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Leukemia Research
Volume 33, Issue 12
, Pages 1581-1583
, December 2009
How do JAK2-inhibitors work in myelofibrosis: An alternative hypothesis
References
- . Hypothesis: how do jak2-inhibitors work in myelofibrosis. Leuk Res. 2009;33:1156–1157
- . Jak2 inhibitor therapy in myeloproliferative disorders: rationale, preclinical studies and ongoing clinical trials. Leukemia. 2008;22:23–30
- . A phase i study of TG101348, an orally bioavailable JAK-selective inhibitor, in patients with myelofibrosis. Blood. 2008;112:97A
- . The JAK inhibitor, INCB018424, demonstrates durable and marked clinical responses in primary myelofibrosis and post-polycythemia/essential thrombocythemia myelofibrosis. Blood. 2008;1762A
- . Pathogenesis of myelofibrosis with myeloid metaplasia: lessons from mouse models of the disease. Semin Oncol. 2005;32:365–372
- . Does primary myelofibrosis involve a defective stem cell niche? From concept to evidence. Blood. 2008;112:3026–3035
- . Leptin stimulates both JAK2_dependent and JAK2-independent signaling pathways. J Biol Chem. 2008;
- . Jaks in pathology: role of janus kinases in hematopoietic malignancies and immunodeficiencies. Semin Cell Dev Biol. 2008;19:385–393
- . A phase 2a study of the histone-deacetylase inhibitor ITF2357 in patients with JAK2V617F positive chronic myeloproliferative neoplasms. Blood. 2008;112:100A
- . The histone deacetylase inhibitor ITF 2357 selectively targets cells bearing mutated JAK2(V617F). Leukemia. 2008;22:740–747
PII: S0145-2126(09)00281-1
doi: 10.1016/j.leukres.2009.06.001
© 2009 Elsevier Ltd. All rights reserved.
« Previous
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Leukemia Research
Volume 33, Issue 12
, Pages 1581-1583
, December 2009
