Heterodimeric JAK–STAT activation as a mechanism of persistence to JAK2 inhibitor therapy-Reference-Cited by-同舟云学术

Heterodimeric JAK–STAT activation as a mechanism of persistence to JAK2 inhibitor therapy

Published:2012-07-22 Issue:7414 Volume:489 Page:155-159
ISSN:0028-0836
Container-title:Nature
language:en
Short-container-title:Nature

Author:

Koppikar Priya,Bhagwat Neha,Kilpivaara Outi,Manshouri Taghi,Adli Mazhar,Hricik Todd,Liu Fan,Saunders Lindsay M.,Mullally Ann,Abdel-Wahab Omar,Leung Laura,Weinstein Abby,Marubayashi Sachie,Goel Aviva,Gönen Mithat,Estrov Zeev,Ebert Benjamin L.,Chiosis Gabriela,Nimer Stephen D.,Bernstein Bradley E.,Verstovsek Srdan,Levine Ross L.

Publisher

Springer Science and Business Media LLC

Subject

Multidisciplinary

Link

http://www.nature.com/articles/nature11303.pdf

Reference32 articles.

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2. Kralovics, R. et al. A gain-of-function mutation of JAK2 in myeloproliferative disorders. N. Engl. J. Med. 352, 1779–1790 (2005)

3. Baxter, E. J. et al. Acquired mutation of the tyrosine kinase JAK2 in human myeloproliferative disorders. Lancet 365, 1054–1061 (2005)

4. Zhao, R. et al. Identification of an acquired JAK2 mutation in polycythemia vera. J. Biol. Chem. 280, 22788–22792 (2005)

5. Pikman, Y. et al. MPLW515L is a novel somatic activating mutation in myelofibrosis with myeloid metaplasia. PLoS Med. 3, e270 (2006)

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