ArticleThe Journal of molecular diagnostics : JMD2005
Microsatellite analysis of hereditary nonpolyposis colorectal cancer-associated colorectal adenomas by laser-assisted microdissection: correlation with mismatch repair protein expression provides new insights in early steps of tumorigenesis.
Article in The Journal of molecular diagnostics : JMD, 2005. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 24 papers.
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24 citing papers in PubMed, 51 citations in OpenAlex.
- Molecular mechanisms and differences in lynch syndrome developing into colorectal cancer and endometrial cancer based on gene expression, methylation, and mutation analysis.Cancer causes & control : CCC · 2022Article
- Complete Loss of EPCAM Immunoexpression IdentifiesCancers · 2020Article
- Enhanced Tumoral MLH1-Expression in MLH1-/PMS2-Deficient Colon Cancer Is Indicative of Sporadic Colon Cancer and Not HNPCC.Pathology oncology research : POR · 2020Article
- Does breast carcinoma belong to the Lynch syndrome tumor spectrum? - Somatic mutational profiles vs. ovarian and colorectal carcinomas.Oncotarget · 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
- [Hereditary colon cancer in Lynch syndrome/HNPCC syndrome in Germany].Der Pathologe · 2019Review
- Advances in Identification of Susceptibility Gene Defects of Hereditary Colorectal Cancer.Journal of Cancer · 2019Review
- Microsatellite instability testing in colorectal cancer using the QiaXcel advanced platform.BMC cancer · 2018Article
- Sequencing of Lynch syndrome tumors reveals the importance of epigenetic alterations.Oncotarget · 2017Article
- Update on Lynch syndrome genomics.Familial cancer · 2016Review
- Mismatch repair deficient-crypts in non-neoplastic colonic mucosa in Lynch syndrome: insights from an illustrative case.Familial cancer · 2015Article
- Getting Down to Specifics: Profiling Gene Expression and Protein-DNA Interactions in a Cell Type-Specific Manner.Advances in genetics · 2015Review
- Article
- Heterogenous mismatch-repair status in colorectal cancer.Diagnostic pathology · 2014Article
- Beyond laser microdissection technology: follow the yellow brick road for cancer research.American journal of cancer research · 2014Review
- Microsatellite instability and DNA mismatch repair protein deficiency in Lynch syndrome colorectal polyps.Cancer prevention research (Philadelphia, Pa.) · 2012Article
- Current hypotheses on how microsatellite instability leads to enhanced survival of Lynch Syndrome patients.Clinical & developmental immunology · 2010Review
- Deficient DNA mismatch repair is common in Lynch syndrome-associated colorectal adenomas.The Journal of molecular diagnostics : JMD · 2009Article
- EGAPP supplementary evidence review: DNA testing strategies aimed at reducing morbidity and mortality from Lynch syndrome.Genetics in medicine : official journal of the American College of Medical Genetics · 2009Review
- Adenoma-infiltrating lymphocytes (AILs) are a potential marker of hereditary nonpolyposis colorectal cancer.The American journal of surgical pathology · 2008Article
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Authors and funding
12 authors at 6 institutions in 3 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Although microsatellite instability (MSI) testing is a useful tool for molecular screening of hereditary nonpolyposis colorectal cancer (HNPCC) carcinomas, conflicting results have been obtained in colorectal adenomas. This might result from different techniques of tissue sampling and MSI analysis. Alternatively, some HNPCC-associated adenomas may follow a molecular route that differs from the MSI pathway. In the present study we examined the MSI status of 18 adenomas from 17 HNPCC patients by comparing manual adenoma dissection under gross visual control with laser microdissection of single adenoma crypts. After manual gross dissection, 50% (9 of 18) and 11.1% (2 of 18) of the adenomas displayed high-level (MSI-H) and low-level (MSI-L) MSI, respectively. The same set of adenomas split into 83.3% (15 of 18) MSI-H and 5.6% (1 of 18) MSI-L after laser microdissection. The expression pattern of mismatch repair (MMR) proteins showed a higher concordance rate with the MSI status in laser-dissected (94%) than gross-dissected (47%) adenomas. Whereas two adenomas remained microsatellite stable (MSS) and MMR proficient even after laser-assisted dissection, two MSI-H cases showed either rare instabilities at coding microsatellites or intratumoral heterogeneity of MSI with and without MSH2 expression. This suggests that in some adenomas development of MMR dysfunction occurs stepwise with MSI, arising before complete loss of MMR gene expression, whereas other HNPCC-associated adenomas might develop independently of MMR deficiency.
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