ArticleInternational journal of colorectal disease2012
Aberrant protein expression and frequent allelic loss of MSH3 in colorectal cancer with low-level microsatellite instability.
Article in International journal of colorectal disease, 2012. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 19 papers.
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19 citing papers in PubMed, 22 citations in OpenAlex.
- Evidence that MutSβ repairs indels generated by mispair initiated template slippage.DNA repair · 2026Article
- Low microsatellite instability revisited: a review.Virchows Archiv : an international journal of pathology · 2026Review
- Low microsatellite instability: A distinct instability type in gastric cancer?Journal of cancer research and clinical oncology · 2023Article
- Article
- Comprehensive Genomic Characterization of Fifteen Early-Onset Lynch-Like Syndrome Colorectal Cancers.Cancers · 2021Article
- Loss of MSH2 and MSH6 due to heterozygous germline defects in MSH3 and MSH6.Familial cancer · 2017Article
- Inactivation of MSH3 by promoter methylation correlates with primary tumor stage in nasopharyngeal carcinoma.International journal of molecular medicine · 2017Article
- Targeted exome sequencing reveals distinct pathogenic variants in Iranians with colorectal cancer.Oncotarget · 2017Article
- Serrated polyposis associated with a family history of colorectal cancer and/or polyps: The preferential location of polyps in the colon and rectum defines two molecular entities.International journal of molecular medicine · 2016Article
- Exome Sequencing Identifies Biallelic MSH3 Germline Mutations as a Recessive Subtype of Colorectal Adenomatous Polyposis.American journal of human genetics · 2016Article
- Detection of DNA repair protein in colorectal cancer of patients up to 50 years old can increase the identification of Lynch syndrome?Tumour biology : the journal of the International Society for Oncodevelopmental Biology and Medicine · 2016Article
- Expression Pattern and Clinicopathological Relevance of the Indoleamine 2,3-Dioxygenase 1/Tryptophan 2,3-Dioxygenase Protein in Colorectal Cancer.Disease markers · 2016Article
- Aberrant methylation of the MSH3 promoter and distal enhancer in esophageal cancer patients exposed to first-hand tobacco smoke.Journal of cancer research and clinical oncology · 2014Article
- Article
- Clinical problems of colorectal cancer and endometrial cancer cases with unknown cause of tumor mismatch repair deficiency (suspected Lynch syndrome).The application of clinical genetics · 2014Review
- The landscape of microsatellite instability in colorectal and endometrial cancer genomes.Cell · 2013Article
- Mismatch repair genes Mlh1 and Mlh3 modify CAG instability in Huntington's disease mice: genome-wide and candidate approaches.PLoS genetics · 2013Article
- How many diseases are colorectal cancer?Gastroenterology research and practice · 2012Article
- Tumor-specific microsatellite instability: do distinct mechanisms underlie the MSI-L and EMAST phenotypes?Mutation researchReview
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Authors and funding
4 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
purposeHigh level of microsatellite instability (MSI-H) in colorectal cancer (CRC) is caused by the inactivation of mismatch repair (MMR) genes; however, it is unknown for tumors with low level MSI (MSI-L). The protein complex involving MSH3 preferentially recognizes insertion/deletion loops (IDLs) of two to eight bases and di- and tetranucleotide repeats are affected in the majority of MSI-L CRC.
methodsWe selected 10 and eight MSI-L CRCs from 228 and 204 patients with sporadic and hereditary disease, respectively. The tumors were analyzed for protein expression of MSH3, MSH2, MSH6, MLH1, and PMS2, and for mutations and loss of heterozygosity (LOH) in MSH3.
resultsFour tumors showed a markedly reduced MSH3 expression, whereas all 18 tumors had normal expression of the remaining MMR proteins. Twenty-five different sequence variants were identified. None of these results in a truncated protein, though L902W represents the first constitutional missense mutation in MSH3 predicted to be functional based on conservation among mutS homologues. All variants have also been found in normal DNA of the patients and in controls. LOH intragenic to MSH3 was evident for 12 of 16 (75%) informative tumors.
conclusionsOccurrence of sequence variants in normal DNA of the patients and in controls excludes somatic mutations and mutations specific to the CRC patient population, respectively. In contrast, the high frequency of LOH as well as the aberrant protein expression in some tumors indicates an involvement of MSH3 impairment in MSI-L CRC.
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