Download Checkpoint Responses in Cancer Therapy (Cancer Drug by Wei Dai PDF

By Wei Dai

ISBN-10: 1588299309

ISBN-13: 9781588299307

ISBN-10: 1597452742

ISBN-13: 9781597452748

Extensive study has exposed a suite of molecular surveillance mechanisms – quite often known as “checkpoints” – which tightly visual display unit cell-cycle tactics. Today’s anticancer drug improvement has pointed out lots of those cell-cycle checkpoint molecules as powerful pursuits. examine now delivers to discover a brand new new release of anticancer medications with superior healing indices in keeping with their skill to focus on rising checkpoint elements. Checkpoint Responses in melanoma remedy summarizes the advances revamped the earlier two decades, settling on parts of cell-cycle checkpoints and their molecular law in the course of checkpoint activation and validating using checkpoint proteins as objectives for the advance of anticancer medications. This book’s uncommon panel of authors takes a detailed examine issues starting from the foremost molecular avid gamers affecting DNA synthesis and the reaction to DNA harm to advances made within the identity of chemicals in a position to inhibiting person mitotic kinases. Illuminating and authoritative, Checkpoint Responses in melanoma remedy deals a severe precis of findings for researchers within the pharmaceutical and biotechnology industries and a important source for tutorial scientists in melanoma learn and the research of cell-cycle rules, sign transduction and apoptosis.

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Additional resources for Checkpoint Responses in Cancer Therapy (Cancer Drug Discovery and Development)

Example text

Later this protective role has been expanded to include a wide variety of oncogenic stresses thus establishing p53 as the “cellular gatekeeper” (11). The p53 tumor suppressor serves as a central node in a complex signal transduction network known as the p53 pathway, which has evolved as a major defense against cancer. This pathway recognizes diverse forms of oncogenic stress within the cellular environment and translates them into appropriate cellular responses to minimize tumorigenic consequences.

Work conducted by independent laboratories have supported part of these findings and have reported a selective induction of apoptosis by PRIMA-1 in mutant p53 cells via the c-JunNH2-kinase pathway (91). Recently, a new family of p53 reactivators derived from the backbone of PRIMA-1 were described (92). Myers et al. (2005) have found that PRIMA-1 and their derivatives selectively eliminate mutant p53 cells, however, they have been unable to find any evidence for restoration of wild-type p53 properties including p53-induced reporter gene activation in vitro (92).

P73: Friend or foe in tumorigenesis. Nat Rev Cancer 2002; 2:605–615. 38. Moll UM, Slade N. p63 and p73: roles in development and tumor formation. Mol Cancer Res 2004; 2:371–386. 39. Arrowsmith CH, Morin P. New insights into p53 function from structural studies. Oncogene 1996; 12:1379–1385. 40. Arrowsmith CH. Structure and function in the p53 family. Cell Death Differ 1999; 6:1169–1173. 41. El-Deiry WS, Kern SE, Pietenpol JA, Kinzler KW, Vogelstein B. Definition of a consensus binding site for p53.

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Checkpoint Responses in Cancer Therapy (Cancer Drug Discovery and Development) by Wei Dai


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