Anticancer Drug Development by Bruce C. Baguley (Author), David J. Kerr (Author)

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By Bruce C. Baguley (Author), David J. Kerr (Author)

The following in one resource is a whole spectrum of rules at the improvement of latest anticancer medicinal drugs. Containing concise studies of multidisciplinary fields of study, this ebook bargains a wealth of principles on present and destiny molecular pursuits for drug layout, together with sign transduction, the telephone department cycle, and programmed mobile dying. distinct descriptions of resources for brand new medicinal drugs and strategies for checking out and medical trial layout also are supplied. KEY FEATURES:* One paintings that may be consulted for all elements of anticancer drug improvement* Concise studies of analysis fields, mixed with functional medical element, written through across the world revered specialists* A wealth of rules on present and destiny molecular objectives for drug layout, together with sign transduction, the cellphone department cycle, and programmed telephone demise * specific descriptions of the assets of recent anticancer medicines, together with combinatorial chemistry, phage show, and typical items* dialogue of the way new medicinal drugs could be established in preclinical platforms, together with the most recent expertise of robot assay platforms, cellphone tradition, and experimental animal concepts* 1000's of references that let the reader to entry suitable medical and clinical literature* transparent illustrations, a few in colour, that offer either realizing of the sphere and fabric for educating

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J. Cell. Sci. 111, 2445–2453. Lane, D. P. (1999). Exploiting the p53 pathway for cancer diagnosis and therapy. Br. J. Cancer 80(Suppl 1), 1–5. 28 POMMIER, YU, AND KOHN Lane, D. , and Hall, P. A. (1997). MDM2—arbiter of p53’s destruction. Trends Biochem. Sci. 22, 372–374. Lau, C. , and Pardee, A. B. (1982). Mechanism by which caffeine potentiates lethality of nitrogen mustard. Proc. Natl. Acad. Sci. USA 79, 2942–2946. , and Jansen-Durr, P. (1999). E2F target genes and cell-cycle checkpoint control.

Direct binding of cyclin D to the retinoblastoma gene product (pRb) and pRb phosphorylation by the cyclin D-dependent kinase CDK4. Genes Dev. 7, 331–342. , and Sausville, E. (1992). Growth inhibition with reversible cell cycle arrest of carcinoma cells by flavone L86-8275. J. Natl. Cancer Inst. 84, 1736–1740. Khanna, K. , Keating, K. , Lees-Miller, S. , and Lavin, M. F. (1998). ATM associates with and phosphorylates p53: mapping the region of interaction. Nat. Genet. 20, 398–400. Khuri, F. , Tannock, I.

Because this radiosensitization is also observed in p53-deficient cells (Price and Youmell, 1996), it is plausible that wortmannin potentiates genotoxic lesions by mechanisms other than ATM inhibition and p53 destabilization. , 1999), as well as potentiation of apoptosis by PI3K inhibition. The reactivity/instability of wortmannin precludes clinical use of the drug. However, other agents that selectively inhibit DNA-PK or ATM might be worth developing. 24 POMMIER, YU, AND KOHN C. Other Sites for Intervention 1.

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