@article{oai:kanazawa-u.repo.nii.ac.jp:00027396,
 author = {Popivanova, Boryana Konstantinova and Kostadinova, Feodora Ivanova and Furuichi, Kengo and Shamekh, Mohamed M. and Kondo, Toshikazu and Wada, Takashi and Egashira, Kensuke and Mukaida, Naofumi},
 issue = {19},
 journal = {Cancer Research},
 month = {Oct},
 note = {Accumulating evidence indicates the crucial contribution of chronic inflammation to various types of carcinogenesis, including colon carcinoma associated with ulcerative colitis and asbestosis-induced malignant mesothelioma. Ulcerative colitis-associated colon carcinogenesis can be recapitulated in mice by azoxymethane administration followed by repetitive dextran sulfate sodium ingestion. In the course of this carcinogenesis process, the expression of a macrophage-tropic chemokine, CCL2, was enhanced together with intracolonic massive infiltration of macrophages, which were a major source of cyclooxygenase (COX)-2, a crucial mediator of colon carcinogenesis. Mice deficient in CCL2-specific receptor, CCR2, exhibited less macrophage infiltration and lower tumor numbers with attenuated COX-2 expression. Moreover, CCL2 antagonists decreased intracolonic macrophage infiltration and COX-2 expression, attenuated neovascularization, and eventually reduced the numbers and size of colon tumors, even when given after multiple colon tumors have developed. These observations identify CCL2 as a crucial mediator of the initiation and progression of chronic colitis-associated colon carcinogenesis and suggest that targeting CCL2 may be useful in treating colon cancers, particularly those associated with chronic inflammation. ©2009 American Association for Cancer Research., 金沢大学がん研究所がん病態制御},
 pages = {7884--7892},
 title = {Blockade of a chemokine, CCL2, reduces chronic colitis-associated carcinogenesis in mice},
 volume = {69},
 year = {2009}
}