Genes and Development

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GENES & DEVELOPMENT 21:2249-2252, 2007
©2007 by Cold Spring Harbor Laboratory Press; ISSN 0890-9369/ $5.00
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PERSPECTIVE

Linking the hematopoietic microenvironment to imatinib-resistant Ph+ B-ALL

Kenneth Dorshkind1,4 and Owen N. Witte2,3

1 Department of Pathology and Laboratory Medicine, David Geffen School of Medicine at University of California at Los Angeles, Los Angeles, California 90095, USA; 2 Department of Microbiology, Immunology and Molecular Genetics and the Howard Hughes Medical Institute, David Geffen School of Medicine at University of California at Los Angeles, Los Angeles, California 90095, USA

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Chronic myeloid leukemia (CML) and a subtype of B-cell acute lymphocytic leukemia (B-ALL) result from the constitutive expression of the Philadelphia (Ph) chromosome, a reciprocal translocation between ABL on chromosome 9 and BCR located on chromosome 22 (Nowell and Hungerford 1960Go; Rowley 1973Go). The chimeric BCR-ABL fusion product encoded by this chromosomal translocation is a tyrosine kinase, and its activity accounts for >90% of CML cases and up to 15% of B-ALL cases (Deininger et al. 2000Go). The treatment of CML has been revolutionized by the development of Imatinib mesylate (Gleevec, STI571), a targeted inhibitor of BCR-ABL . . . [Full Text of this Article]


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Related Article

Cytokine-dependent imatinib resistance in mouse BCR-ABL+, Arf-null lymphoblastic leukemia
Richard T. Williams, Willem den Besten, and Charles J. Sherr
Genes & Dev. 2007 21: 2283-2287. [Abstract] [Full Text] [PDF]





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