Patients with inflammatory bowel disease (IBD) (an acronym that includes both ulcerative colitis [UC] and Crohn’s colitis [CC]) are at risk to develop dysplasia in the cryptal epithelium, polypoid and nonpolypoid adenomatous growths, and selleck screening library IBD-independent sporadic polypoid and nonpolypoid adenomas. All these lesions may proceed to colorectal carcinoma (CRC). Information concerning the histogenesis of CRC in IBD is derived from studies done in patients with UC. At present, 7 alternative pathways have been proposed:

(1) from UC-dependent histologically detected dysplastic gland, referred to as dysplasia in flat mucosa in the literature; (2) from UC-dependent adenomatoid neoplastic growths1; (3) from UC-independent, age-dependent, sporadic adenomas1; (4) from gut-associated lymphoid tissue (GALT)2; (5) from nonpolypoid (UC-dependent and UC-independent) adenomas3; (6) from UC-dependent discrete villous dysplastic changes4; or (7) from apparently nondysplastic mucosa (de novo carcinomas). 1 Histologically detected dysplasia in IBD

may be found in colorectal glands exhibiting parallel tubules Selleckchem ATM/ATR inhibitor or bifurcations; in those instances, the dysplasia is initially found in the basal aspect of the crypts and progresses gradually toward the superficial aspect of the crypts (base-to-surface progression). In mucosa with advanced atrophy without crypts, dysplasia may be found in the superficial epithelium. A recent search in the literature revealed that most of the publications on flat adenomas in IBD concerned dysplasia in flat mucosa, flat dysplasia, flat dysplastic tissue, or flat low-grade dysplasia. These terms Morin Hydrate should not be confused with nonpolypoid adenomas, as these adenomas

are also flat dysplasias albeit showing a circumscribed clustering of abnormal crypts lined with dysplastic cells. It is crucial to distinguish between these 2 different histologic alterations, as cases of nonpolypoid adenomas are even today being referred to in the literature as flat adenomas. In this article the term “flat” is reserved for nonpolypoid adenomas. In 1975, Mr Bussey from the St. Mark’s Hospital, London, UK published a monograph on colectomy specimens from patients with familial adenomatous polyposis (FAP). The caption in one of the illustrations reads as follows: “a lesion consisting of adenomatous tubules, which have not produced any thickening of the mucosa”. This appears to be the first description of nonpolypoid (flat) colonic adenomas in FAP.5 In 1985, Muto and colleagues6 launched the colonoscopic-histologic concept “flat adenoma-carcinoma sequence”, uncovering thereby an alternative route to sporadic colorectal carcinogenesis. Hurlstone postulated that the variability in histologic diagnostic criteria used by Western and Japanese pathologists have made comparative studies difficult.