Janus kinase 2 inhibitors in myeloproliferative disorders

Bibliography

• Levine RL, Pardanani A, Tefferi A, Gilliland DG. Role of JAK2 in the pathogenesis and therapy of myeloproliferative disorders. Nat Rev Cancer 2007;7:673-83
   PubMed Web of Science ®Google Scholar
• Campbell PJ, Green AR. The myeloproliferative disorders. N Engl J Med 2006;355:2452-66
   PubMed Web of Science ®Google Scholar
• Mesa RA. Navigating the evolving paradigms in the diagnosis and treatment of myeloproliferative disorders. Am Soc Hematol Educ Program 2007;2007:355-62
   Google Scholar
• Tefferi A, Skoda R, Vardiman JW. Myeloproliferative neoplasms: contemporary diagnosis using histology and genetics. Nat Rev Clin Oncol 2009;11:627-37
   Google Scholar
• Kralovics R, Passamonti F, Buser AS, A gain-of-function mutation of JAK2 in myeloproliferative disorders. N Engl J Med 2005;352:1779-90
   PubMed Web of Science ®Google Scholar
• Ihle JN, Kerr IM. Jaks and Stats in signaling by the cytokine receptor superfamily. Trends Genet 1995;11:69-74
   PubMed Web of Science ®Google Scholar
• Ihle JN. The Janus protein tyrosine kinases in hematopoietic cytokine signaling. Semin Immunol 1995;7:247-54
   PubMedGoogle Scholar
• Ihle JN, Nosaka T, Thierfelder W, Jaks and Stats in cytokine signaling. Stem Cells 1997;15(Suppl 1):105-11, discussion 112
   PubMed Web of Science ®Google Scholar
• Valentino L, Pierre J. JAK/STAT signal transduction: regulators and implication in hematological malignancies. Biochem Pharmacol 2006;71:713-21
   PubMed Web of Science ®Google Scholar
• Murray PJ. The JAK-STAT signaling pathway: input and output integration. J Immunol 2007;178:2623-9
   PubMed Web of Science ®Google Scholar
• Pardanani A. JAK2 inhibitor therapy in myeloproliferative disorders: rationale, preclinical studies and ongoing clinical trials. Leukemia 2008;22:23-30
   PubMed Web of Science ®Google Scholar
• Pardanani A, Lasho T, Smith G, CYT387, a selective JAK1/JAK2 inhibitor: in vitro assessment of kinase selectivity and preclinical studies using cell lines and primary cells from polycythemia vera patients. Leukemia 2009;23:1441-5
   PubMed Web of Science ®Google Scholar
• Pardanani A, Hood J, Lasho T, TG101209, a small molecule JAK2-selective kinase inhibitor potently inhibits myeloproliferative disorder-associated JAK2V617F and MPLW515L/K mutations. Leukemia 2007;21:1658-68
   PubMed Web of Science ®Google Scholar
• Lasho TL, Tefferi A, Hood JD, TG101348, a JAK2-selective antagonist, inhibits primary hematopoietic cells derived from myeloproliferative disorder patients with JAK2V617F, MPLW515K or JAK2 exon 12 mutations as well as mutation negative patients. Leukemia 2008;22:1790-2
   PubMed Web of Science ®Google Scholar
• Vainchenker W, Dusa A, Constantinescu SN. JAKs in pathology: role of Janus kinases in hematopoietic malignancies and immunodeficiencies. Semin Cell Dev Biol 2008;19:385-93
   PubMed Web of Science ®Google Scholar
• Constantinescu SN, Girardot M, Pecquet C. Mining for JAK-STAT mutations in cancer. Trends Biochem Sci 2008;33:122-31
   PubMed Web of Science ®Google Scholar
• Wadleigh M, Tefferi A. Classification and diagnosis of myeloproliferative neoplasms according to the 2008 World Health Organization criteri. Int J Hematol 2010;91:174-9
   PubMed Web of Science ®Google Scholar
• James C, Ugo V, Le Couedic JP, A unique clonal JAK2 mutation leading to constitutive signalling causes polycythaemia vera. Nature 2005;434:1144-8
   PubMed Web of Science ®Google Scholar
• Levine RL, Wadleigh M, Cools J, Activating mutation in the tyrosine kinase JAK2 in polycythemia vera, essential thrombocythemia, and myeloid metaplasia with myelofibrosis. Cancer Cell 2005;7:387-97
