The New England Journal of Medicine
e-mail icon  FREE NEJM E-TOC    HOME   |   SUBSCRIBE   |   CURRENT ISSUE   |   PAST ISSUES   |   COLLECTIONS   |    Advanced Search
Sign in | Get NEJM's E-Mail Table of Contents — Free | Subscribe
 
Editorial
PreviousPrevious
Volume 344:1084-1086 April 5, 2001 Number 14
NextNext

Targeting the BCR-ABL Tyrosine Kinase in Chronic Myeloid Leukemia

Since this article has no abstract, we have provided an extract of the first 100 words of the full text and any section headings.

 Sign up for free e-toc
 

This Article
-Full Text
- PDF
-Purchase this article

Tools and Services
-Add to Personal Archive
-Add to Citation Manager
-Notify a Friend
-E-mail When Cited

More Information
-PubMed Citation
Chronic myeloid leukemia (CML) is one of the most remarkable cancers.1,2 It was probably the first type of leukemia to be recognized, in the 1840s, as a distinct entity. A landmark was the discovery of the Philadelphia (Ph) chromosome in 1960.3 This led to the identification in CML cells of the BCR-ABL fusion gene and its corresponding protein, which is now firmly established as the unique cause of the initial, or "chronic," phase of CML. ABL and BCR, which are located on chromosomes 9 and 22, respectively, are normal genes whose function is still unknown. The ABL gene encodes a . . . [Full Text of this Article]

References


This article has been cited by other articles:



HOME  |  SUBSCRIBE  |  SEARCH  |  CURRENT ISSUE  |  PAST ISSUES  |  COLLECTIONS  |  PRIVACY  |  HELP  |  beta.nejm.org

Comments and questions? Please contact us.

The New England Journal of Medicine is owned, published, and copyrighted © 2008 Massachusetts Medical Society. All rights reserved.