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タイトル: Blocking TNF-α in mice reduces colorectal carcinogenesis associated with chronic colitis
著者: Popivanova, Boryana K.
Kitamura, Kazuya
Wu, Yu
Kondo, Toshikazu
Kagaya, Takashi link image
Kaneko, Shuichi link image link image
Oshima, Masanobu link image link image
Fujii, Chifumi
Mukaida, Naofumi link image link image
加賀谷, 尚史
金子, 周一
大島, 正伸
向田, 直史
発行日: 2008年 2月 1日
出版社(者): American Society for Clinical Investigation
雑誌名: Journal of Clinical Investigation
ISSN: 0021-9738
巻: 118
号: 2
開始ページ: 560
終了ページ: 570
抄録: The inflammatory bowel disease ulcerative colitis (UC) frequently progresses to colon cancer. To understand the mechanisms by which UC patients develop colon carcinomas, we used a mouse model of the disease whereby administration of azoxymethane (AOM) followed by repeated dextran sulfate sodium (DSS) ingestion causes severe colonic inflammation and the subsequent development of multiple tumors. We found that treating WT mice with AOM and DSS increased TNF-α expression and the number of infiltrating leukocytes expressing its major receptor, p55 (TNF-Rp55), in the lamina propria and submucosal regions of the colon. This was followed by the development of multiple colonic tumors. Mice lacking TNF-Rp55 and treated with AOM and DSS showed reduced mucosal damage, reduced infiltration of macrophages and neutrophils, and attenuated subsequent tumor formation. WT mice transplanted with TNF-Rp55-deficient bone marrow also developed significantly fewer tumors after AOM and DSS treatment than either WT mice or TNF-Rp55-deficient mice transplanted with WT bone marrow. Furthermore, administration of etanercept, a specific antagonist of TNF-α, to WT mice after treatment with AOM and DSS markedly reduced the number and size of tumors and reduced colonic infiltration by neutrophils and macrophages. These observations identify TNF-α as a crucial mediator of the initiation and progression of colitis-associated colon carcinogenesis and suggest that targeting TNF-α may be useful in treating colon cancer in individuals with UC.
URI: http://hdl.handle.net/2297/9041
資料種別: Journal Article
版表示: publisher
出現コレクション:1. 査読済論文

このアイテムを引用あるいはリンクする場合は次の識別子を使用してください。 http://hdl.handle.net/2297/9041



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