Total submissions: 4
Submitter | RCV | SCV | Clinical significance | Condition | Last evaluated | Review status | Method | Comment |
---|---|---|---|---|---|---|---|---|
Counsyl | RCV000409401 | SCV000487329 | likely pathogenic | Familial adenomatous polyposis 2 | 2015-12-30 | criteria provided, single submitter | clinical testing | |
Color Diagnostics, |
RCV001176292 | SCV001340192 | pathogenic | Hereditary cancer-predisposing syndrome | 2020-01-15 | criteria provided, single submitter | clinical testing | This variant deletes 1 nucleotide in exon 12 of the MUTYH gene, creating a frameshift and premature translation stop signal. This variant is expected to result in an absent or non-functional protein product. This variant has not been identified in the general population by the Genome Aggregation Database (gnomAD). Loss of MUTYH function is a known mechanism of disease (clinicalgenome.org). Based on the available evidence, this variant is classified as Pathogenic. |
Labcorp Genetics |
RCV000409401 | SCV002234292 | pathogenic | Familial adenomatous polyposis 2 | 2023-03-02 | criteria provided, single submitter | clinical testing | This variant has not been reported in the literature in individuals affected with MUTYH-related conditions. ClinVar contains an entry for this variant (Variation ID: 371676). For these reasons, this variant has been classified as Pathogenic. This variant is not present in population databases (gnomAD no frequency). This sequence change creates a premature translational stop signal (p.Arg360Glufs*48) 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). |
Baylor Genetics | RCV000409401 | SCV004199442 | likely pathogenic | Familial adenomatous polyposis 2 | 2021-03-24 | criteria provided, single submitter | clinical testing |