Skip to main content

Therapeutic Targeting of Apoptotic Pathways in Cancer

Buy Article:

$63.00 plus tax (Refund Policy)

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.





No References
No Citations
No Supplementary Data
No Data/Media
No Metrics

Keywords: BH3-only proteins; Mouse-double-minute-2 (MDM-2); TNF receptor superfamily; p53 Gene Transfer; pro-apoptotic genes

Document Type: Research Article

Affiliations: Department of Medicine III,Johannes Gutenberg University, Langenbeckstrasse 1, D-55131 Mainz,Germany.

Publication date: 2006-10-01

More about this publication?
  • Current Drug Targets aims to cover the latest and most outstanding developments on the medicinal chemistry and pharmacology of molecular drug targets e.g. disease specific proteins, receptors, enzymes, genes. Each issue of the journal will be devoted to a single timely topic, with series of in-depth reviews, written by leaders in the field, covering a range of current topics on drug targets. These issues will be organized and led by a guest editor who is a recognized expert in the overall topic. As the discovery, identification, characterisation and validation of novel human drug targets for drug discovery continues to grow; this journal will be essential reading for all pharmaceutical scientists involved in drug discovery and development.
  • Access Key
  • Free content
  • Partial Free content
  • New content
  • Open access content
  • Partial Open access content
  • Subscribed content
  • Partial Subscribed content
  • Free trial content
Cookie Policy
X
Cookie Policy
Ingenta Connect website makes use of cookies so as to keep track of data that you have filled in. I am Happy with this Find out more