Total submissions: 3
Submitter | RCV | SCV | Clinical significance | Condition | Last evaluated | Review status | Method | Comment |
---|---|---|---|---|---|---|---|---|
International Society for Gastrointestinal Hereditary Tumours |
RCV000075539 | SCV000106539 | likely pathogenic | Lynch syndrome | 2019-06-21 | reviewed by expert panel | curation | Interrupts canonical donor splice site |
Labcorp Genetics |
RCV001314807 | SCV001505355 | likely pathogenic | Hereditary nonpolyposis colorectal neoplasms | 2024-06-17 | criteria provided, single submitter | clinical testing | This sequence change affects an acceptor splice site in intron 18 of the MLH1 gene. RNA analysis indicates that disruption of this splice site induces altered splicing and likely disrupts the C-terminus of the protein. This variant is not present in population databases (gnomAD no frequency). Disruption of this splice site has been observed in individual(s) with colorectal or ovarian cancer (PMID: 8592341, 14635101, 15365995, 24362816). It has also been observed to segregate with disease in related individuals. ClinVar contains an entry for this variant (Variation ID: 90054). Variants that disrupt the consensus splice site are a relatively common cause of aberrant splicing (PMID: 17576681, 9536098). Studies have shown that disruption of this splice site results in skipping of exon 19 and introduces a new termination codon (PMID: 24362816). However the mRNA is not expected to undergo nonsense-mediated decay. 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, |
RCV003451105 | SCV004185827 | likely pathogenic | Colorectal cancer, hereditary nonpolyposis, type 2 | 2023-07-25 | 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. |