs*11) 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). |
Baylor Genetics | RCV004571154 | SCV005057617 | likely pathogenic | Fanconi anemia complementation group C | 2023-12-01 | criteria provided, single submitter | clinical testing |