Annals
Established in 1927 by the American College of Physicians
:
Advanced search
box Article
 arrow  Table of Contents                
space
 arrow  Full Text of this article Free
space
 arrow  Figures/Tables List
space
box Services
 arrow  Send comment/rapid response letter
space
 arrow  Notify a friend about this article
space
 arrow  Alert me when this article is cited
space
 arrow  Add to Personal Archive
space
 arrow  Download to Citation Manager
space
 arrow  ACP Search                        
space
 arrow  Get Permissions
space
box Google Scholar
 arrow  Search for Related Content
space
box PubMed
Articles in PubMed by Author:
  arrow  Chabner, B. A.
space
 arrow  Related Articles in PubMed
space
 arrow  PubMed Citation
space
 arrow  PubMed
space

PERSPECTIVE

Biological Basis for Cancer Treatment

right arrow Bruce A. Chabner

15 April 1993 | Volume 118 Issue 8 | Pages 633-637

The new knowledge of the regulation of cell growth and the genetic and biochemical changes that lead to malignancy have created many new opportunities for cancer drug discovery. These new targets include oncogenes, growth factors and their receptors, signal transduction pathways, and cell differentiation signals. Attempts to identify new therapies based on these targets can complement traditional drug discovery efforts that rely on high-volume screening of candidate natural products and synthetic chemicals against human tumor cell lines and against defined molecular reactions. Through modern computer-based data analysis, drug screening data can be used to establish mechanisms of drug action of new agents; these analyses shed light on patterns of cross-resistance of new compounds and their interactions with defined molecular targets as well as allow selection of chemically and biologically unique agents as candidates for clinical development.

Author and Article Information
space

From the National Cancer Institute, National Institutes of Health, Bethesda, Maryland.
Requests for Reprints: Bruce A. Chabner, MD, Division of Cancer Treatment, National Cancer Institute, NIH, Bethesda, MD 20892.
Acknowledgments: The author thanks Drs. Michael Grever, Michael Friedman, and Dan Longo, Greg Curt, Steve Brown and their colleagues in the Division of Cancer Treatment, National Cancer Institute, Bethesda, Maryland.




This article has been cited by other articles:


Home page
J. Virol.Home page
Y. Zhu, H. A. Gelbard, M. Roshal, S. Pursell, B. D. Jamieson, and V. Planelles
Comparison of Cell Cycle Arrest, Transactivation, and Apoptosis Induced by the Simian Immunodeficiency Virus SIVagm and Human Immunodeficiency Virus Type 1 vpr Genes
J. Virol., April 15, 2001; 75(8): 3791 - 3801.
[Abstract] [Full Text]




 Home | Current Issue | Past Issues | In the Clinic | ACP Journal Club | CME | Collections | Audio/Video | Mobile | Subscribe | Tools | Help | ACP Online 

Copyright © 1993 by the American College of Physicians.