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      TNF- and cancer therapy-induced apoptosis: potentiation by inhibition of NF-kappaB.

      Science (New York, N.Y.)

      Antibiotics, Antineoplastic, pharmacology, Antineoplastic Combined Chemotherapy Protocols, therapeutic use, Apoptosis, drug effects, radiation effects, Cell Nucleus, metabolism, Cycloheximide, DNA-Binding Proteins, Daunorubicin, Humans, I-kappa B Proteins, Interleukin-1, Leupeptins, NF-kappa B, antagonists & inhibitors, physiology, Neoplasms, drug therapy, radiotherapy, Protein Synthesis Inhibitors, Radiation, Ionizing, Staurosporine, Transcription Factor RelA, Tumor Cells, Cultured, Tumor Necrosis Factor-alpha

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          Abstract

          Many cells are resistant to stimuli that can induce apoptosis, but the mechanisms involved are not fully understood. The activation of the transcription factor nuclear factor-kappa B (NF-kappaB) by tumor necrosis factor (TNF), ionizing radiation, or daunorubicin (a cancer chemotherapeutic compound), was found to protect from cell killing. Inhibition of NF-kappaB nuclear translocation enhanced apoptotic killing by these reagents but not by apoptotic stimuli that do not activate NF-kappaB. These results provide a mechanism of cellular resistance to killing by some apoptotic reagents, offer insight into a new role for NF-kappaB, and have potential for improvement of the efficacy of cancer therapies.

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          8864119

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