Abstract
Programmed cell death (apoptosis) is a key tumor suppressor mechanism. Consequently, most if not all cancers develop mechanisms to abolish or circumvent this genetic program. Besides enabling malignant transformation and tumor progression, defects in apoptosis can result in resistance to cytotoxic cancer therapies. Much progress has been made in the delineation of the molecular pathways leading to apoptosis. This allows the identification of target molecules and lead compounds to develop novel therapies, which make use of this intrinsic death program for the treatment of cancer. Here, we review the current understanding of apoptotic signal transduction pathways, and strategies of their therapeutic modulation in relation to lymphoma and other cancers.
Keywords: BH3-only proteins, p53 Gene Transfer, pro-apoptotic genes, TNF receptor superfamily, Mouse-double-minute-2 (MDM-2)
Current Drug Targets
Title: Therapeutic Targeting of Apoptotic Pathways in Cancer
Volume: 7 Issue: 10
Author(s): Johannes Meiler and Martin Schuler
Affiliation:
Keywords: BH3-only proteins, p53 Gene Transfer, pro-apoptotic genes, TNF receptor superfamily, Mouse-double-minute-2 (MDM-2)
Abstract: Programmed cell death (apoptosis) is a key tumor suppressor mechanism. Consequently, most if not all cancers develop mechanisms to abolish or circumvent this genetic program. Besides enabling malignant transformation and tumor progression, defects in apoptosis can result in resistance to cytotoxic cancer therapies. Much progress has been made in the delineation of the molecular pathways leading to apoptosis. This allows the identification of target molecules and lead compounds to develop novel therapies, which make use of this intrinsic death program for the treatment of cancer. Here, we review the current understanding of apoptotic signal transduction pathways, and strategies of their therapeutic modulation in relation to lymphoma and other cancers.
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Cite this article as:
Meiler Johannes and Schuler Martin, Therapeutic Targeting of Apoptotic Pathways in Cancer, Current Drug Targets 2006; 7 (10) . https://dx.doi.org/10.2174/138945006778559175
DOI https://dx.doi.org/10.2174/138945006778559175 |
Print ISSN 1389-4501 |
Publisher Name Bentham Science Publisher |
Online ISSN 1873-5592 |
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