ArticleClinical and translational gastroenterology2019
Inflammation-Associated Microsatellite Alterations Caused by MSH3 Dysfunction Are Prevalent in Ulcerative Colitis and Increase With Neoplastic Advancement.
Article in Clinical and translational gastroenterology, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 23 papers.
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Who cites it
23 citing papers in PubMed, 25 citations in OpenAlex.
- Prevalence of germline MSH3 polymorphisms in ulcerative colitis and early-onset colorectal cancer patients that potentiates inflammation-to-cancer transformation.Human molecular genetics · 2026Article
- Inflammation Drives Phosphorylation and Acetylation of MutS Homolog 3 and Interaction with Cytosolic HDAC6.Journal of Cancer · 2026Article
- Novel African American Colorectal CancerHuman mutation · 2026Article
- Double-Strand Breaks Induce Nuclear-Cytosolic Shuttling of Polymorphic DNA Mismatch Repair Protein MutS Homolog 3 and Binding to NEMO/IKKγ in Colon Cancer Cells.Gastro hep advances · 2025Article
- Association of Functional Polymorphisms inCancers · 2024Article
- Curative resection via right hemicolectomy and regional lymph node dissection for colonic adenomatous polyposis of unknown etiology with adenocarcinomas localized in the right side of the colon: a case report.Surgical case reports · 2024Article
- Article
- Compound heterozygous MSH3 germline variants and associated tumor somatic DNA mismatch repair dysfunction.NPJ precision oncology · 2024Article
- Fusobacterium nucleatum Load Correlates with KRAS Mutation and Sessile Serrated Pathogenesis in Colorectal Adenocarcinoma.Cancer research communications · 2023Article
- EMAST Type of Microsatellite Instability-A Distinct Entity or Blurred Overlap between Stable and MSI Tumors.Genes · 2023Review
- Epidemiology and biology of early onset colorectal cancer.EXCLI journal · 2022Review
- Genetic and epigenetic dependencies in colorectal cancer development.Gastroenterology report · 2022Review
- Inflammatory Bowel Disease-Associated Colorectal Cancer: Translational Risks from Mechanisms to Medicines.Journal of Crohn's & colitis · 2021Review
- Article
- Racial and ethnic disparities in colorectal cancer incidence and mortality.Advances in cancer research · 2021Article
- miR‑31 promotes tumorigenesis in ulcerative colitis‑associated neoplasia via downregulation of SATB2.Molecular medicine reports · 2020Article
- MUC1-C drives stemness in progression of colitis to colorectal cancer.JCI insight · 2020Article
- The Human DNA Mismatch Repair Protein MSH3 Contains Nuclear Localization and Export Signals That Enable Nuclear-Cytosolic Shuttling in Response to Inflammation.Molecular and cellular biology · 2020Article
- Altered ARID1A expression in colorectal cancer.BMC cancer · 2020Article
- Article
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Authors and funding
16 authors at 4 institutions in 2 countries.
Funding
Abstract
objectivesInflammation-associated microsatellite alterations (also known as elevated microsatellite alterations at selected tetranucleotide repeats [EMAST]) result from IL-6-induced nuclear-to-cytosolic displacement of the DNA mismatch repair (MMR) protein MSH3, allowing frameshifts of dinucleotide or longer microsatellites within DNA. MSH3 also engages homologous recombination to repair double-strand breaks (DSBs), making MSH3 deficiency contributory to both EMAST and DSBs. EMAST is observed in cancers, but given its genesis by cytokines, it may be present in non-neoplastic inflammatory conditions. We examined ulcerative colitis (UC), a preneoplastic condition from prolonged inflammatory duration.
methodsWe assessed 70 UC colons without neoplasia, 5 UC specimens with dysplasia, 14 UC-derived colorectal cancers (CRCs), and 19 early-stage sporadic CRCs for microsatellite instability (MSI) via multiplexed polymerase chain reaction capable of simultaneous detection of MSI-H, MSI-L, and EMAST. We evaluated UC specimens for MSH3 expression via immunohistochemistry.
resultsUC, UC with dysplasia, and UC-derived CRCs demonstrated dinucleotide or longer microsatellite frameshifts, with UC showing coincident reduction of nuclear MSH3 expression. No UC specimen, with or without neoplasia, demonstrated mononucleotide frameshifts. EMAST frequency was higher in UC-derived CRCs than UC (71.4% vs 31.4%, P = 0.0045) and higher than early-stage sporadic CRCs (66.7% vs 26.3%, P = 0.0426). EMAST frequency was higher with UC duration >8 years compared with ≤8 years (40% vs 16%, P = 0.0459). DISCUSSION: Inflammation-associated microsatellite alterations/EMAST are prevalent in UC and signify genomic mutations in the absence of neoplasia. Duration of disease and advancement to neoplasia increases frequency of EMAST. MSH3 dysfunction is a potential contributory pathway toward neoplasia in UC that could be targeted by therapeutic intervention.
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