Total submissions: 3
Submitter | RCV | SCV | Clinical significance | Condition | Last evaluated | Review status | Method | Comment |
---|---|---|---|---|---|---|---|---|
Ambry Genetics | RCV000167124 | SCV000217954 | pathogenic | Hereditary cancer-predisposing syndrome | 2023-09-05 | criteria provided, single submitter | clinical testing | The c.1803dupG (p.L602Afs*42) alteration, located in exon 12 (coding exon 12) of the MSH2 gene, consists of a duplication of G at position 1803, causing a translational frameshift with a predicted alternate stop codon after 42 amino acids. This alteration is expected to result in loss of function by premature protein truncation or nonsense-mediated mRNA decay. This variant was not reported in population-based cohorts in the Genome Aggregation Database (gnomAD). This mutation has been identified in a patient undergoing multi-gene panel testing for a personal and/or family history of cancer (Espenschied, 2017). Based on the available evidence, this alteration is classified as pathogenic. |
Labcorp Genetics |
RCV001385381 | SCV001585216 | pathogenic | Hereditary nonpolyposis colorectal neoplasms | 2024-08-20 | criteria provided, single submitter | clinical testing | This sequence change creates a premature translational stop signal (p.Leu602Alafs*42) 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). This variant is not present in population databases (gnomAD no frequency). This premature translational stop signal has been observed in individual(s) with hereditary cancer predisposition (PMID: 28514183). ClinVar contains an entry for this variant (Variation ID: 187400). For these reasons, this variant has been classified as Pathogenic. |
Myriad Genetics, |
RCV003454419 | SCV004186962 | pathogenic | Lynch syndrome 1 | 2023-08-03 | criteria provided, single submitter | clinical testing | This variant is considered pathogenic. This variant creates a frameshift predicted to result in premature protein truncation. |