Heterodimeric JAK-STAT Activation as a Mechanism of Persistence to JAK2 Inhibitor Therapy

The identification of somatic activating mutations in JAK2(1–4) and in the thrombopoietin receptor (MPL)(5) in the majority of myeloproliferative neoplasm (MPN) patients led to the clinical development of JAK2 kinase inhibitors(6,7). JAK2 inhibitor therapy improves MPN-associated splenomegaly and sy...

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Autors principals: 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.
Format: Artigo
Idioma:Inglês
Publicat: 2012
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Article
Accés en línia:https://ncbi.nlm.nih.gov/pmc/articles/PMC3991463/
https://ncbi.nlm.nih.gov/pubmed/22820254
https://ncbi.nlm.nih.govhttp://dx.doi.org/10.1038/nature11303
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