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Friday, November 30, 2012 12:51:13 PM
Inflammation and cancer: How hot is the link?
Bharat B. Aggarwal a,*, Shishir Shishodia b, Santosh K. Sandur a,
Manoj K. Pandey a, Gautam Sethi a
a Cytokine Research Laboratory, Department of Experimental Therapeutics, The University of Texas M.D. Anderson Cancer Center,
1515 Holcombe Boulevard, Houston, TX 77030, United States
b Department of Biology, Texas Southern University, 3100 Cleburne Street, Houston, TX 77004, United States
a b s t r a c t
Although inflammation has long been known as a localized protective reaction of tissue to
irritation, injury, or infection, characterized by pain, redness, swelling, and sometimes loss
of function, there has been a new realization about its role in a wide variety of diseases,
including cancer. While acute inflammation is a part of the defense response, chronic
inflammation can lead to cancer, diabetes, cardiovascular, pulmonary, and neurological
diseases. Several pro-inflammatory gene products have been identified that mediate a
critical role in suppression of apoptosis, proliferation, angiogenesis, invasion, and metastasis.
Among these gene products are TNF and members of its superfamily, IL-1a, IL-1b, IL-6,
IL-8, IL-18, chemokines, MMP-9, VEGF, COX-2, and 5-LOX. The expression of all these genes
are mainly regulated by the transcription factor NF-kB, which is constitutively active in most
tumors and is induced by carcinogens (such as cigarette smoke), tumor promoters, carcinogenic
viral proteins (HIV-tat, HIV-nef, HIV-vpr, KHSV, EBV-LMP1, HTLV1-tax, HPV, HCV,
and HBV), chemotherapeutic agents, and g-irradiation. These observations imply that antiinflammatory
agents that suppress NF-kB or NF-kB-regulated products should have a
potential in both the prevention and treatment of cancer. The current review describes
in detail the critical link between inflammation and cancer.
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