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- Volume 17, Issue 6, 2011
Current Pharmaceutical Design - Volume 17, Issue 6, 2011
Volume 17, Issue 6, 2011
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Editorial [Hot Topic: Pharmaceutical Reactivation of p53 Pathways in Cancer (Executive Guest Editor: Asfar S. Azmi)]
More LessP53 was discovered 30 years ago and research during the last three decades has produced over 55,000 publications leading to deeper understanding of this crucial protein [1]. Majority of cancers have dysfunctional p53, either through mutation of the p53 gene itself or alterations in factors that modulate p53's stability and activity. This has led to numerous strategies to combat cancer by re-activating p53 or related p Read More
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Small-Molecule Inhibitors of p53-MDM2 Interaction: the 2006-2010 Update
Authors: Melissa Millard, Divya Pathania, Fedora Grande, Shili Xu and Nouri NeamatiIncreasing knowledge of the relationship between p53 and MDM2 has led to development of potential small molecule inhibitors useful for clinical studies. Herein, we discuss the patented (2006-2010) inhibitors of p53-MDM2 interaction. The anticancer agents discussed in this review belong to several different chemical classes including benzodiazepinediones, cis-imidazolines, oxindoles, spirooxindoles, and numerous miscellane Read More
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Pharmacologic Activation of p53 by Small-Molecule MDM2 Antagonists
Authors: Hong Shen and Carl G. MakiRestoring p53 activity by inhibiting the interaction between p53 and MDM2 represents an attractive approach for cancer therapy. To this end, a number of small-molecule p53-MDM2 binding inhibitors have been developed during the past several years. Nutlin-3 is a potent and selective small-molecule MDM2 antagonist that has shown considerable promise in pre-clinical studies. This review will highlight recent advances in the Read More
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Recent Advances in the Therapeutic Perspectives of Nutlin-3
Authors: Paola Secchiero, Raffaella Bosco, Claudio Celeghini and Giorgio ZauliNutlin-3 is a small molecule inhibitor of the MDM2/p53 interaction, which leads to the non-genotoxic p53 stabilization, activation of cell cycle arrest and apoptosis pathways. A series of recent studies have strengthened the concept that selective, non-genotoxic p53 activation by Nutlin-3 might represent an alternative to the current cytotoxic chemotherapy, in particular for pediatric tumors and for hematological malignancies, Read More
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p73 as a Pharmaceutical Target for Cancer Therapy
Authors: Andrea Bisso, Licio Collavin and Giannino Del SalAbout half of all human tumors contain an inactivating mutation of p53, while in the remaining tumors, the p53 pathway is frequently abrogated by alterations of other components of its signaling pathway. In humans, the p53 tumor suppressor is part of a small gene family that includes two other members, p73 and p63, structurally and functionally related to p53. Accumulating evidences indicate that all p53-family proteins f Read More
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Targeting p73 - a Potential Approach in Cancer Treatment
Authors: Neda Slade and Andela HorvatThe p53 family consists of three members: p53, p63 and p73. All three of them have a role in cell cycle arrest and induction of apoptosis. However, despite structural and partly functional similarity, there are striking differences in their functions and each of them has its own and unique identity. All three genes encode multiple variants with opposing functions in cancer development - full length transactivation forms with proapopt Read More
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Peptide Activators of the p53 Tumor Suppressor
Authors: Changyou Zhan and Wuyuan LuThe oncoproteins MDM2 and MDMX negatively regulate the activity and stability of the p53 tumor suppressor, directly contributing to the development and progression of many tumors harboring wild type p53. Antagonizing MDM2 and MDMX to activate the p53 pathway has thus become an attractive new strategy for anticancer drug design. Several different classes of MDM2 and MDMX antagonists have been rep Read More
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p53 Activation by Blocking Snail : A Novel Pharmacological Strategy for Cancer
Authors: Sun-Hye Lee and Bum-Joon ParkSince p53 is the strongest tumor suppressor gene, which can regulate apoptosis, cell cycle arrest and senescence, re-activation of p53 and its pathway seem to be very plausible target for cancer therapy. However, in 50% of human cancers, p53 itself is mutated. In addition, in remaining half of cancers, it is inactivated by distortion of signaling pathways. Moreover, differentially from typical tumor suppressor genes such as Read More
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Tissue-Specific Therapeutic Targeting of p53 in Cancer: One Size Does Not Fit All
Authors: Nikolina Vlatkovic, Kerryanne Crawford, Carlos P. Rubbi and Mark T. Boydp53, the “guardian of the genome” and the most mutated gene in cancer presents a considerable therapeutic opportunity as well as a challenge. In the past decade, several therapeutic strategies have been developed that aim to take advantage of a wealth of knowledge about p53, including insights into the biology and patho-biology of p53. Nevertheless, considerable challenges remain, not least as a result of tissue- and can Read More
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Pharmacological Activation of p53 in Cancer Cells
Authors: Mohammad Athar, Craig A. Elmets and Levy KopelovichTumor suppressor p53 is a transcription factor that regulates a large number of genes and guards against genomic instability. Under multiple cellular stress conditions, p53 functions to block cell cycle progression transiently unless proper DNA repair occurs. Failure of DNA repair mechanisms leads to p53-mediated induction of cell death programs. p53 also induces permanent cell cycle arrest known as cellular se Read More
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Network Perspectives on HDM2 Inhibitor Chemotherapy Combinations
Authors: Asfar S. Azmi, Frances W.J. Beck, Fazlul H. Sarkar and Ramzi M. MohammadThe discovery of small molecule inhibitors of HDM2-p53 interaction is considered one of the most significant therapeutic developments in the area p53 research. Intensive work on different classes of HDM2 inhibitors has proven their therapeutic utility as activators of p53 in multiple tumor models. Many laboratories have shown that HDM2 inhibitors can synergize with chemotherapeutic agents resulting in enhanced efficacy Read More
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Volumes & issues
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Volume 31 (2025)
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Volume 30 (2024)
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Volume 29 (2023)
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Volume 28 (2022)
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Volume 27 (2021)
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Volume 26 (2020)
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Volume 25 (2019)
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Volume 24 (2018)
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Volume 23 (2017)
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Volume 22 (2016)
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Volume 21 (2015)
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Volume 20 (2014)
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Volume 19 (2013)
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Volume 18 (2012)
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Volume 17 (2011)
- Issue 38
- Issue 37
- Issue 36
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- Issue 31
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- Issue 14
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- Issue 12
- Issue 11
- Issue 10
- Issue 9
- Issue 8
- Issue 7
- Issue 6
- Issue 5
- Issue 4
- Issue 3
- Issue 2
- Issue 1
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Volume 16 (2010)
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Volume 15 (2009)
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Volume 14 (2008)
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Volume 13 (2007)
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Volume 12 (2006)
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Volume 11 (2005)
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Volume 10 (2004)
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Volume 9 (2003)
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Volume 8 (2002)
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Volume 7 (2001)
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Volume 6 (2000)
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