Document Detail


Recent advances in targeting regulators of apoptosis in cancer cells for therapeutic gain.
MedLine Citation:
PMID:  16732718     Owner:  NLM     Status:  MEDLINE    
Abstract/OtherAbstract:
Apoptosis is a fundamental cellular death process that is essential for normal tissue homeostasis, whose deregulation is associated with several human disease states, including cancer. Increased understanding of cancer biology has led to the hypothesis that although cancer cells are inherently resistant to the engagement of apoptosis due to the deregulation of molecular components of core apoptotic machinery or of survival signalling cascades, they are primed to die as a result of microenvironmental and oncogenic proapoptotic stress. Recently, deeper insight into the molecular regulation of apoptosis and, specifically, into its deregulation in cancer has led to the development of promising therapies to restore apoptosis and enable selective tumour cell kill. It is hoped that these mechanism-based therapies will exhibit less problematic toxicity profiles than those of conventional agents. Moreover, the development of tailored therapies directed at malignancies bearing specific alterations in apoptotic or survival signalling components may be used in combination approaches to overcome the resistance to other forms of treatment.
Authors:
Kathryn Taylor; Dimitra Micha; Malcolm Ranson; Caroline Dive
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Publication Detail:
Type:  Journal Article; Review    
Journal Detail:
Title:  Expert opinion on investigational drugs     Volume:  15     ISSN:  1744-7658     ISO Abbreviation:  Expert Opin Investig Drugs     Publication Date:  2006 Jun 
Date Detail:
Created Date:  2006-05-30     Completed Date:  2007-10-26     Revised Date:  2007-11-15    
Medline Journal Info:
Nlm Unique ID:  9434197     Medline TA:  Expert Opin Investig Drugs     Country:  England    
Other Details:
Languages:  eng     Pagination:  669-90     Citation Subset:  IM    
Affiliation:
Paterson Institute for Cancer Research, Clinical and Experimental Pharmacology Group, University of Manchester, Wilmslow Road, Withington, Manchester, M20 4BX, UK.
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MeSH Terms
Descriptor/Qualifier:
1-Phosphatidylinositol 3-Kinase / antagonists & inhibitors,  metabolism
Alkaloids / pharmacology,  therapeutic use
Animals
Antineoplastic Agents / pharmacology,  therapeutic use*
Apoptosis* / drug effects,  genetics
Benzophenanthridines / pharmacology,  therapeutic use
Caspases / metabolism
Clinical Trials as Topic
Drug Evaluation, Preclinical
Humans
Neoplasms / drug therapy,  genetics,  metabolism*
Oligonucleotides, Antisense / genetics,  metabolism*
Protein Kinase Inhibitors / pharmacology,  therapeutic use
Proto-Oncogene Proteins c-bcl-2 / genetics,  metabolism
Receptors, Tumor Necrosis Factor / drug effects,  metabolism
Recombinant Proteins / pharmacology,  therapeutic use
Signal Transduction / drug effects
TNF-Related Apoptosis-Inducing Ligand / genetics,  pharmacology,  therapeutic use
Thionucleotides / genetics,  metabolism
X-Linked Inhibitor of Apoptosis Protein / genetics,  metabolism
bcl-X Protein / genetics,  metabolism
Chemical
Reg. No./Substance:
0/Alkaloids; 0/Antineoplastic Agents; 0/Benzophenanthridines; 0/Oligonucleotides, Antisense; 0/Protein Kinase Inhibitors; 0/Proto-Oncogene Proteins c-bcl-2; 0/Receptors, Tumor Necrosis Factor; 0/Recombinant Proteins; 0/TNF-Related Apoptosis-Inducing Ligand; 0/Thionucleotides; 0/X-Linked Inhibitor of Apoptosis Protein; 0/bcl-X Protein; 0/oblimersen; 34316-15-9/chelerythrine; EC 2.7.1.137/1-Phosphatidylinositol 3-Kinase; EC 3.4.22.-/Caspases

From MEDLINE®/PubMed®, a database of the U.S. National Library of Medicine


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