Abstract
The wider use of gastrointestinal endoscopic procedures has led to an increased detection of small intestinal preneoplastic and neoplastic epithelial lesions, most of which are identified in the duodenum and ampullary region. Like their malignant counterparts, small intestinal glandular precursor lesions, which include adenomas and hamartomas, may arise sporadically or be associated with hereditary tumor syndromes, such as familial adenomatous polyposis, MUTYH-associated polyposis, Lynch syndrome, Peutz-Jeghers syndrome, juvenile polyposis syndrome, and Cowden syndrome. In addition, dysplastic, preinvasive lesions have been observed adjacent to small bowel adenocarcinomas complicating immune-related disorders, such as celiac or Crohn’s disease. Adenomatous lesions may exhibit an intestinal-type, gastric-type, or, very rarely, serrated differentiation, related to different molecular pathogenetic mechanisms. Finally, in the background of multiple endocrine neoplasia 1 syndrome, precursor neuroendocrine growths have been described. In this review we offer a comprehensive description on the histo-molecular features of the main histotypes of small bowel epithelial precursors lesions, including: (i) sporadic adenomas (intestinal-type and gastric-type; non-ampullary and ampullary); (ii) syndromic adenomas; (iii) small bowel dysplasia in celiac and Crohn’s disease; (iv) serrated lesions; (v) hamartomatous lesions; and (vi) neuroendocrine precursor lesions.
Highlights
The widespread use of gastrointestinal endoscopic procedures has led to increased detection of small bowel polyps, most of which are incidental lesions located in the duodenum [1,2,3]
Screening of remaining organs and family members, when they are associated with hereditary tumor syndromes, such as familial adenomatous polyposis 1 (FAP), MUTYHassociated polyposis (MAP) or multiple endocrine neoplasia 1 syndrome (MEN1)
TP53 mutations have been identified in only 5% of non-ampullary duodenal adenomas (NADAs) by Ota et al [16], while recent studies indicate that TP53 (38–58%), KRAS (27–54%), and APC (11–27%) are the most frequently mutated genes in small bowel adenocarcinomas [9,10,11,20], suggesting that this molecular alteration is a late event in tumorigenesis
Summary
The widespread use of gastrointestinal endoscopic procedures has led to increased detection of small bowel polyps, most of which are incidental lesions located in the duodenum [1,2,3]. Small bowel (ampullary and non-ampullary) adenomas may show intestinal or gastric differentiation, as well as, very rarely, serrated morphology and may be either sporadic or related to polyposis syndromes or immune-mediated disorders [1,2,4]. The identification of such precursor lesions may have clinical implications, requiring specific endoscopic surveillance programs on the bases of their malignant potential [5]. The aim of this review is to provide a global view of the molecular aspects of precursor epithelial lesions of the small intestine
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