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1)Barbui T, Barosi G, Birgegard G, et al. Philadelphia-negative classical myeloproliferative neoplasms: Critical Concepts and Management Recommendations From European LeukemiaNet. J Clin Oncol. 2011; 29: 761-70
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2)骨髄線維症の診断基準と診療の参照ガイド作成のためのWG. 骨髄線維症診療の参照ガイド.特発性造血障害疾患の診療の参照ガイド(平成22年度改訂版).小澤敬也,編.2011
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3)James C, Ugo V, Le Couedic JP, et al. A unique clonal JAK2 mutation leading to constitutive signalling causes polycythaemia vera. Nature. 2005; 434: 1144-8
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4)Kralovics R, Passamonti F, Buser AS, et al. A gain-of-function mutation of JAK2 in myeloproliferative disorders. N Engl J Med. 2005; 352: 1779-90
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5)Pikman Y, Lee BH, Mercher T, et al. MPLW515L is a novel somatic activating mutation in myelo-fibrosis with myeloid metaplasia. PLoS Med. 2006; 3: e270
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6)Grand FH, Hidalgo-Curtis CE, Ernst T, et al. Frequent CBL mutations associated with 11q acquired uniparental disomy in myeloproliferative neoplasms. Blood. 2009; 113: 6182-92
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7)Oh ST, Simonds EF, Jones C, et al. Novel mutations in the inhibitory adaptor protein LNK drive JAK-STAT signaling in patients with myeloproliferative neoplasms. Blood. 2010; 116: 988-92
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8)Harrison C, Kiladjian JJ, Al-Ali HK, et al. JAK inhibition with ruxolitinib versus best available therapy for myelofibrosis. N Engl J Med. 2012; 366: 787-98
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9)Verstovsek S, Mesa RA, Gotlib J, et al. A double-blind, placebo-controlled trial of ruxolitinib for myelofibrosis. N Engl J Med. 2012; 366: 799-807
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10)Cervantes F, Kiladjian JJ, Niederwieser D, et al. Long-term safety, efficacy, and survival findings from COMFORT-II, a phase 3 study comparing ruxolitinib with best available therapy (BAT) for the treatment of myelofibrosis (MF). ASH Annual Meeting Abstracts. 2012; 120: 801
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11)Verstovsek S, Mesa RA, Gotlib J, et al. Long-term outcome of ruxolitinib treatment in patients with myelofibrosis: durable reductions in spleen volume, improvements in quality of life, and overall survival advantage in COMFORT-I. ASH Annual Meeting Abstracts. 2012; 120: 800
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12)Komrokji RS, Wadleigh M, Seymour JF, et al. Results of a phase 2 study of pacritinib (SB1518), a novel oral JAK2 inhibitor, in patients with primary, post-polycythemia vera, and post-essential thrombocythemia myelofibrosis. ASH Annual Meeting Abstracts. 2011; 118: 282
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13)Pardanani A, Gotlib JR, Jamieson C, et al. Safety and efficacy of TG101348, a selective JAK2 inhibitor, in myelofibrosis. J Clin Oncol. 2011; 29: 789-96
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14)Pardanani A, Laborde RR, Lasho TL, et al. Safety and efficacy of CYT387, a JAK1 and JAK2 inhibitor, in myelofibrosis. Leukemia. 2013; 27: 1322-7
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15)Verstovsek S, Kantarjian H, Mesa RA, et al. Safety and efficacy of INCB018424, a JAK1 and JAK2 inhibitor, in myelofibrosis. N Engl J Med. 2010; 363: 1117-27
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16)Apperley JF. Part I: Mechanisms of resistance to imatinib in chronic myeloid leukaemia. Lancet Oncol. 2007; 8: 1018-29
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17)Koppikar P, Bhagwat N, Kilpivaara O, et al. Heterodimeric JAK-STAT activation as a mechanism of persistence to JAK2 inhibitor therapy. Nature. 2012; 489: 155-9
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18)Bareng J, Jilani I, Gorre M, et al. A potential role for HSP90 inhibitors in the treatment of JAK2 mutant-positive diseases as demonstrated using quantitative flow cytometry. Leuk Lymphoma. 2007; 48: 2189-95
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19)Fiskus W, Verstovsek S, Manshouri T, et al. Heat shock protein 90 inhibitor is synergistic with JAK2 inhibitor and overcomes resistance to JAK2-TKI in human myeloproliferative neoplasm cells. Clin Cancer Res. 2011; 17: 7347-58
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20)Levine RL, Koppikar P, Marubayashi S, et al. Combination therapy using JAK2 and HSP90 inhibitors increased efficacy in myelofibrosis in vivo. ASH Annual Meeting Abstracts. 2012; 120: 805
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21)Bali P, Pranpat M, Bradner J, et al. Inhibition of histone deacetylase 6 acetylates and disrupts the chaperone function of heat shock protein 90: A novel basis for antileukemia activity of histone deacetylase inhibitors. J Biol Chem. 2005; 280: 26729-34
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22)Guerini V, Barbui V, Spinelli O, et al. The histone deacetylase inhibitor ITF2357 selectively targets cells bearing mutated JAK2V617F. Leukemia. 2007; 22: 740-7
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23)Wang Y, Fiskus W, Chong DG, et al. Cotreatment with panobinostat and JAK2 inhibitor TG101209 attenuates JAK2V617F levels and signaling and exerts synergistic cytotoxic effects against human myeloproliferative neoplastic cells. Blood. 2009; 114: 5024-33
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24)Baffert F, Evrot E, Ebel N, et al. Improved efficacy upon combined JAK1/2 and pan-deacetylase inhibition using ruxolitinib (INC424) and panobinostat (LBH589) in preclinical mouse models of JAK2V617F-driven disease. ASH Annual Meeting Abstracts. 2011; 118: 798
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25)Nakaya Y, Shide K, Niwa T, et al. Efficacy of NS-018, a potent and selective JAK2/Src inhibitor, in primary cells and mouse models of myeloproliferative neoplasms. Blood Cancer J. 2011; 1: e29
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26)Purandare AV, McDevitt TM, Wan H, et al. Characterization of BMS-911543, a functionally selective small-molecule inhibitor of JAK2. Leukemia. 2012; 26: 280-8
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27)Ma L, Clayton JR, Walgren RA, et al. Discovery and characterization of LY2784544, a small-molecule tyrosine kinase inhibitor of JAK2V617F. Blood Cancer J. 2013; 3: e109
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28)Fang Z, Grütter C, Rauh D. Strategies for the selective regulation of kinases with allosteric modulators: exploiting exclusive structural features. ACS Chemical Biology. 2012; 8: 58-70
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29)Liu Y, Gray NS. Rational design of inhibitors that bind to inactive kinase conformations. Nat Chem Biol. 2006; 2: 358-64
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30)Andraos R, Qian Z, Bonenfant D, et al. Modulation of activation-loop phosphorylation by JAK inhibitors is binding mode dependent. Cancer Discov. 2012; 2: 512-23
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31)Harrison C, Verstovsek S, McMullin MF, et al. Janus kinase inhibition and its effect upon the therapeutic landscape for myelofibrosis: from palliation to cure? Br J Haematol. 2012; 157: 426-37
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32)Vannucchi AM, Harrison CN. Promise and pitfalls of therapy with JAK2 inhibitors in myeloproliferative neoplasms. Int J Clin Rev. 2012; doi: 10.5275/ijcr
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