By Ian S. Fentiman
Guy's health center, London, united kingdom. specializes in present examine and destiny advancements within the box. hugely topical textual content designed for the expert looking the newest pondering at the debatable parts surrounding breast melanoma. Sections comprise biology, prognosis, preliminary remedy difficulties, and systemic treatment. References are superstar rated. DNLM: Breast Neoplasms.
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Extra resources for Challenges in Breast Cancer
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).