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JNCI Journal of the National Cancer Institute 1999 91(22):1910-1911; doi:10.1093/jnci/91.22.1910
© 1999 by Oxford University Press
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Journal of the National Cancer Institute, Vol. 91, No. 22, 1910-1911, November 17, 1999
© 1999 Oxford University Press


EDITORIALS

Radiosensitivity and Transcription Factor NF-{kappa}B Inhibition—Progress and Pitfalls

Anatoly Dritschilo

Correspondence to: Anatoly Dritschilo, M.D., Department of Radiation Medicine, Georgetown University Medical Center, TRB E202A-B, 3970 Reservoir Rd., N.W., Washington, DC 20007 (e-mail: dritscha@gunet.georgetown.edu).

Cellular responses to ionizing radiation include activation of signal transduction cascades that may originate at the plasma membrane, cytoplasm, or nucleus. The cell's success in dealing with radiation "stress" determines its survival or death. Activation of transcription factor NF-{kappa}B, an immediate early response after exposure to ionizing radiations, functions to protect cells from apoptosis (programmed cell death), but the role of NF-{kappa}B in mitotic cell death has not been fully defined (1,2). NF-{kappa}B is constitutively activated in lymphoid cells, immortal ataxia telangiectasia (AT) fibroblasts, and other cells (3-. . . [Full Text of this Article]

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