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10.1002/cam4.1460

http://scihub22266oqcxt.onion/10.1002/cam4.1460
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C5943478!5943478!29624892
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suck abstract from ncbi


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pmid29624892      Cancer+Med 2018 ; 7 (5): 2003-12
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  • Antibiotic?mediated bacteriome depletion in ApcMin/+ mice is associated with reduction in mucus?producing goblet cells and increased colorectal cancer progression #MMPMID29624892
  • Kaur K; Saxena A; Debnath I; O'Brien JL; Ajami NJ; Auchtung TA; Petrosino JF; Sougiannis A; Depaep S; Chumanevich A; Gummadidala PM; Omebeyinje MH; Banerjee S; Chatzistamou I; Chakraborty P; Fayad R; Berger FG; Carson JA; Chanda A
  • Cancer Med 2018[May]; 7 (5): 2003-12 PMID29624892show ga
  • Recent epidemiological evidence suggests that exposure to antibiotics in early?to?middle adulthood is associated with an increased risk of colorectal adenoma. However, mechanistic studies in established preclinical cancer to examine these claims are extremely limited. Therefore, we investigated the effect of long?term exposure of an antibiotic cocktail composed of Vancomycin, Neomycin, and Streptomycin, on tumor development and progression in the ApcMin/+ mouse, an established genetic model for familial adenomatous polyposis. Clinical pathologies related to tumor development as well as intestinal and colon tissue histopathology were studied at ages 8, 12, and 16 weeks of age, which correspond to the approximate ages of development of neoplasia, gut inflammation with polyposis, and cancer progression, respectively, in this animal model. We show that the antibiotics significantly increase the severity of clinical symptoms, including effects on intestinal histology and goblet cell numbers. In addition, they promote small intestinal polyposis. Finally, metagenomic analysis of fecal samples demonstrated that antibiotic exposure is associated with a significant but nonuniform depletion of the animal's natural gut flora. Overall, these findings support the premise that long?term antibiotic exposure mediates the selected depletion of gut microbial communities and the concomitant thinning of the protective mucus layer, resulting in an increase in tumor development.
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