| |||||||||||||||||||||||||||||||||||||||||||||||||||||||
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
From the National Cancer Institute, National Institutes of Health, Bethesda, Maryland.
PERSPECTIVE
Biological Basis for Cancer Treatment
![]()
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:
![]() |
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] |
||||