In recent years there have been many intensive studies on the molecular mechanisms involving the carcinogenesis of colorectal cancer (CRC). An inflammatory process and genetics play the key role in neoplasia of CRC. Currently, there are two known pathways of CRC carcinogenesis, such as the adenoma and the serrated adenoma, which are referred to as "classic" and "alternative", respectively. Among all the components of the inflammatory process, the proinflammatory and anti-inflammatory cytokines play a major role as a factor influencing the process of malignant transformation. In our study we focused on key inflammatory factors such as cytokines interleukin (IL)-10, IL-1β, IL-4, tumor necrosis factor α (TNF-α) and cyclooxygenase-2 (COX-2) in adenomas, serrated adenomas, hyperplastic polyps, adenocarcinomas and normal mucosa. Our study confirmed the hypothesis that inflammation has a major effect on carcinogenesis of CRC. Our studies also showed the difference in carcinogenesis of CRC. It showed a greater effect of the inflammatory process in carcinogenesis of CRC by a "serrated" (alternative) way as compared to the classic way. In a serrated way all the inflammatory factors had a higher expression. It might suggest that effectiveness of cancer prevention with the use of NSAIDs has a greater impact in patients whose tumors were formed in an alternative way. Additionally, it also showed that the inflammatory process has no influence on the final form of cancer.

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http://dx.doi.org/10.5114/pjp.2012.32768DOI Listing

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