By Erik S. Knudsen, Wesley A. Braden (auth.), Wei Dai PhD (eds.)
Extensive examine has exposed a suite of molecular surveillance mechanisms – usually known as "checkpoints" – which tightly computer screen cell-cycle tactics. Today’s anticancer drug improvement has pointed out lots of those cell-cycle checkpoint molecules as potent pursuits. learn now provides to discover a brand new new release of anticancer medications with enhanced healing indices in accordance with their skill to focus on rising checkpoint elements. Checkpoint Responses in melanoma remedy summarizes the advances revamped the previous two decades, deciding upon parts of cell-cycle checkpoints and their molecular law in the course of checkpoint activation and validating using checkpoint proteins as ambitions for the improvement of anticancer medicinal drugs. This book’s uncommon panel of authors takes an in depth examine issues starting from the foremost molecular gamers affecting DNA synthesis and the reaction to DNA harm to advances made within the id of chemical substances able to inhibiting person mitotic kinases. Illuminating and authoritative, Checkpoint Responses in melanoma treatment bargains a severe precis of findings for researchers within the pharmaceutical and biotechnology industries and a necessary source for educational scientists in melanoma study and the research of cell-cycle legislation, sign transduction and apoptosis.
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Additional resources for Checkpoint Responses in Cancer Therapy
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). Despite multiple attempts to show interaction of CP-31398 and PRIMA1 with p53 by biophysical methods there have been no data reported supporting a direct interaction of CP-31398 (86) or PRIMA-1 with p53.
In addition, the high concentrations needed to mediate CP-31398 and PRIMA-1 action on p53 (up to 150 μM in in vitro and cellular assays) compared to a lower IC50 in cell proliferation assays (ca. 20 μM for PRIMA-1) suggests Chapter 2 / Targeting the p53/MDM2 Pathway for Cancer Therapy 27 that PRIMA-1 might exhibit off-target activities. Taken together the mode of action of both CP-31398 and PRIMA-1 remains elusive and somewhat controversial. The first proof-of-concept for rescuing of mutant p53 by a peptide stabilizing wild-type p53 conformation has come from studies with a short SH3 domain peptide CDB3.
2. THE p53 TUMOR SUPPRESSOR PROTEIN The p53 protein has been described for the first time in 1979 as an oncoprotein. However, in the following years, it has been recognized that only mutated p53 acts as oncoprotein whereas the normal wild-type protein possess the properties of a tumor suppressor (8,9). Lane first proposed that p53 functions as a “guardian of the genome” protecting mammalian cells from the consequences of DNA damage (10). Later this protective role has been expanded to include a wide variety of oncogenic stresses thus establishing p53 as the “cellular gatekeeper” (11).