Total submissions: 3
Submitter | RCV | SCV | Clinical significance | Condition | Last evaluated | Review status | Method | Comment |
---|---|---|---|---|---|---|---|---|
Ambry Genetics | RCV000491446 | SCV000580489 | pathogenic | Hereditary cancer-predisposing syndrome | 2016-05-09 | criteria provided, single submitter | clinical testing | The c.2393_2396delATAA pathogenic mutation, located in coding exon 14 of the MSH2 gene, results from a deletion of 4 nucleotides at nucleotide positions 2393 to 2396, causing a translational frameshift with a predicted alternate stop codon (p.N798Ifs*13). 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 |
RCV001856945 | SCV002228685 | pathogenic | Hereditary nonpolyposis colorectal neoplasms | 2020-12-23 | 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 MSH2-related conditions. ClinVar contains an entry for this variant (Variation ID: 428481). This variant is not present in population databases (ExAC no frequency). This sequence change creates a premature translational stop signal (p.Asn798Ilefs*13) 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). |
Myriad Genetics, |
RCV003449352 | SCV004188946 | pathogenic | Lynch syndrome 1 | 2023-08-08 | criteria provided, single submitter | clinical testing | This variant is considered pathogenic. This variant creates a frameshift predicted to result in premature protein truncation. |