The Journal of Experimental Medicine
Keystone Symposia
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Published online March 12, 2007
doi:10.1084/jem.20062335
The Journal of Experimental Medicine, Vol. 204, No. 3, 461-465
The Rockefeller University Press, 0022-1007 $30.00
© 2007 Van Etten
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COMMENTARY

 Oncogenic signaling: new insights and controversies from chronic myeloid leukemia

Richard A. Van Etten

CORRESPONDENCE R.A.V.: rvanetten{at}tufts-nemc.org


ABSTRACT
Chronic myeloid leukemia (CML), which is caused by the BCR–ABL fusion tyrosine kinase, is one of the most intensively studied human cancers. ABL kinase inhibitors have been spectacularly successful in treating CML, but disease persistence and acquired drug resistance can prevent eradication and cure of the leukemia. The development of better therapies will depend on a full understanding of signaling pathways in CML, facilitated by model studies using mutant mice.

R.A.V. is at the Molecular Oncology Research Institute and the Division of Hematology/Oncology, Tufts-New England Medical Center, Boston, MA 02111.


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