   PubMed Web of Science ®Google Scholar
• Baxter EJ, Scott LM, Campbell PJ, Acquired mutation of the tyrosine kinase JAK2 in human myeloproliferative disorders. Lancet 2005;365:1054-61
   PubMed Web of Science ®Google Scholar
• Steensma DP, McClure RF, Karp JE, JAK2 V617F is a rare finding in de novo acute myeloid leukemia, but STAT3 activation is common and remains unexplained. Leukemia 2006;20:971-8
   PubMed Web of Science ®Google Scholar
• Steensma DP, Dewald GW, Lasho TL, The JAK2 V617F activating tyrosine kinase mutation is an infrequent event in both ‘atypical’ myeloproliferative disorders and myelodysplastic syndromes. Blood 2005;106:1207-9
   PubMed Web of Science ®Google Scholar
• Inami M, Yamaguchi H, Hasegawa S, Analysis of the exon 12 and 14 mutations ofthe JAK2 gene in Philadelphia chromosome-positive leukemia. Leukemia 2008;22:216
   PubMed Web of Science ®Google Scholar
• Hussein K, Bock O, Theophile K, Chronic myeloproliferative diseases with concurrent BCRABL junction and JAK2V617F mutation. Leukemia 2008;22:1059-62
   PubMed Web of Science ®Google Scholar
• Melzner I, Weniger MA, Menz CK, Moller P. Absence of the JAK2 V617F activating mutation in classical Hodgkin lymphoma and primary mediastinal B-cell lymphoma. Leukemia 2006;20:157-8
   PubMed Web of Science ®Google Scholar
• Levine RL, Loriaux M, Huntly BJ, The JAK2V617F activating mutation occurs in chronic myelomonocytic leukemia and acute myeloid leukemia, but not in acute lymphoblastic leukemia or chronic lymphocytic leukemia. Blood 2005;106:3377-9
   PubMed Web of Science ®Google Scholar
• Kilpivaara O, Levine RL. JAK2 and MPL mutations in myeloproliferative neoplasms: discovery and science. Leukemia 2008;22:1813-17
   PubMed Web of Science ®Google Scholar
• Neubauer H, Cumano A, Muller M, Jak2 deficiency defines an essential developmental checkpoint in definitive hematopoiesis. Cell 1998;93:397-409
   PubMed Web of Science ®Google Scholar
• Tefferi A, Gilliland DG. The JAK2V617F tyrosine kinase mutation in myeloproliferative disorders: status report and immediate implications for disease classification and diagnosis. Mayo Clin Proc 2005;80:947-58
   PubMed Web of Science ®Google Scholar
• Lacout C, Pisani DF, Tulliez M, JAK2V617F expression in murine hematopoietic cells leads to MPD mimicking human PV with secondary myelofibrosis. Blood 2006;108:1652-60
   PubMed Web of Science ®Google Scholar
• Wernig G, Mercher T, Okabe R, Expression of Jak2V617F causes a polycythemia vera-like disease with associated myelofibrosis in a murine bone marrow transplant model. Blood 2006;107:4274-81
   PubMed Web of Science ®Google Scholar
• Bumm TG, Elsea C, Corbin AS, Characterization of murine JAK2V617F-positive myeloproliferative disease. Cancer Res 2006;66:11156-65
   PubMed Web of Science ®Google Scholar
• Zaleskas VM, Krause DS, Lazarides K, Molecular pathogenesis and therapy of polycythemia induced in mice by JAK2 V617F. PLoS One 2006;1:e18
   PubMed Web of Science ®Google Scholar
• Marty C, Lacout C, Martin A, Myeloproliferative neoplasm induced by constitutive expression of JAK2V617F in knock-in mice. Blood 2010;116:783-7
   PubMed Web of Science ®Google Scholar
• Moliterno AR, Williams DM, Rogers O, Molecular mimicry in the chronic myeloproliferative disorders: reciprocity between quantitative JAK2 V617F and Mpl expression. Blood 2006;108:3913-15
   PubMed Web of Science ®Google Scholar
• Bellanne-Chantelot C, Chaumarel I, Labopin M, Genetic and clinical implications of the Val617Phe JAK2 mutation in 72 families with myeloproliferative disorders. Blood 2006;108:346-52
   PubMed Web of Science ®Google Scholar
