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Blood, 22 October 2009, Vol. 114, No. 17, pp. 3625-3628. Prepublished online as a Blood First Edition Paper on August 26, 2009; DOI 10.1182/blood-2009-05-220285. This Article Full Text Full Text (PDF) All Versions of this Article: blood-2009-05-220285v1 114/17/3625    most recent Alert me when this article is cited Alert me if a correction is posted Services Email this article to a friend Similar articles in this journal Similar articles in PubMed Alert me to new issues of the journal Download to citation manager Rights and Permissions Citing Articles Citing Articles via CrossRef Google Scholar Articles by Zheng, Y. Articles by Yi, Q. PubMed PubMed Citation Articles by Zheng, Y. Articles by Yi, Q. Related Collections Lymphoid Neoplasia Brief Reports Social Bookmarking                   What's this?  Previous Article  |  Table of Contents  |  Next Article  LYMPHOID NEOPLASIA Brief report Macrophages are an abundant component of myeloma microenvironment and protect myeloma cells from chemotherapy drug–induced apoptosis Yuhuan Zheng1,*, Zhen Cai1,2,*, Siqing Wang1,*, Xiang Zhang1, Jianfei Qian1, Sungyoul Hong1, Haiyan Li1, Michael Wang1, Jing Yang1, and Qing Yi1 1 Department of Lymphoma and Myeloma, Division of Cancer Medicine, Center for Cancer Immunology Research, University of Texas M. D. Anderson Cancer Center, Houston; and 2 Department of Hematology, First Affiliated Hospital, Medical School of Zhejiang University, Zhejiang, China Multiple myeloma remains an incurable disease. One of the major problems is that myeloma cells develop drug resistance on interaction with bone marrow stromal cells. In this study, we examined the effects of macrophages (Ms), a type of stromal cells, on myeloma cell survival and response to chemotherapy. We showed that M, in particular tumor-associated M, is a protector of myeloma cells. The protective effect was dependent on direct contact between Ms and myeloma cells. Ms protected both myeloma cell lines and primary myeloma cells from spontaneous and chemotherapy drug-induced apoptosis by attenuating the activation and cleavage of caspase-dependent apoptotic signaling. These findings are clinically relevant because we found that CD68+ Ms heavily infiltrate the bone marrow of patients with myeloma but not the bone marrow of control patients. Thus, our results indicate that Ms may contribute to myeloma cell survival and resistance to chemotherapeutic treatment in vivo. CiteULike    Connotea    Del.icio.us    Digg    Reddit    Technorati    What's this?

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