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Molecular Pathways |
Authors' Affiliation: Phase I Program, Division of Cancer Medicine, The University of Texas M. D. Anderson Cancer Center, Houston, Texas
Requests for reprints: Razelle Kurzrock, Division of Cancer Medicine, M. D. Anderson Cancer Center, Unit 422, P.O. Box 301402, Houston, TX 77030. Phone: 713-794-1226; Fax: 713-563-0566; E-mail: rkurzroc{at}mdanderson.org and Laura S. Angelo, Division of Cancer Medicine, M. D. Anderson Cancer Center. Phone: 713-817-2123; E-mail: langelo{at}alltel.net.
Abstract
Inflammation occurs in response to host injury or infection, as the result of an autoimmune disease, or in response to the development of a tumor. Although the immune system may be helpful in fighting the tumor, it may also fuel the tumorigenic process. In fact, recent data suggest a strong link between chronic inflammation, angiogenesis, and the development of cancer. For example, inflammation and scarring caused by recurring infections with Mycobacterium tuberculosis may be a cause for cancers of the lung. Inflammatory breast cancer exhibits increased angiogenesis and lymphangiogenesis and has a higher metastatic potential than noninflammatory breast cancer. Nonsteroidal anti-inflammatory drugs have been proposed as preventives for the development of colon carcinoma and ovarian cancer. Inhibition of nuclear factor-
B contributes to the proposed mechanism of action. Inflammatory cytokines, including interleukin-6, serve as autocrine and paracrine growth factors for several cancers, and high levels of these cytokines may correlate with a poor prognosis and increased production of angiogenic factors. The state of the art of our understanding of this critical interaction is reviewed.
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