Apoptosis Senescence and Cancer by David A Gewirtz (Editor), Shawn Edan Holt (Editor), Steven

By David A Gewirtz (Editor), Shawn Edan Holt (Editor), Steven Grant (Editor)

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249. Rampino N, Yamamoto H, Ionov Y, et al. Somatic frameshift mutations in the BAX gene in colon cancers of the microsatellite mutator phenotype. Science 1997; 275(5302):967–9. 250. Degenhardt K, Chen G, Linsten T, White E. BAX and BAK mediate p53-independent suppression of tumorigenesis. Cancer Cell 2002; 2:193–203. 251. Vivanco I, Sawyers CL. The phosphatidylinositol 3-kinase AKT pathway in human cancer. Nat Rev Cancer 2002; 2:489–501. 252. Samuels Y, Wang Z, Bardelli A, et al. High frequency of mutations of the PIK3CA gene in human cancers.

As indicated elsewhere in this monograph, cells can also suffer other fates after drug treatment, and these other fates are not necessarily modulated by changes in the apoptotic machinery. Clinical studies examining the correlation between expression of various components of the apoptotic machinery and treatment outcome have been extensively reviewed (15,263,264). These studies, while potentially important for identifying predictive markers that might alter treatment and for confirming activation of various pathways that might serve as drug targets in future trials, do not establish causality.

64. Newmeyer DD, Ferguson-Miller S. Mitochondria: releasing power for life and unleashing the machineries of death. Cell 2003; 112:481–90. 65. Jiang X, Wang X. Cytochrome C-mediated apoptosis. Annu Rev Biochem 2004; 73:87–106. 66. Anflous K, Armstrong DD, Craigen WJ. Altered mitochondrial sensitivity for ADP and maintenance of creatine-stimulated respiration in oxidative striated muscles from VDAC1-deficient mice. J Biol Chem 2001; 276:1954–60. 67. Graham BH, Waymire KG, Cottrell B, Trounce IA, MacGregor GR, Wallace DC.

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