Magali Svrcek © ECCO
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In addition to the “classical” pathway of colorectal carcinogenesis, involving development of cancer from an adenomatous precursor lesion, an alternative pathway, the serrated pathway, is now recognised to exist, and it is estimated that approximately 30% of colorectal cancers (CRC) arise via this alternative pathway [1]. In the last WHO classification, serrated polyps were classified as (i) hyperplastic polyps (HP), (ii) sessile serrated adenoma/polyps (SSA/P), with or without dysplasia, and (iii) traditional serrated adenomas (TSA). The possibility of a serrated pathway has also been suggested in colorectal carcinoma complicating Inflammatory Bowel Disease (IBD) [2–4]. Little is known concerning immunohistochemical and molecular features of serrated lesions in IBD: Data are limited to small series of patients or case reports and findings are controversial due to the rarity of the cases. However, the clinical, pathological and biological characteristics of serrated polyps in patients with IBD do seem to resemble those of their sporadic counterparts.