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Updated: May 20, 2026

Deficient Pms2, ERCC1, Ku86, CcOI in Field Defects During Progression to Colon Cancer
Published on: July 28, 2010
Early changes in carcinogenesis of colorectal adenomas
1Akdeniz University Pathology Department, Antalya, Turkey. serap_toru@yahoo.com
Objectives:
Adenocarcinoma of the colon and rectum is the third most common cause of cancer deaths and the sixth most common cancer in the world. Adenomas are benign neoplastic lesions which can be transformed into carcinomas, but this is usually not the case. There should be some risk factors which lead to the development of carcinomas into adenomas. The aim of this study is to find out the early changes and high risk factors related to carcinogenesis in colonic polyps.
Methods:
In this study, we reviewed nearly 1000 colonoscopic biopsies and chose 72 biopsies. We developed three groups (tubular adenomas group 1, villous adenomas group 2, normal mucosa group 3); each group had 24 different biopsies. P53, Ki-67, bcl-2, cyclin D1, E-cadherin, c-erb B2 immunohistochemistry and human papillomavirus (HPV) in-situ hybridization were used for analysis.
Results:
Five of the seventy-two cases were positive in HPV in-situ analysis. Four of them were villous adenomas and one was a tubular adenoma. Ki-67 expression was limited only to crypts in group 3 but in groups 1 and 2, Ki-67 expression was seen both in crypt epithelium and surface epithelium. Cyclin D1, c-erb B2, bcl-2 expression was significantly increased in neoplastic polyps.
Conclusion:
Ki-67 expression, both in the crypt and surface epithelium, and cyclin D1, c-erb B2, bcl-2 over-expression may be a clue of dysplastic epithelium and if the role of HPV is elucidated and shown to be important in colonic carcinogenesis, then vaccination might prevent carcinogenesis caused by HPV.
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