Apoptosis and Cancer Chemotherapy by J. Martin Brown PhD, Bradly G. Wouters PhD (auth.), John A.

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

The prior few years have witnessed an staggering overseas attempt that demonstrated the function of a few 20 new molecules in apoptosis and extra activation or suppression of apoptosis to the authorised organic services of a superb many others already favourite in melanoma biology. a few of these molecules are receptors, transducing cytokine-mediated indications; others seem to accentuate or curb the danger compro­ mised phone will fireplace its apoptosis effector mechanism. All are of curiosity as power goals for tumor treatment, and a few could turn out to be keep an eye on issues encouraged within the pathogenesis of melanoma and different illnesses as assorted as viral an infection, neurodegenerative problems, and stroke. occasionally, in the middle of those advancements, one of those euphoria ap­ pears to have gripped the learn neighborhood, with the expectancy that apoptosis will have the funds for factors to many unsolved questions in cellu­ lar law. This e-book, in a chain of considerate and provocative ar­ ticles--some from tested leaders within the box, and others from more youthful scientists--seeks to redress the balance.

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Also, the fact that p53 loss leads to less damage of normal tissue provides proof-of-concept data that inhibitors of p53 function might act as chemoprotective agents. 34 Lowe ""49. Sjogren S, Inganas M, Norberg T, Lindgren A, Nordgren H, Holmberg L, Bergh 1. p53 gene in breast cancer: prognostic value of complementary DNA sequencing versus immunohistochemistry. J Natl Cancer Inst 1996; 88: 173-182. Provides a clear example of how the use of different methodological approaches can alter the interpretation of clinical studies.

REGULATORS OF p53 Because p53 may be the most important suppressor of human cancer, there has been an intense effort to identify its mechanism of action. One of the basic approaches to this question has been to identify what proteins interact with p53, and how the interactions modulate its function. Historically, the first group of p53-interacting proteins discovered were several transforming viral oncoproteins. In fact, p53 was discovered as an SV40 large T-antigen interacting protein. It is also targeted for inactivation by HPV E6, which, through E6-associated protein, an E3-ubiquitin ligase, resulted in its degradation.

Chapter 1 I Apoptosis and Cell Sensitivity 19 052. Brown JM. NCI's anticancer drug screening program may not be selecting for clinically active compounds. Oncol Res 1997; 9: 213-215. Points out that the 60-cell-line screen for anticancer drugs used by the NCI measures growth delay rather than cell killing, and therefore may not be selecting for agents that would be effective anticancer drugs. 053. Rupnow BA, Murtha AD, Alarcon RM, Giaccia AJ, Knox SJ. Direct evidence that apoptosis enhances tumor responses to fractionated radiotherapy.

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