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Distribution of intestinal stem cell markers in colorectal precancerous lesions
Author(s) -
Jang Bo Gun,
Kim Hye Sung,
Kim Kyung Ju,
Rhee YeYoung,
Kim Woo Ho,
Kang Gyeong Hoon
Publication year - 2016
Publication title -
histopathology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.626
H-Index - 124
eISSN - 1365-2559
pISSN - 0309-0167
DOI - 10.1111/his.12787
Subject(s) - lgr5 , ectopic expression , pathology , dysplasia , stem cell , biology , stem cell marker , paneth cell , hyperplastic polyp , progenitor cell , cancer research , colorectal cancer , medicine , cancer stem cell , cancer , cell culture , colonoscopy , small intestine , microbiology and biotechnology , genetics , biochemistry
Aims Intestinal stem cell ( ISC ) markers such as LGR 5 , ASCL 2 , EPHB 2 and OLFM 4 , and their clinical implications have been studied extensively in colorectal cancers ( CRC s). However, little is known about their expression in precancerous lesions of CRC s. Here, we investigated the expression and distribution of ISC markers in serrated polyps and conventional adenomas. Methods and results Reverse transcription–polymerase chain reaction ( RT – PCR ) analysis revealed that all ISC markers were up‐regulated significantly in conventional adenomas with low‐grade dysplasia ( CALG s) compared with other lesions. RNA in‐situ hybridization confirmed that CALG s exhibited strong and diffuse expression of all ISC markers, which indicate a stem cell‐like phenotype. However, normal colonic mucosa, hyperplastic polyps and sessile serrated adenomas harboured LGR 5 + cells that were confined to the crypt base and demonstrated an organized expression of ISC markers. Notably, in traditional serrated adenomas, expression of LGR 5 and ASCL 2 was localized to the ectopic crypts as in the normal crypts, but expression of EPHB 2 and OLFM 4 was distributed in a diffuse manner, which is suggestive of a progenitor‐like features. Conclusions The expression and distribution profile of ISC markers possibly provides insights into the organization of stem and progenitor‐like cells in each type of precancerous lesion of CRC .