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A role for CDK9 in UV damage response

Cell Cycle
Landes Bioscience
Publication Date
DOI: 10.4161/cc.20963
  • Cell Cycle News & Views
  • Medicine


© 2012 Landes Bioscience. Do not distribute. Cell Cycle 2227 Cell Cycle 11:12 2227-2232; June 15, 2012; © 2012 Landes Bioscience CeLL CyCLe news & views CeLL CyCLe news & views The occurrence of intolerable side effects in patients undergoing chemotherapy is still a major clinical hurdle. Finding tumor-spe- cific therapy and exploiting the differences between normal cells and tumor cells has led to strategies targeting oncogenic mutations or the deficiency of tumor suppressor pathways in cancers. Alternatively, focusing efforts to protect normal cells from the side effects of chemotherapy has gained much interest, and harnessing cell cycle checkpoints to target tumor cells while sparing normal cells is an attractive strategy. Contrary to achieving drug synergism when targeting tumor cells, one hopes to achieve drug “antagonism” on normal cells in a proposed strategy, termed “cyclotherapy.”1 The concept requires the use of two drugs, the first to arrest the normal cells and the second, to kill only cycling (tumor) cells (Fig. 1). The high frequency of p53 mutations in human cancers presents an opportunity for selectively targeting the p53-deficient tumors using s- or M-phase poisons, by activating a checkpoint arrest only in the normal cells. indeed, several recent studies demonstrate that p53 activation Cell Cycle News & Views Protecting normal cells from the cytotoxicity of chemotherapy Comment on: van Leeuwen IMM, et al. Cell Cycle 2012; 11:1851–61; PMID:22517433; Chit Fang Cheok; IFOM-p53 Lab Joint Research Laboratory; The FIRC Institute of Molecular Oncology; Milan, Italy and Agency for Science, Technology and Research; Singapore; Email: [email protected] or [email protected]; protects normal cells from the toxicity of drugs acting in the s-phase or M-phase, including Ara-C,2 taxol,3 Aurora kinase inhibitors4 and Polo-like k

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