Total submissions: 2
Submitter | RCV | SCV | Clinical significance | Condition | Last evaluated | Review status | Method | Comment |
---|---|---|---|---|---|---|---|---|
Labcorp Genetics |
RCV000803405 | SCV000943274 | likely pathogenic | Hereditary nonpolyposis colorectal neoplasms | 2018-12-08 | criteria provided, single submitter | clinical testing | This sequence change affects an acceptor splice site in intron 2 of the MSH6 gene. It is expected to disrupt RNA splicing and likely results in an absent or disrupted protein product. This variant is not present in population databases (ExAC no frequency). Disruption of this splice site has been observed in combination with another MSH6 variant in an individual affected with constitutional mismatch repair deficiency syndrome (PMID: 17259933). Donor and acceptor splice site variants typically lead to a loss of protein function (PMID: 16199547), and loss-of-function variants in MSH6 are known to be pathogenic (PMID: 18269114, 24362816). In summary, the currently available evidence indicates that the variant is pathogenic, but additional data are needed to prove that conclusively. Therefore, this variant has been classified as Likely Pathogenic. |
Myriad Genetics, |
RCV003453672 | SCV004185570 | likely pathogenic | Lynch syndrome 5 | 2023-08-10 | criteria provided, single submitter | clinical testing | This variant is considered likely pathogenic. This variant occurs within a consensus splice junction and is predicted to result in abnormal mRNA splicing of either an out-of-frame exon or an in-frame exon necessary for protein stability and/or normal function. |