• Kralovics R, Teo SS, Li S, Acquisition of the V617F mutation of JAK2 is a late genetic event in a subset of patients with myeloproliferative disorders. Blood 2006;108:1377-80
   PubMed Web of Science ®Google Scholar
• Kralovics R. Genetic complexity of myeloproliferative neoplasms. Leukemia 2008;22:1841-8
   PubMed Web of Science ®Google Scholar
• Theocharides A, Boissinot M, Girodon F, Leukemic blasts in transformed JAK2-V617F-positive myeloproliferative disorders are frequently negative for the JAK2-V617F mutation. Blood 2007;110:375-9
   PubMed Web of Science ®Google Scholar
• Nussenzveig RH, Swierczek SI, Jelinek J, Polycythemia vera is not initiated by JAK2V617F mutation. Exp Hematol 2007;35:32-8
   PubMed Web of Science ®Google Scholar
• Beer PA, Delhommeau F, LeCouedic JP, Two routes to leukemic transformation after a JAK2 mutation-positive myeloproliferative neoplasm. Blood 2010;115:2891-900
   PubMed Web of Science ®Google Scholar
• Thoennissen NH, Krug UO, Lee DH, Prevalence and prognostic impact of allelic imbalances associated with leukemic transformation of Philadelphia chromosome-negative myeloproliferative neoplasms. Blood 2010;115:2882-90
   PubMed Web of Science ®Google Scholar
• Scott LM, Tong W, Levine RL, JAK2 exon 12 mutations in polycythemia vera and idiopathic erythrocytosis. N Engl J Med 2007;356:459-68
   PubMed Web of Science ®Google Scholar
• Williams DM, Kim AH, Rogers O, Phenotypic variations and new mutations in JAK2 V617F-negative polycythemia vera, erythrocytosis, and idiopathic myelofibrosis. Exp Hematol 2007;35:1641-6
   PubMed Web of Science ®Google Scholar
• Lu X, Levine R, Tong W, Expression of a homodimeric type I cytokine receptor is required for JAK2V617F-mediated transformation. Proc Natl Acad Sci USA 2005;102:18962-7
   PubMed Web of Science ®Google Scholar
• Mullally A, Lane SW, Ball B, Physiological Jak2V617F expression causes a lethal myeloproliferative neoplasm with differential effects on hematopoietic stem and progenitor cells. Cancer Cell 2010;17(6):584-96
   PubMed Web of Science ®Google Scholar
• Shide K, Shimoda HK, Kumano T, Development of ET, primary myelofibrosis and PV in mice expressing JAK2 V617F. Leukemia 2008;22:87-95
   PubMed Web of Science ®Google Scholar
• Barosi G, Bergamaschi G, Marchetti M, JAK2 V617F mutational status predicts progression to large splenomegaly and leukemic transformation in primary myelofibrosis. Blood 2007;110:4030-6
   PubMed Web of Science ®Google Scholar
• Tefferi A, Lasho TL, Schwager SM, The JAK2 tyrosine kinase mutation in myelofibrosis with myeloid metaplasia: lineage specificity and clinical correlates. Br J Haematol 2005;131:320-8
   PubMed Web of Science ®Google Scholar
• Tefferi A, Strand JJ, Lasho TL, Bone marrow JAK2V617F allele burden and clinical correlates in polycythemia vera. Leukemia 2007;21:2074-5
   PubMed Web of Science ®Google Scholar
• Kittur J, Knudson RA, Lasho TL, Clinical correlates of JAK2V617F allele burden in essential thrombocythemia. Cancer 2007;109:2279-84
   PubMed Web of Science ®Google Scholar
• Campbell PJ, Griesshammer M, Dohner K, V617F mutation in JAK2 is associated with poorer survival in idiopathic myelofibrosis. Blood 2006;107:2098-100
   PubMed Web of Science ®Google Scholar
• Guglielmelli P, Barosi G, Specchia G, Identification of patients with poorer survival in primary myelofibrosis based on the burden of JAK2V617F mutated allele. Blood 2009;114:1477-83
   PubMed Web of Science ®Google Scholar
• Tefferi A, Lasho TL, Huang J, Low JAK2V617F allele burden in primary myelofibrosis, compared to either a higher allele burden or unmutated status, is associated with inferior overall and leukemia-free survival. Leukemia 2008;22:756-61
