Disease relevance of Intestinal Polyposis

• In humans, mutations in BMPR1A, SMAD4 and PTEN are responsible for juvenile polyposis syndrome, juvenile intestinal polyposis and Cowden disease, respectively [1].
• These results indicate that LRD can suppress intestinal polyposis compared with HRD which does not, and suggest that its suppression is at the initiation of polyp formation [2].
• Familial adenomatous polyposis (FAP) is an autosomal dominant condition characterized by diffuse intestinal polyposis, specific gene mutation, and predisposition for developing colon cancer [3].
• Cataract continues to be associated with a number of systemic diseases and syndromes such as atherosclerosis, diabetes mellitus, atopy, juvenile rheumatoid arthritis, Marfan's syndrome, and the Cronkhite-Canada syndrome [4].

High impact information on Intestinal Polyposis

• Here we show that conditional inactivation of Bmpr1a in mice disturbs homeostasis of intestinal epithelial regeneration with an expansion of the stem and progenitor cell populations, eventually leading to intestinal polyposis resembling human juvenile polyposis syndrome [1].
• Suppression of intestinal polyposis in Apc delta716 knockout mice by inhibition of cyclooxygenase 2 (COX-2) [5].
• We treated Apc(min) mice, which are predisposed to intestinal polyposis, with a selective synthetic agonist of peroxisome proliferator-activated receptor-delta (PPAR-delta) [6].
• Loss of the Lkb1 tumour suppressor provokes intestinal polyposis but resistance to transformation [7].
• COX-2, the inducible COX isozyme, has a key role in intestinal polyposis [8].

Chemical compound and disease context of Intestinal Polyposis

• Treatment of Cronkhite-Canada syndrome with home total parenteral nutrition [9].
• Chemoprevention of intestinal polyposis in the Apcdelta716 mouse by rofecoxib, a specific cyclooxygenase-2 inhibitor [10].
• A patient whose major complaint was taste disturbance and who was diagnosed as having Cronkhite-Canada syndrome was prescribed zinc sulfate [11].

Gene context of Intestinal Polyposis

• Suppression of intestinal polyposis in Mdr1-deficient ApcMin/+ mice [12].
• In contrast, the mutant Nkd1 did not affect intestinal polyposis in Apc(Delta716) mice [13].
• Gastrin is a target of the beta-catenin/TCF-4 growth-signaling pathway in a model of intestinal polyposis [14].
• Intestinal polyposis in mice with a dominant stable mutation of the beta-catenin gene [15].
• Cooperation of cyclooxygenase 1 and cyclooxygenase 2 in intestinal polyposis [16].

Analytical, diagnostic and therapeutic context of Intestinal Polyposis

• Chemoprevention of intestinal polyposis by COX-2 inhibition: from mouse to man [17].
• Autopsy revealed intestinal polyposis and hemochromatosis secondary to massive blood transfusions [18].

References