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.
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.
Authors: Xinwei Hua; Polly A Newcomb; Jessica Chubak; Rachel C Malen; Rebecca Ziebell; Aruna Kamineni; Lee-Ching Zhu; Melissa P Upton; Michelle A Wurscher; Sushma S Thomas; Hana Newman; Sheetal Hardikar; Andrea N Burnett-Hartman Journal: Cancer Causes Control Date: 2020-05-01 Impact factor: 2.506
Authors: Oscar Murcia; Miriam Juárez; Eva Hernández-Illán; Cecilia Egoavil; Mar Giner-Calabuig; María Rodríguez-Soler; Rodrigo Jover Journal: World J Gastroenterol Date: 2016-04-07 Impact factor: 5.742
Authors: Martha L Slattery; Jennifer S Herrick; Roger K Wolff; Lila E Mullany; John R Stevens; Wade Samowitz Journal: Genes Chromosomes Cancer Date: 2017-02-01 Impact factor: 5.006
Authors: Karam S Boparai; Evelien Dekker; Mirjam M Polak; Alex R Musler; Susanne van Eeden; Carel J M van Noesel Journal: Am J Pathol Date: 2011-06 Impact factor: 4.307