   PubMed Web of Science ®Google Scholar
• Vannucchi AM, Antonioli E, Guglielmelli P, Clinical profile of homozygous JAK2 617V4F mutation in patients with polycythemia vera or essential thrombocythemia. Blood 2007;110:840-6
   PubMed Web of Science ®Google Scholar
• Lucet IS, Fantino E, Styles M, The structural basis of Janus kinase 2 inhibition by a potent and specific pan-Janus kinase inhibitor. Blood 2006;107:176-83
   PubMed Web of Science ®Google Scholar
• Verstovsek S, Kantarjian H, Pardanani A, INCB018424, an oral, selective JAK2 inhibitor, shows significant clinical activity in a phase I/II study in patients with primary myelofibrosis (PMF) and post polycythemia vera/essential thrombocythemia myelofibrosis (post-PV/ET MF) [abstract]. Blood 2007:110:558
   Google Scholar
• Cervantes F. Modern management of myelofibrosis. Br J Haematol 2005;128:583-92
   PubMed Web of Science ®Google Scholar
• Stewart WA, Pearce R, Kirkland KE, The role of allogeneic SCT in primary myelofibrosis: a British Society for Blood and Marrow Transplantation study. Bone Marrow Transplant 2010;45:1587-93
   Google Scholar
• Patriarca F, Bacigalupo A, Speretto A, Allogeneic hematopoietic stem cell transplantation in myelofibrosis: the 20-year experience of the Gruppo Italiano di Midollo Osseo (GITMO). Haematologica 2008;93:1514-22
   PubMed Web of Science ®Google Scholar
• Quintas-Cardama A, Vaddi K, Liu P, Preclinical characterization of the selective JAK1/2 inhibitor INCB018424: therapeutic implications for the treatment of myeloproliferative neoplasms. Blood 2010;115:3109-17
   PubMed Web of Science ®Google Scholar
• Verstovsek S, Kantarjian H, Mesa RA, Safety and efficacy of INCB018424, a JAK1 and JAK2 inhibitor, in myelofibrosis. N Engl J Med 2010;363:1117-27
   PubMed Web of Science ®Google Scholar
• Verstovsek S, Kantarjian HM, Pardanani AD, Characterization of JAK2 V617F allele burden in advanced myelofibrosis (MF) patients: no change in V617F:WT JAK2 ratio in patients with high allele burdens despite profound clinical improvement following treatment with the JAK inhibitor, INCB018424 [abstract]. Blood 2008;112:2802
   Google Scholar
• Vannucchi AM. From palliation to targeted therapy in myelofibrosis. N Engl J Med 2010;363(12):1180-2
   PubMed Web of Science ®Google Scholar
• Wernig G, Kharas MG, Okabe R, Efficacy of TG101348, a selective JAK2 inhibitor, in treatment of a murine model of JAK2V617F-induced polycythemia vera. Cancer Cell 2008;13:311-20
   PubMed Web of Science ®Google Scholar
• Pardanani D, Gotlib J, Jamieson C, A phase I evaluation of TG101348, a selective JAK2 inhibitor, in myelofibrosis: clinical response is accompanied by significant reduction in JAK2V617F allele burden. Blood (ASH Annual Meeting Abstracts) 2009;114:755
   Google Scholar
• Paquette R, Sokol L, Shah NP, A phase I study of XL019, a selective JAK2 inhibitor, in patients with polycythemia vera. Blood (ASH Annual Meeting Abstracts) 2008;112:2810
   PubMed Web of Science ®Google Scholar
• Verstovsek S, Pardanani AD, Shah NP, A phase I study of XL019, a selective JAK2 inhibitor, in patients with primary myelofibrosis and post-polycythemia vera/essential thrombocythemia myelofibrosis. Blood (ASH Annual Meeting Abstracts) 2007;110:170a
   Web of Science ®Google Scholar
• Shah NP, Olszynski P, Sokol L, A phase I study of XL019, a selective JAK2 inhibitor, in patients with primary myelofibrosis, post-polycythemia vera, or post-essential thrombocythemia myelofibrosis. Blood (ASH Annual Meeting Abstracts) 2008;112:98
   Google Scholar
