Total submissions: 3
Submitter | RCV | SCV | Clinical significance | Condition | Last evaluated | Review status | Method | Comment |
---|---|---|---|---|---|---|---|---|
Counsyl | RCV000669566 | SCV000794331 | likely pathogenic | Familial adenomatous polyposis 2 | 2017-09-22 | criteria provided, single submitter | clinical testing | |
Labcorp Genetics |
RCV000669566 | SCV000827218 | pathogenic | Familial adenomatous polyposis 2 | 2021-06-08 | criteria provided, single submitter | clinical testing | For these reasons, this variant has been classified as Pathogenic. This variant has not been reported in the literature in individuals with MUTYH-related conditions. ClinVar contains an entry for this variant (Variation ID: 554017). This variant is not present in population databases (ExAC no frequency). This sequence change creates a premature translational stop signal (p.Gln187*) 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 | RCV002343420 | SCV002647460 | pathogenic | Hereditary cancer-predisposing syndrome | 2016-11-02 | criteria provided, single submitter | clinical testing | The p.Q187* pathogenic mutation (also known as c.559C>T), located in coding exon 7 of the MUTYH gene, results from a C to T substitution at nucleotide position 559. This changes the amino acid from a glutamine to a stop codon within coding exon 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. |