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B Activation: From Bench to BedsideCytokine Research Laboratory, Department of Experimental Therapeutics, The University of Texas M. D. Anderson Cancer Center, 1515 Holcombe Boulevard, Box 143, Houston, Texas 77030
To whom requests for reprints should be addressed at 1 Bharat B. Aggarwal, Cytokine Research Laboratory, Department of Experimental Therapeutics, The University of Texas M. D. Anderson Cancer Center, 1515 Holcombe Boulevard, Box 143, Houston, TX 77030. Email: aggarwal{at}mdanderson.org
Nuclear factor-
B (NF-
B) is a proinflammatory transcription factor that has emerged as an important player in the development and progression of malignant cancers. NF-
B targets genes that promote tumor cell proliferation, survival, metastasis, inflammation, invasion, and angiogenesis. Constitutive or aberrant activation of NF-
is frequently encountered in many human tumors and is associated with a resistant phenotype and poor prognosis. The mechanism of such persistent NF-
B activation is not clear but may involve defects in signaling pathways, mutations, or chromosomal rearrangements. Suppression of constitutive NF-
B activation inhibits the oncogenic potential of transformed cells and thus makes NF-
B an interesting new therapeutic target in cancer.
Key Words: NF-
B cancer IKK metastasis invasion
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