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JNCI Journal of the National Cancer Institute 2004 96(8):583-585; doi:10.1093/jnci/djh095
© 2004 by Oxford University Press
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© 2004 Oxford University Press

COMMENTARY

Cancer Stem Cells: Are We Missing the Target?

Richard J. Jones, William H. Matsui, B. Douglas Smith

Affiliation of authors: Sidney Kimmel Comprehensive Cancer Center at Johns Hopkins, Baltimore, MD

Correspondence to: Richard J. Jones, MD, Bunting-Blaustein Cancer Research Building, 1650 Orleans St., Rm. 207, Baltimore, MD 21231 (e-mail: rjjones@jhmi.edu)

The first 150 words of the full text of this article appear below.


    INTRODUCTION
 
Most conventional anticancer agents are nonselective cellular poisons with broad activities against most dividing cells, regardless of whether they are malignant or not; any preferential effects of these agents on cancer cells usually reflect their relatively high rates of cell division. The widely acclaimed success of imatinib mesylate (also known as STI571 or Gleevec, and herein referred to as imatinib) in chronic myeloid leukemia (CML) highlights the enormous possibilities that the development of drugs directed against cancer-specific targets has for improving cancer treatment. Targeted anticancer agents have the potential to favorably influence patient survival by decreasing toxicity and improving disease control. However, recent laboratory and clinical data raise questions about whether new anticancer agents will effectively target relevant subsets of cancer cells. These issues have implications for interpreting results of clinical studies with targeted therapies as well as for the future development of new anticancer treatments.


    IMATINIB IN CHRONIC MYELOID LEUKEMIA: A MODEL OF TARGETED THERAPY
 
The cytogenetic hallmark of . . . [Full Text of this Article]


    RESISTANCE TO IMATINIB
 

    CANCER STEM CELLS AND TARGETED THERAPY
 

    DRUG DEVELOPMENT FOR CANCER: ARE WE OFF TARGET?
 

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