Total submissions: 2
Submitter | RCV | SCV | Clinical significance | Condition | Last evaluated | Review status | Method | Comment |
---|---|---|---|---|---|---|---|---|
Ambry Genetics | RCV000571703 | SCV000662335 | pathogenic | Hereditary cancer-predisposing syndrome | 2017-02-07 | criteria provided, single submitter | clinical testing | The c.2421_2422delTGinsCT pathogenic mutation, located in coding exon 14 of the MSH2 gene, results from an in-frame deletion of TG and insertion of CT at nucleotide positions 2421 to 2422, leading to an immediate stop codon (p.E808*). 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. |
Labcorp Genetics |
RCV001858108 | SCV002171679 | pathogenic | Hereditary nonpolyposis colorectal neoplasms | 2021-12-08 | 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: 479848). This premature translational stop signal has been observed in individual(s) with colorectal and endometrial cancer (PMID: 15520370). Information on the frequency of this variant in the gnomAD database is not available, as this variant may be reported differently in the database. This sequence change creates a premature translational stop signal (p.Glu808*) in the MSH2 gene. It is expected to result in an absent or disrupted protein product. Loss-of-function variants in MSH2 are known to be pathogenic (PMID: 15849733, 24362816). |