• Goh KC, Ong WC, Hu C, SB1518: a potent and orally active JAK2 inhibitor for the treatment of myeloproliferative disorders. Blood (ASH Annual Meeting Abstracts) 2007;110(11):538
   Google Scholar
• Verstovsek S, Odenike O, Scott B, Phase I dose-escalation trial of SB1518, a novel JAK2/FLT3 inhibitor, in acute and chronic myeloid diseases, including primary or post-essential thrombocythemia/polycythemia vera myelofibrosis. Blood (ASH Annual Meeting Abstracts) 2009;114: abstract 3905
   Google Scholar
• Seymour F, Goh A, Meadows L, First report of the phase-i study of the novel oral JAK2 inhibitor SB1518 in patients with myelofibrosis. [ABS] 2005;EHA 15th Congress Abstracts
   Google Scholar
• Tyner JW, Bumm TG, Deininger J, CYT387, a novel JAK2 inhibitor, induces hematologic responses and normalizes inflammatory cytokines in murine myeloproliferative neoplasms. Blood 2010;115:5232-40
   PubMed Web of Science ®Google Scholar
• Napper A. Drug discovery and development of innovative therapeutics—IBC's 13th annual world congress. Approaches to cancer therapy. IDrugs 2008;11:705-9
   PubMed Web of Science ®Google Scholar
• Hedvat M, Huszar D, Herrmann A, The JAK2 inhibitor AZD1480 potently blocks Stat3 signaling and oncogenesis in solid tumors. Cancer Cell 2009;16:487-97
   PubMed Web of Science ®Google Scholar
• Levis M, Tse KF, Smith BD, A FLT3 tyrosine kinase inhibitor is selectively cytotoxic to acute myeloid leukemia blasts harboring FLT3 internal tandem duplication mutations. Blood 2001;98:885-7
   PubMed Web of Science ®Google Scholar
• Smith BD, Levis M, Beran M, Single-agent CEP-701, a novel FLT3 inhibitor, shows biologic and clinical activity in patients with relapsed or refractory acute myeloid leukemia. Blood 2004;103:3669-76
   PubMed Web of Science ®Google Scholar
• Hexner EO, Serdikoff C, Jan M, Lestaurtinib (CEP701) is a JAK2 inhibitor that suppresses JAK2/ STAT5 signaling and the proliferation of primary erythroid cells from patients with myeloproliferative disorders. Blood 2008;111:5663-71
   PubMed Web of Science ®Google Scholar
• Levis M, Smith BD, Beran M, A randomized, open-label study of lestaurtinib (CEP-701), an oral FLT3 inhibitor, administered in sequence with chemotherapy in patients with relapsed AML harboring FLT3 activating mutations: clinical response correlates with successful FLT3 inhibition [abstract]. Blood 2005;106:403
   Google Scholar
• Santos FP, Kantarjian HM, Jain N, Phase 2 study of CEP-701, an orally available JAK2 inhibitor, in patients with primary or post-polycythemia vera/essential thrombocythemia myelofibrosis. Blood 2010;115:1131-6
   PubMed Web of Science ®Google Scholar
• Moliterno AR, Hexner E, Roboz GJ, An Open-Label Study of CEP-701 in patients with JAK2 V617F-positive PV and ET: update of 39 enrolled patients. Blood (ASH Annual Meeting Abstracts) 2009;114:753
   PubMedGoogle Scholar
• Harrington EA, Bebbington D, Moore J, VX-680, a potent and selective small-molecule inhibitor of the Aurora kinases, suppresses tumor growth in vivo. Nat Med 2004;10:262-7
   PubMed Web of Science ®Google Scholar
• Giles F, Bergstrom D, Garcia-Manero G, MK-0457 is a novel aurora kinase and janus kinase 2 (JAK2) inhibitor with activity in transformed JAK2-positive myeloproliferative disease (MPD). Blood (ASH Annual Meeting Abstracts) 2006;108:4893
   Google Scholar
• Carter TA, Wodicka LM, Shah NP, Inhibition of drug-resistant mutants of ABL, KIT, and EGF receptor kinases. Proc Natl Acad Sci USA 2005;102:11011-16
   PubMed Web of Science ®Google Scholar
• Fei F, Stoddart S, Groffen J, Heisterkamp N. Activity of the Aurora kinase inhibitor VX-680 against Bcr/Abl-positive acute lymphoblastic leukemias. Mol Cancer Ther 2010;9:1318-27
   PubMed Web of Science ®Google Scholar
