Skip Navigation


Journal of the National Cancer Institute Advance Access originally published online on June 24, 2008
JNCI Journal of the National Cancer Institute 2008 100(13):908-909; doi:10.1093/jnci/djn204
This Article
Right arrow Full Text Freely available
Right arrow FREE Full Text (PDF) Freely available
Right arrow All Versions of this Article:
100/13/908    most recent
djn204v1
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 O'Hare, T.
Right arrow Articles by Deininger, M. W.
Right arrow Search for Related Content
PubMed
Right arrow PubMed Citation
Right arrow Articles by O'Hare, T.
Right arrow Articles by Deininger, M. W.
Related Collections
Right arrowRelated Articles in JNCI
Social Bookmarking
Add to CiteULike   Add to Connotea   Add to Del.icio.us  
What's this?

© The Author 2008. Published by Oxford University Press.

EDITORIAL

Persistent LYN Signaling in Imatinib-Resistant, BCR-ABL–Independent Chronic Myelogenous Leukemia

Thomas O'Hare, Christopher A. Eide, Michael W. Deininger

Affiliation of authors: Oregon Health & Science University Cancer Institute, L592, 3181 SW Sam Jackson Park Rd, Portland, OR

Correspondence to: Michael W. Deininger MD, PhD, Oregon Health & Science University Cancer Institute, L592, 3181 SW Sam Jackson Park Rd, Portland, OR 97239 (e-mail: deininge@ohsu.edu).

The first 10% of the full text of this article appears below.

Resistance to imatinib is commonly associated with reactivation of BCR-ABL signaling. Many such patients harbor a mutation in BCR-ABL that confers resistance to imatinib. In other patients, the leukemia cells appear to express increased amounts of BCR-ABL kinase. Identification of a BCR-ABL mutation provides an explanation for onset of imatinib resistance and indicates a clear treatment strategy: second-line therapy with an ABL kinase inhibitor that is active against the particular BCR-ABL variant kinase. In the clinical setting, nilotinib and dasatinib are used for this purpose; additional inhibitors are under development.

However, not all cases of resistance can be attributed to a BCR-ABL mutation or enhanced expression. The phenomenon of BCR-ABL–independent resistance is probably . . . [Full Text of this Article]


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

Related Articles in JNCI

IN THIS ISSUE
J Natl Cancer Inst 2008 100: 907. [Extract] [Full Text] [PDF]

Activation of LYN Kinase Is Associated with Imatinib-Resistance in CML Patients
J Natl Cancer Inst 2008 100: 907. [Extract] [Full Text] [PDF]