Serrated polyps of the large intestine: a molecular study comparing sessile serrated adenomas and hyperplastic polyps
| Autor: | Hanifa Bouzourene, Dominique Sandmeier, Jean Benhattar, Patricia Martin |
|---|---|
| Rok vydání: | 2009 |
| Předmět: |
Adenoma
Proto-Oncogene Proteins B-raf Pathology medicine.medical_specialty Histology Colon Colonic Polyps Biology MLH1 medicine.disease_cause DNA Mismatch Repair Methylation Pathology and Forensic Medicine Proto-Oncogene Proteins p21(ras) CDKN2A Proto-Oncogene Proteins hemic and lymphatic diseases medicine Humans Intestine Large neoplasms beta Catenin Adaptor Proteins Signal Transducing Hyperplasia Genes p16 Nuclear Proteins Microsatellite instability DNA Neoplasm General Medicine medicine.disease Immunohistochemistry eye diseases digestive system diseases Hyperplastic Polyp MSH2 Mutation DNA methylation ras Proteins Cancer research KRAS MutL Protein Homolog 1 Microsatellite Repeats Sessile serrated adenoma |
| Zdroj: | Histopathology. 55:206-213 |
| ISSN: | 1365-2559 0309-0167 |
| DOI: | 10.1111/j.1365-2559.2009.03356.x |
| Popis: | AIMS: To compare the molecular profile of a series of sessile serrated adenomas (SSAs) and hyperplastic polyps (HPs), in order to distinguish these lesions, SSAs having a potential role in the genesis of serrated adenocarcinomas through a serrated pathway in which methylation plays a key role. METHODS AND RESULTS: Twelve HPs and sixteen SSAs of the right and left colon were investigated for microsatellite instability, DNA mismatch repair genes, p53, p16, and beta-catenin expression, MLH1 and p16 (CDKN2A) gene methylation, and KRAS and BRAF mutations. Both SSAs and HPs were microsatellite stable. MLH1 and MSH2 protein silencing, aberrant cytoplasmic expression and methylation of p16 were found to be exclusive to right-sided SSAs. The MLH1 promoter gene was frequently methylated in right-sided SSAs in contrast with HPs. Abnormal p53 and beta-catenin expression was present in both SSAs and HPs. BRAF and KRAS mutation were mutually exclusive, but KRAS mutation was present only in left-sided SSAs and HPs. CONCLUSIONS: HPs and SSAs may be related lesions. However, at least right-sided SSAs differ from left-sided SSAs and HPs in the occurrence of MLH1 and p16 methylation, supporting the hypothesis that SSAs could be precursors of serrated adenocarcinomas. |
| Databáze: | OpenAIRE |
| Externí odkaz: |
|