Total submissions: 2
Submitter | RCV | SCV | Clinical significance | Condition | Last evaluated | Review status | Method | Comment |
---|---|---|---|---|---|---|---|---|
Labcorp Genetics |
RCV000460168 | SCV000545763 | pathogenic | Familial adenomatous polyposis 2 | 2022-05-12 | 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: 406847). 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.Arg36Glyfs*22) 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). |
Ambry Genetics | RCV002379435 | SCV002689323 | pathogenic | Hereditary cancer-predisposing syndrome | 2020-06-17 | criteria provided, single submitter | clinical testing | The c.102delA pathogenic mutation, located in coding exon 2 of the MUTYH gene, results from a deletion of one nucleotide at nucleotide position 102, causing a translational frameshift with a predicted alternate stop codon (p.R36Gfs*22). 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. |