Enterotoxigenic Bacteroides fragilis (ETBF)-mediated colitis in Min (Apc+/-) mice: a human commensal-based murine model of colon carcinogenesis.
作者信息
Housseau Franck, Sears Cynthia L
出版信息
Cell Cycle. 2010 Jan 1;9(1):3-5. doi: 10.4161/cc.9.1.10352. Epub 2010 Jan 18.
Abstract
摘要
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本文引用的文献
1
A human colonic commensal promotes colon tumorigenesis via activation of T helper type 17 T cell responses.一种人类结肠共生菌通过激活17型辅助性T细胞反应促进结肠肿瘤发生。
Nat Med. 2009 Sep;15(9):1016-22. doi: 10.1038/nm.2015. Epub 2009 Aug 23.
2
IL-17 can promote tumor growth through an IL-6-Stat3 signaling pathway.白细胞介素-17可通过白细胞介素-6-信号转导和转录激活因子3信号通路促进肿瘤生长。
J Exp Med. 2009 Jul 6;206(7):1457-64. doi: 10.1084/jem.20090207. Epub 2009 Jun 29.
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Cancer statistics, 2009.2009年癌症统计数据。
CA Cancer J Clin. 2009 Jul-Aug;59(4):225-49. doi: 10.3322/caac.20006. Epub 2009 May 27.
4
Enterotoxigenic Bacteroides fragilis: a rogue among symbiotes.产肠毒素脆弱拟杆菌：共生菌中的异类。
Clin Microbiol Rev. 2009 Apr;22(2):349-69, Table of Contents. doi: 10.1128/CMR.00053-08.
5
Induction of persistent colitis by a human commensal, enterotoxigenic Bacteroides fragilis, in wild-type C57BL/6 mice.人共生菌产肠毒素脆弱拟杆菌在野生型C57BL/6小鼠中诱导持续性结肠炎。
Infect Immun. 2009 Apr;77(4):1708-18. doi: 10.1128/IAI.00814-08. Epub 2009 Feb 2.
6
Apc mice: models, modifiers and mutants.Apc小鼠：模型、修饰基因与突变体。
Pathol Res Pract. 2008;204(7):479-90. doi: 10.1016/j.prp.2008.03.004. Epub 2008 Jun 5.
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The genetics and immunopathogenesis of inflammatory bowel disease.炎症性肠病的遗传学与免疫发病机制
Nat Rev Immunol. 2008 Jun;8(6):458-66. doi: 10.1038/nri2340.
8
Crosstalk between cancer and immune cells: role of STAT3 in the tumour microenvironment.癌症与免疫细胞之间的相互作用：STAT3在肿瘤微环境中的作用
Nat Rev Immunol. 2007 Jan;7(1):41-51. doi: 10.1038/nri1995.
9
A possible role of Bacteroides fragilis enterotoxin in the aetiology of colorectal cancer.脆弱拟杆菌肠毒素在结直肠癌病因学中的可能作用。
Clin Microbiol Infect. 2006 Aug;12(8):782-6. doi: 10.1111/j.1469-0691.2006.01494.x.
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Nuclear factor-kappaB in cancer development and progression.核因子-κB在癌症发生发展中的作用
Nature. 2006 May 25;441(7092):431-6. doi: 10.1038/nature04870.
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