Total submissions: 3
Submitter | RCV | SCV | Clinical significance | Condition | Last evaluated | Review status | Method | Comment |
---|---|---|---|---|---|---|---|---|
Ambry Genetics | RCV000573409 | SCV000670183 | pathogenic | Hereditary cancer-predisposing syndrome | 2017-07-17 | criteria provided, single submitter | clinical testing | The c.394delG variant, located in coding exon 5 of the MUTYH gene, results from a deletion of one nucleotide at nucleotide position 394, causing a translational frameshift with a predicted alternate stop codon (p.V132Sfs*14). 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 |
RCV003614048 | SCV004374960 | pathogenic | Familial adenomatous polyposis 2 | 2023-07-25 | 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: 483932). This variant has not been reported in the literature in individuals affected with MUTYH-related conditions. This variant is not present in population databases (gnomAD no frequency). This sequence change creates a premature translational stop signal (p.Val132Serfs*14) in the MUTYH gene. It is expected to result in an absent or disrupted protein product. Loss-of-function variants in MUTYH are known to be pathogenic (PMID: 18534194, 20663686). |
All of Us Research Program, |
RCV003614048 | SCV004830749 | likely pathogenic | Familial adenomatous polyposis 2 | 2023-11-30 | criteria provided, single submitter | clinical testing |