© 1999 by Oxford University Press
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-
B InhibitionProgress and Pitfalls
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-
B, an immediate early response after
exposure to ionizing radiations, functions to protect cells from
apoptosis (programmed cell death), but the role of NF-
B in mitotic
cell death has not been fully defined (1,2). NF-
B is
constitutively activated in lymphoid cells, immortal ataxia
telangiectasia (AT) fibroblasts, and other cells (3-
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