ArticleFamilial cancer2015
Mismatch repair deficient-crypts in non-neoplastic colonic mucosa in Lynch syndrome: insights from an illustrative case.
Article in Familial cancer, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 17 papers.
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Who cites it
17 citing papers in PubMed, 28 citations in OpenAlex.
- Routes to colorectal cancer in Lynch syndrome: a decade of molecular and clinical insights converging on Schrödinger's cat.Familial cancer · 2026Review
- [The role of immunosurveillance and immunoediting in hereditary cancer predisposition syndromes].Magyar onkologia · 2025Review
- Defining precancer: a grand challenge for the cancer community.Nature reviews. Cancer · 2024Review
- Article
- Acetaldehyde and defective mismatch repair increase colonic tumours in a Lynch syndrome model with Aldh1b1 inactivation.Disease models & mechanisms · 2023Article
- Multi-omic analysis in normal colon organoids highlights MSH4 as a novel marker of defective mismatch repair in Lynch syndrome and microsatellite instability.Cancer medicine · 2023Article
- Vaccines for immunoprevention of DNA mismatch repair deficient cancers.Journal for immunotherapy of cancer · 2022Review
- Ethanol-induced formation of colorectal tumours and precursors in a mouse model of Lynch syndrome.The Journal of pathology · 2021Article
- Discordant DNA mismatch repair protein status between synchronous or metachronous gastrointestinal carcinomas: frequency, patterns, and molecular etiologies.Familial cancer · 2021Article
- Complete Loss of EPCAM Immunoexpression IdentifiesCancers · 2020Article
- Frequent loss of mutation-specific mismatch repair protein expression in nonneoplastic endometrium of Lynch syndrome patients.Modern pathology : an official journal of the United States and Canadian Academy of Pathology, Inc · 2020Article
- Detection of DNA mismatch repair deficient crypts in random colonoscopic biopsies identifies Lynch syndrome patients.Familial cancer · 2020Article
- Immune Activation in Mismatch Repair-Deficient Carcinogenesis: More Than Just Mutational Rate.Clinical cancer research : an official journal of the American Association for Cancer Research · 2020Review
- DNA methylation changes and somatic mutations as tumorigenic events in Lynch syndrome-associated adenomas retaining mismatch repair protein expression.EBioMedicine · 2019Article
- Diagnosing colorectal medullary carcinoma: interobserver variability and clinicopathological implications.Human pathology · 2017Article
- CTNNB1-mutant colorectal carcinomas with immediate invasive growth: a model of interval cancers in Lynch syndrome.Familial cancer · 2016Article
- Mismatch repair-deficient crypt foci in Lynch syndrome--molecular alterations and association with clinical parameters.PloS one · 2015Article
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Authors and funding
9 authors at 2 institutions in 1 country.
Funding
Abstract
Mono-allelic germline mutations in DNA mismatch repair (MMR) genes lead to Lynch syndrome (LS). Questions remain as to the timing of the inactivation of the wild-type allele in LS-associated tumorigenesis. Speculation exists that it happens after the neoplasia has been initiated. However, a recent study reported the presence of MMR-deficiency in non-neoplastic colonic crypts in LS; thus the possibility can be raised that these crypts may be tumor precursors, and as such, biallelic loss of MMR may occur prior to neoplasia. Here we report a unique case that showed findings supporting both of the two seemingly conflicting notions. The patient was a 40-year-old female with LS, MSH2 type, who underwent a segmental colectomy for an adenocarcinoma. By immunohistochemistry, the carcinoma lost MSH2/MSH6. Interestingly, there was also complete loss of MSH2/MSH6 in a distinct focus of 20 colonic crypts that were morphologically non-neoplastic, thus supporting the possibility of biallelic loss of MMR before initiation of neoplasia. However, in a separate adenoma, MMR was preserved in neoplastic glands with low grade dysplasia and lost only in glands with high grade dysplasia, i.e., MMR loss after tumor initiation. These are relevant findings with regard to the timing of MMR deficiency in LS tumorigenesis, and bring forth the possibility that varied tumorigenic pathways may exist. Additionally, we observed that the MMR-deficient non-neoplastic crypts harbored increased intraepithelial CD8-positive T-lymphocytes similar to the patient's carcinoma, providing a potential new venue for the study of the natural antitumor immune responses in LS individuals.
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