Document Detail


Combined modality therapy with TRAIL or agonistic death receptor antibodies.
MedLine Citation:
PMID:  21263219     Owner:  NLM     Status:  MEDLINE    
Abstract/OtherAbstract:
Molecularly targeted therapies, such as antibodies and small molecule inhibitors have emerged as an important breakthrough in the treatment of many human cancers. One targeted therapy under development is tumor necrosis factor-related apoptosis-inducing ligand (TRAIL) due to its ability to induce apoptosis in a variety of human cancer cell lines and xenografts, while lacking toxicity in most normal cells. TRAIL and apoptosis-inducing agonistic antibodies to the TRAIL death receptors have been the subject of many preclinical and clinical studies in the past decade. However, the sensitivity of individual cancer cell lines of a particular tumor type to these agents varies from highly sensitive to resistant. Various chemotherapy agents have been shown to enhance the apoptosis-inducing capacity of TRAIL receptor-targeted therapies and induce sensitization of TRAIL-resistant cells. This review provides an overview of the mechanisms associated with chemotherapy enhancement of TRAIL receptor-targeted therapies including modulation of the apoptotic (death receptor expression, FLIP, and Bcl-2 or inhibitors of apoptosis (IAP) families) as well as cell signaling (NFκB, Akt, p53) pathways. These mechanisms will be important in establishing effective combinations to pursue clinically and in determining relevant targets for future cancer therapies.
Authors:
Hope M Amm; Patsy G Oliver; Choo Hyung Lee; Yufeng Li; Donald J Buchsbaum
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Publication Detail:
Type:  Journal Article; Research Support, N.I.H., Extramural; Research Support, Non-U.S. Gov't; Review     Date:  2011-03-01
Journal Detail:
Title:  Cancer biology & therapy     Volume:  11     ISSN:  1555-8576     ISO Abbreviation:  Cancer Biol. Ther.     Publication Date:  2011 Mar 
Date Detail:
Created Date:  2011-03-03     Completed Date:  2011-09-14     Revised Date:  2013-06-30    
Medline Journal Info:
Nlm Unique ID:  101137842     Medline TA:  Cancer Biol Ther     Country:  United States    
Other Details:
Languages:  eng     Pagination:  431-49     Citation Subset:  IM    
Affiliation:
Department of Pharmacology and Toxicology, University of Alabama at Birmingham, USA.
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MeSH Terms
Descriptor/Qualifier:
Antibodies, Monoclonal / therapeutic use
Antineoplastic Agents / metabolism,  therapeutic use*
Apoptosis
Combined Modality Therapy
Humans
Molecular Targeted Therapy
Neoplasms / drug therapy*,  metabolism
Receptors, TNF-Related Apoptosis-Inducing Ligand / agonists*,  immunology,  metabolism
Signal Transduction / drug effects
TNF-Related Apoptosis-Inducing Ligand / metabolism*,  therapeutic use*
Grant Support
ID/Acronym/Agency:
5P50CA089019-08/CA/NCI NIH HHS
Chemical
Reg. No./Substance:
0/Antibodies, Monoclonal; 0/Antineoplastic Agents; 0/Receptors, TNF-Related Apoptosis-Inducing Ligand; 0/TNF-Related Apoptosis-Inducing Ligand
Comments/Corrections

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