Skip Navigation

JNCI Journal of the National Cancer Institute 2002 94(2):78-79; doi:10.1093/jnci/94.2.78
© 2002 by Oxford University Press
This Article
Right arrow Full Text Freely available
Right arrow FREE Full Text (PDF) Freely available
Right arrow Alert me when this article is cited
Right arrow Alert me if a correction is posted
Services
Right arrow Email this article to a friend
Right arrow Similar articles in this journal
Right arrow Similar articles in PubMed
Right arrow Alert me to new issues of the journal
Right arrow Add to My Personal Archive
Right arrow Download to citation manager
Right arrow Request Permissions
Google Scholar
Right arrow Articles by Balis, F. M.
Right arrow Search for Related Content
PubMed
Right arrow PubMed Citation
Right arrow Articles by Balis, F. M.
Social Bookmarking
 Add to CiteULike   Add to Connotea   Add to Del.icio.us  
What's this?

Journal of the National Cancer Institute, Vol. 94, No. 2, 78-79, January 16, 2002
© 2002 Oxford University Press


EDITORIAL

Evolution of Anticancer Drug Discovery and the Role of Cell-Based Screening

Frank M. Balis

Affiliation of author: Pediatric Oncology Branch, Center for Cancer Research, National Cancer Institute, Bethesda, MD.

Correspondence to: Frank M. Balis, M.D., National Institutes of Health, Bldg. 10, Rm. 13C103, 10 Center Dr., Bethesda, MD 20892–1920 (e-mail: balisf@nih.gov).

The approach to the discovery of new anticancer drugs has recently evolved from a reliance on empiric cell-based screening for antiproliferative effects to a more mechanistically based approach that targets the specific molecular lesions thought to be responsible for the development and maintenance of the malignant phenotype in various forms of cancer. The ultimate goal of the development of molecularly targeted drugs is to improve the efficacy and selectivity of cancer treatment by exploiting the differences between cancer cells and normal cells. The success of recently developed molecularly targeted agents, such as tretinoin (all-trans-retinoic acid) for acute promyelocytic leukemia (1,2) and imatinib (STI-571) for chronic myelogenous leukemia (CML) (3,4) and gastrointestinal stromal tumors . . . [Full Text of this Article]

REFERENCES


Add to CiteULike CiteULike   Add to Connotea Connotea   Add to Del.icio.us Del.icio.us    What's this?


This article has been cited by other articles:


Home page
Clin. Cancer Res.Home page
B. Freidlin and R. Simon
Adaptive Signature Design: An Adaptive Clinical Trial Design for Generating and Prospectively Testing A Gene Expression Signature for Sensitive Patients
Clin. Cancer Res., November 1, 2005; 11(21): 7872 - 7878.
[Abstract] [Full Text] [PDF]


Home page
JCOHome page
B. Freidlin and R. Simon
Evaluation of Randomized Discontinuation Design
J. Clin. Oncol., August 1, 2005; 23(22): 5094 - 5098.
[Abstract] [Full Text] [PDF]


Home page
Clin. Cancer Res.Home page
R. Simon and A. Maitournam
Evaluating the Efficiency of Targeted Designs for Randomized Clinical Trials
Clin. Cancer Res., October 15, 2004; 10(20): 6759 - 6763.
[Abstract] [Full Text] [PDF]


Home page
J Biomol ScreenHome page
L. A. Kunz-Schughart, J. P. Freyer, F. Hofstaedter, and R. Ebner
The Use of 3-D Cultures for High-Throughput Screening: The Multicellular Spheroid Model
J Biomol Screen, June 1, 2004; 9(4): 273 - 285.
[Abstract] [PDF]


Home page
J. Cell Sci.Home page
K. L. Schmeichel and M. J. Bissell
Modeling tissue-specific signaling and organ function in three dimensions
J. Cell Sci., June 15, 2003; 116(12): 2377 - 2388.
[Abstract] [Full Text] [PDF]


Home page
The OncologistHome page
E. Fox, G. A. Curt, and F. M. Balis
Clinical Trial Design for Target-Based Therapy
Oncologist, October 1, 2002; 7(5): 401 - 409.
[Abstract] [Full Text] [PDF]