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- W1006465369 abstract "Radiation is an important modality of therapy for a variety of cancers, including squamous cell carcinomas (SCC) of the head and neck and skin. Cell survival and resistance following radiation are mediated by cytoprotective molecules that regulate cellcycle progression and cell death. Constitutive and radiation-induced activation of the transcription factor nuclear factor-κB (NF-κB) and cell-cycle regulatory proteins have been shown to contribute to differences in resistance of SCC to radiation (Kato et al., Head Neck 2000;22:748–759). NF-κB and one of its target genes, cyclin D1, are regulated by signal activation and degradation of inhibitor-κBs by the proteasome. In addition, the proteasome degrades cyclin inhibitors. We investigated the effects of the proteasome inhibitor bortezomib (PS-341, Velcade) on NF-κB activation and cell-cycle regulatory protein expression, as well as cell-cycle and radiosensitizing effects in SCC. Bortezomib produced accumulation of cyclin inhibitor p21 and inhibited activation of NF-κB and cyclin D1. Bortezomib had direct cytotoxic activity, and an accumulation of SCC cells in the radiosensitive G2/M phase of the cell cycle was accompanied by further radiosensitization. Clinical studies of concomitant therapy with bortezomib and radiation are under way in patients with SCC of the head and neck." @default.
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- W1006465369 date "2004-01-01" @default.
- W1006465369 modified "2023-09-23" @default.
- W1006465369 title "Radiosensitization and Proteasome Inhibition" @default.
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- W1006465369 doi "https://doi.org/10.1007/978-1-59259-794-9_10" @default.
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