• Giles FJ, Cortes J, Jones D, MK-0457, a novel kinase inhibitor, is active in patients with chronic myeloid leukemia or acute lymphocytic leukemia with the T315I BCR-ABL mutation. Blood 2007;109:500-2
   PubMed Web of Science ®Google Scholar
• Li Y, Zhang ZF, Chen J, The BT. VX680/MK-0457, a potent and selective Aurora kinase inhibitor, targets both tumor and endothelial cells in clear cell renal cell carcinoma. Am J Transl Res 2010;2:296-308
   PubMedGoogle Scholar
• Traynor AM, Hewitt M, Liu G, Phase I dose escalation study of MK-0457, a novel Aurora kinase inhibitor, in adult patients with advanced solid tumors. Cancer Chemother Pharmacol 2010; DOI: 10.1007/s00280-010-1318-9
   Google Scholar
• Howard S, Berdini V, Boulstridge J, Fragment-based discovery of AT9283, a multi-targeted kinase inhibitor with potent Aurora kinase activity. J Med Chem 2009;52:379-88
   PubMed Web of Science ®Google Scholar
• Curry J, Angove H, Fazal L, Aurora B kinase inhibition in mitosis: strategies for optimising the use of Aurora kinase inhibitors such as AT9283. Cell Cycle 2009;8:1921-9
   PubMedGoogle Scholar
• Dawson MA, Curry JE, Barber K, AT9283, a potent inhibitor of the Aurora kinases and Jak2, has therapeutic potential in myeloproliferative disorders. Br J Haematol 2010;150:46-57
   PubMed Web of Science ®Google Scholar
• Tanaka R, Squires MS, Kimura S, Activity of the multi-targeted kinase inhibitor, AT9283, in imatinib-resistant BCR-ABL positive leukemic cells. Blood 2010;116:2089-95
   PubMed Web of Science ®Google Scholar
• Lyons JF, Squires MS, Goodall J, The activity of AT9283 in acute myeloid leukemia in vitro and in the clinic is karyotype dependent. Blood (ASH Annual Meeting Abstracts) 2009;114:4159
   Google Scholar
• Ravandi F, Foran J, Verstovsek S, A Phase I Trial of AT9283, a multitargeted kinase inhibitor, in patients with refractory hematological malignancies (ASH Annual Meeting Abstracts). Blood 2007;110:904
   Google Scholar
• Barbetti V, Gozzini A, Rovida E, Selective anti-leukaemic activity of low-dose histone deacetylase inhibitor ITF2357 on AML1/ETO-positive cells. Oncogene 2008;27:1767-78
   PubMed Web of Science ®Google Scholar
• Petrini M, Galimberti S, Canestraro M, Histone deacetylase inhibitor ITF2357 is effective on the P39 cells. A gene expression study. J Clin Oncol 2008;26:5156-64
   PubMedGoogle Scholar
• Golay J, Cuppini L, Leoni F, The histone deacetylase inhibitor ITF2357 has anti-leukemic activity in vitro and in vivo and inhibits IL-6 and VEGF production by stromal cells. Leukemia 2007;21:1892-900
   PubMed Web of Science ®Google Scholar
• Guerini V, Barbui V, Spinelli O, The histone deacetylase inhibitor ITF2357 selectively targets cells bearing mutated JAK2(V617F). Leukemia 2008;22:740-7
   PubMed Web of Science ®Google Scholar
• Rambaldi A, Dellacasa CM, Finazzi G, A pilot study of the histone-deacetylase inhibitor givinostat in patients with JAK2V617F positive chronic myeloproliferative neoplasms. Br J Haematol 2010;150:446-55
   PubMed Web of Science ®Google Scholar
• Markovtsov V, Tonkin E, Fang S, In vitro and in vivo inhibition of JAK2 signaling by potent and selective JAK2 inhibitor blood (ASH Annual Meeting Abstracts) 2008:112:3721
   Google Scholar
• Shide K, Kameda T, Markovtsov V, Efficacy of R723, a potent and selective JAK2 inhibitor, in JAK2V617F-induced murine MPD model. Blood (ASH Annual Meeting Abstracts) 2009;114:3897
   Google Scholar
• Koppikar P, Abdel-Wahab O, Hedvat C, Efficacy of the JAK2 inhibitor INCB16562 in a murine model of MPLW515L-induced thrombocytosis and myelofibrosis. Blood 2010;115:2919-27
   PubMed Web of Science ®Google Scholar