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本文引用的文献

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Microbial genomic analysis reveals the essential role of inflammation in bacteria-induced colorectal cancer.微生物基因组分析揭示炎症在细菌诱导的结直肠癌中的关键作用。
Nat Commun. 2014 Sep 3;5:4724. doi: 10.1038/ncomms5724.
2
High-fat-diet-mediated dysbiosis promotes intestinal carcinogenesis independently of obesity.高脂饮食介导的肠道菌群失调独立于肥胖促进肠道癌变。
Nature. 2014 Oct 23;514(7523):508-12. doi: 10.1038/nature13398. Epub 2014 Aug 31.
3
Gut microbial metabolism drives transformation of MSH2-deficient colon epithelial cells.肠道微生物代谢驱动 MSH2 缺陷型结肠上皮细胞的转化。
Cell. 2014 Jul 17;158(2):288-299. doi: 10.1016/j.cell.2014.04.051.
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The multifaceted role of the intestinal microbiota in colon cancer.肠道微生物群在结肠癌中的多方面作用。
Mol Cell. 2014 Apr 24;54(2):309-20. doi: 10.1016/j.molcel.2014.03.039.
5
Interplay of host microbiota, genetic perturbations, and inflammation promotes local development of intestinal neoplasms in mice.宿主微生物群、遗传扰动和炎症的相互作用促进了小鼠肠道肿瘤的局部发展。
J Exp Med. 2014 Mar 10;211(3):457-72. doi: 10.1084/jem.20131587. Epub 2014 Mar 3.
6
Activation of Gpr109a, receptor for niacin and the commensal metabolite butyrate, suppresses colonic inflammation and carcinogenesis.Gpr109a 的激活,作为烟酸和共生代谢物丁酸盐的受体,可抑制结肠炎症和癌变。
Immunity. 2014 Jan 16;40(1):128-39. doi: 10.1016/j.immuni.2013.12.007. Epub 2014 Jan 9.
7
Inflammation-induced cancer: crosstalk between tumours, immune cells and microorganisms.炎症相关癌症:肿瘤、免疫细胞和微生物之间的串扰。
Nat Rev Cancer. 2013 Nov;13(11):759-71. doi: 10.1038/nrc3611.
8
Obesity and colorectal cancer.肥胖与结直肠癌。
Gut. 2013 Jun;62(6):933-47. doi: 10.1136/gutjnl-2013-304701. Epub 2013 Mar 12.
9
Microbial ecology: human gut microbes associated with obesity.微生物生态学:与肥胖相关的人类肠道微生物
Nature. 2006 Dec 21;444(7122):1022-3. doi: 10.1038/4441022a.
10
Dietary fat influences on polyp phenotype in multiple intestinal neoplasia mice.饮食脂肪对多发性肠道肿瘤小鼠息肉表型的影响。
Proc Natl Acad Sci U S A. 1997 Apr 1;94(7):3308-13. doi: 10.1073/pnas.94.7.3308.

细菌与食物:引发癌症的因素?

Bugs and food: a recipe for cancer?

作者信息

Ohland Christina L, Jobin Christian

机构信息

Department of Medicine, University of Florida, Gainesville, FL 32610, USA.

Department of Medicine, University of Florida, Gainesville, FL 32610, USA; Department of Infectious Diseases and Pathology, University of Florida, Gainesville, FL 32610, USA.

出版信息

Cell Metab. 2014 Dec 2;20(6):937-8. doi: 10.1016/j.cmet.2014.11.010.

DOI:10.1016/j.cmet.2014.11.010
PMID:25470545
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC4364408/
Abstract

Obesity and the associated state of subchronic inflammation are risk factors for numerous pathologies, including carcinogenesis. Recently, Schulz et al. (2014) demonstrated that high-fat diet-induced intestinal dysbiosis promotes cancer development in K-ras(G12Dint) mice without inducing obesity or mucosal inflammation, positioning microbial activities as a central component of diet-induced carcinogenesis.

摘要

肥胖以及相关的亚慢性炎症状态是包括致癌作用在内的多种病症的风险因素。最近,舒尔茨等人(2014年)证明,高脂饮食诱导的肠道微生物失调会促进携带K-ras(G12Dint)基因的小鼠发生癌症,且不会导致肥胖或黏膜炎症,这表明微生物活动是饮食诱导致癌作用的核心组成部分。