Skip Navigation

JNCI Journal of the National Cancer Institute 2007 99(9):662-663; doi:10.1093/jnci/djk176
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 ISI Web of Science
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 Rodrigues, M. S.
Right arrow Articles by Sattler, M.
Right arrow Search for Related Content
PubMed
Right arrow PubMed Citation
Right arrow Articles by Rodrigues, M. S.
Right arrow Articles by Sattler, M.
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 2007. Published by Oxford University Press.

EDITORIALS

Chronic Myelogenous Leukemia Progenitors Display a Genetically Unstable Personality

Margret S. Rodrigues, Martin Sattler

Affiliations of authors: Department of Medical Oncology, Dana-Farber Cancer Institute, Boston, MA (MSR, MS); Department of Medicine, Brigham and Women's Hospital and Harvard Medical School, Boston, MA (MSR, MS)

Correspondence to: Martin Sattler, PhD, Department of Medical Oncology, Dana-Farber Cancer Institute, 44 Binney St, Boston, MA 02115 (e-mail: martin_sattler@dfci.harvard.edu).

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

Chronic myelogenous leukemia (CML) is a hematopoietic stem cell disorder caused by the BCR–ABL tyrosine kinase oncogene, which induces constitutive activation of growth and viability signaling pathways (1). CML cells are dependent on the elevated kinase activity of BCR–ABL, as demonstrated by the high rates of hematologic remissions induced by the ABL kinase inhibitor imatinib mesylate (Gleevec). Although complete hematologic remission rates occur in more than 95% of patients, only a minority enter a molecular remission in which BCR–ABL is undetectable by polymerase chain reaction. In acute phase, characterized by an increase of immature blast cells in the peripheral blood, only . . . [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

Instability of BCR–ABL Gene in Primary and Cultured Chronic Myeloid Leukemia Stem Cells
Xiaoyan Jiang, Kyi Min Saw, Allen Eaves, and Connie Eaves
J Natl Cancer Inst 2007 99: 680-693. [Abstract] [Full Text] [PDF]

IN THIS ISSUE
J Natl Cancer Inst 2007 99: 657. [Extract] [Full Text] [PDF]

Press Release: Unstable Leukemia Stem Cells May Predispose Patients to Drug Resistance
Liz Savage
J Natl Cancer Inst 2007 99: 657. [Extract] [Full Text]