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By Bruce C Baguley; David J Kerr

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1997). Chk1 is a wee1 kinase in the G2 DNA damage checkpoint inhibiting cdc2 by Y15 phosphorylation. EMBO J. 16, 545–554. , and Ui, M. (1994). Essential role of phosphatidylinositol 3-kinase in insulin-induced glucose transport and antilipolysis in rat adipocytes. Studies with a selective inhibitor wortmannin. J. Biol. Chem. 269, 3568–3573. , Pei, X. , and Hara, N. (2000). Alteration of drug chemosensitivity caused by the adenovirusmediated transfer of the wild-type p53 gene in human lung cancer cells.

1996). Both of these pathways are involved in mitogenesis and cell survival. 34 LEOPOLD ET AL. B. , 1994; Depotter, 1994; Hynes and Stern, 1994; Davies and Chamberlin, 1996; Qian and Greene, 1997). , 1994). , 1997). , 1996). , 1995). These data, coupled with the fact that the tyrosine kinase activity is absolutely required for their mitogenic and transforming properties, provide a strong rationale to focus on these receptors as viable targets for cancer chemotherapy. Thus far two approaches have been taken to attack this family of receptors on tumors.

Cancer cell cycles. Science 274, 1672–1677. Sherr, C. , and Roberts, J. M. (1999). CDK inhibitors: positive and negative regulators of G1-phase progression. Genes Dev. 13, 1501–1512. Shieh, S. , and Prives, C. (2000). The human homologs of checkpoint kinases Chk1 and Cds1 (Chk2) phosphorylate p53 at multiple DNA damage-inducible sites. Genes Dev. 14, 289–300. 30 POMMIER, YU, AND KOHN Shieh, S. , and Prives, C. (1997). DNA damageinduced phosphorylation of p53 alleviates inhibition by MDM2. Cell 91, 325–334.

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