BCR-ABL uncouples canonical JAK2-STAT5 signaling in chronic myeloid leukemia-Reference-Cited by-同舟云学术

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BCR-ABL uncouples canonical JAK2-STAT5 signaling in chronic myeloid leukemia

Published:2012-01-29 Issue:3 Volume:8 Page:285-293
ISSN:1552-4450
Container-title:Nature Chemical Biology
language:en
Short-container-title:Nat Chem Biol

Author:

Hantschel Oliver,Warsch Wolfgang,Eckelhart Eva,Kaupe Ines,Grebien Florian,Wagner Kay-Uwe,Superti-Furga Giulio,Sexl Veronika

Publisher

Springer Science and Business Media LLC

Subject

Cell Biology,Molecular Biology

Link

http://www.nature.com/articles/nchembio.775.pdf

Reference50 articles.

1. Wong, S. & Witte, O.N. The BCR-ABL story: bench to bedside and back. Annu. Rev. Immunol. 22, 247–306 (2004).

2. Goldman, J.M. & Melo, J.V. Chronic myeloid leukemia–advances in biology and new approaches to treatment. N. Engl. J. Med. 349, 1451–1464 (2003).

3. Lugo, T.G., Pendergast, A.M., Muller, A.J. & Witte, O.N. Tyrosine kinase activity and transformation potency of bcr-abl oncogene products. Science 247, 1079–1082 (1990).

4. Capdeville, R., Buchdunger, E., Zimmermann, J. & Matter, A. Glivec (STI571, imatinib), a rationally developed, targeted anticancer drug. Nat. Rev. Drug Discov. 1, 493–502 (2002).

5. Weisberg, E., Manley, P.W., Cowan-Jacob, S.W., Hochhaus, A. & Griffin, J.D. Second generation inhibitors of BCR-ABL for the treatment of imatinib-resistant chronic myeloid leukemia. Nat. Rev. Cancer 7, 345–356 (2007).

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