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By J. Martin Brown PhD, Bradly G. Wouters PhD (auth.), John A. Hickman, Caroline Dive (eds.)

The previous few years have witnessed an excellent overseas attempt that proven the position of a few 20 new molecules in apoptosis and extra activation or suppression of apoptosis to the approved organic services of an excellent many others already usual in melanoma biology. a few of these molecules are receptors, transducing cytokine-mediated indications; others seem to accentuate or minimize the danger compro­ mised phone will hearth its apoptosis effector mechanism. All are of curiosity as power objectives for tumor treatment, and a few may well turn out to be keep watch over issues motivated within the pathogenesis of melanoma and different ailments as diversified as viral an infection, neurodegenerative issues, and stroke. occasionally, in the middle of those advancements, one of those euphoria ap­ pears to have gripped the study group, with the expectancy that apoptosis will manage to pay for reasons to many unsolved questions in cellu­ lar legislation. This booklet, in a chain of considerate and provocative ar­ ticles--some from demonstrated leaders within the box, and others from more youthful scientists--seeks to redress the balance.

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16. Skipper HE, Schabel FM, Wilcox WS. Experimental evaluation of potential anticancer agents, XIII. On the criteria and kinetics associated with "curability" of experimental leukemias. Cancer Chemother Rep 1964; 35: 1-111. 17. Lamb JR, Friend SH. Which guesstimate is the best guesstimate? Predicting chemotherapeutic outcomes. Nature Med 1997; 3: 962,963. 18. Gura T. Cancer models: systems for identifying new drugs are often faulty. Science 1997; 278: 1041,1042. ··19. Tannock IF. Biological properties of anticancer drugs.

Jung M, Notario V, Dritschilo A. Mutations in the p53 gene in radiation-sensitive and -resistant human squamous carcinoma cells. Cancer Res 1992; 52: 6390-3693. 30. Ribeiro JC, Barnetson AR, Fisher RJ, Mameghan H, Russell PI. Relationship between radiation response and p53 status in human bladder cancer cells. Int J Radiat Bioi 1997; 72: 11-20. 31. Zolzer F, Hillebrandt S, Streffer C. Radiation induced G I-block and p53 status in six human cell lines. Radiother Onco11995; 37: 20-28. 32. Biard DS, Martin M, Rhun YL, Duthu A, Lefaix JL, May E, May P.

Still, p53 can enhance drug-induced toxicity in clonogenic survival assays (21-,46-,47) or, more importantly, in vivo (10--,20--,48"). A more likely explanation for this paradox is methodological, because current technologies are unable to properly classify tumors based on p53 functional status. Finally, the diversity of p53 activities and subsequent 26 Lowe consequences of p53 loss may vary between settings. Because defects in damage-induced checkpoints may enhance chemosensitivity, but defects in apoptosis promote drug resistance, the clinical impact of p53 mutation may be determined by which effect predominates.

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