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Fig. 6.26 A, B Crypt adenoma in a patient with FAP.

Fig. 6.24 Tubulovillous adenoma. Pedunculated with long stalk of non-neoplastic mucosa.
Fig. 6.25 A Sessile villous adenoma. B Section through a villous adenoma.

sia (dysplasia) is the hallmark of these lesions. Depressed adenomas are usually smaller than flat or protruding ones and tend to give rise to adenocarcinoma while still relatively small (mean diameter 11 mm) due to a greater tendency to progress {1628}. These adenomas have a lower frequency of ras mutation than polypoid adenomas {974}.

Histopathology. Tubular adenomas are usually protruding, spherical and pedun-culated, or non-protruding (flat). Microscopically, dysplastic glandular structures occupy at least 80% of the luminal surface. Villous adenomas are typically sessile with a hairy-appearing surface. Microscopically, leaf-like projections lined by dysplastic glandular epithelium comprise more than 80% of the luminal surface. Distinction of villous structures from elongated separated tubules is sometimes problematical. Villous architecture is defined arbitrarily by the length of the glands exceeding twice the thickness of normal colorectal mucosa. Tubulovillous adenomas have a mixture of tubular and villous structures with a ratio between 80%/20% and 20%/80%. Serrated adenomas are characterized by the saw-tooth configuration of a hyperplastic (metaplas-tic) polyp on low power microscopy, but the epithelium lining the upper portion of the crypts and luminal surface is dysplas-tic. Serrated adenomas can also have a tubular or villous component, but low-levels of microsatellite instability (MSI-L) and altered mucin are characteristic of these serrated lesions {840}. By contrast, mixed hyperplastic polyp/adenoma contains separate identifiable areas of each histo-pathological type {1092}. Occasionally some villous adenomas show in the slopes of the villi closely packed small glands; those adenomas have been referred to as villo-microglandular adenomas {972}.

Although tiny flat or depressed adeno-carcinomas are well-described, it is difficult to determine if de novo adenocarcinomas without a benign histopathologi-cal precursor lesion ever occur in the large bowel, because adenocarcinoma can overgrow the precursor lesion. The prolonged time interval usually required for progression of intraepithelial to invasive neoplasia offers opportunities for prevention or interruption of the process to reduce mortality due to colorectal carcinoma.

Intraepithelial neoplasia can also occur in the absence of an adenoma, in a preexisting lesion of another type (such as a hamartomatous polyp in juvenile polyposis syndrome and Peutz-Jeghers syndrome), and in chronic inflammatory diseases.

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