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Advances in Hematology
Volume 2012 (2012), Article ID 535709, 6 pages
JAK2 Inhibition: Reviewing a New Therapeutical Option in Myeloproliferative Neoplasms
Department of Hematology, Erasmus University Medical Center, P.O. Box 2040, 3000 CA Rotterdam, The Netherlands
Received 12 September 2011; Revised 29 November 2011; Accepted 4 December 2011
Academic Editor: Mark R. Litzow
Copyright © 2012 Mar Bellido and Peter A. W. te Boekhorst. This is an open access article distributed under the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited.
- M. Bennett and D. F. Stroncek, “Recent advances in the bcr-abl negative chronic myeloproliferative diseases,” Journal of Translational Medicine, vol. 4, article 41, 2006.
- A. Stoddart, M. L. Dykstra, B. K. Brown, W. Song, S. K. Pierce, and F. M. Brodsky, “Lipid rafts unite signaling cascades with clathrin to regulate BCR internalization,” Immunity, vol. 17, no. 4, pp. 451–462, 2002.
- I. Duran, S. J. Hotté, H. Hirte et al., “Phase I targeted combination trial of sorafenib and erlotinib in patients with advanced solid tumors,” Clinical Cancer Research, vol. 13, no. 16, pp. 4849–4857, 2007.
- M. C. Heinrich, H. Joensuu, G. D. Demetri et al., “Phase II, open-label study evaluating the activity of imatinib in treating life-threatening malignancies known to be associated with imatinib-sensitivetyrosine kinases,” Clinical Cancer Research, vol. 14, no. 9, pp. 2717–2725, 2008.
- M. E. Weinblatt, A. Kavanaugh, M. C. Genovese, T. K. Musser, E. B. Grossbard, and D. B. Magilavy, “An oral spleen tyrosine kinase (Syk) inhibitor for rheumatoid arthritis,” The New England Journal of Medicine, vol. 363, no. 14, pp. 1303–1312, 2010.
- E. Scott, E. Hexner, A. Perl, and M. Carroll, “Targeted signal transduction therapies in myeloid malignancies,” Current Oncology Reports, vol. 12, no. 6, pp. 358–365, 2010.
- H. Grant, X. Jiang, J. Stebbing et al., “Analysis of BCR-ABL1 tyrosine kinase domain mutational spectra in primitive chronic myeloid leukemia cells suggests a unique mutator phenotype,” Leukemia, vol. 24, no. 10, pp. 1817–1821, 2010.
- O. Abdel-Wahab, A. Mullally, C. Hedvat et al., “Genetic characterization of TET1, TET2, and TET3 alterations in myeloid malignancies,” Blood, vol. 114, no. 1, pp. 144–147, 2009.
- A. J. Mead, D. C. Linch, R. K. Hills, K. Wheatley, A. K. Burnett, and R. E. Gale, “FLT3 tyrosine kinase domain mutations are biologically distinct from and have a significantly more favorable prognosis than FLT3 internal tandem duplications in patients with acute myeloid leukemia,” Blood, vol. 110, no. 4, pp. 1262–1270, 2007.
- M. M. Patnaik, R. A. Knudson, N. Gangat et al., “Chromosome 9p24 abnormalities: prevalence, description of novel JAK2 translocations, ,JAK2V617F mutation analysis and clinicopathologic correlates,” European Journal of Haematology, vol. 84, no. 6, pp. 518–524, 2010.
- C. Walz, A. Chase, C. Schoch et al., “The t(8;17) (p11;q23) in the 8p11 myeloproliferative syndrome fuses MYO18A to FGFR1,” Leukemia, vol. 19, no. 6, pp. 1005–1009, 2005.
- A. de Klein, A. G. van Kessel, G. Grosveld, et al., “A celllular oncogene is translocated to the Philadelphia chromosome in chronic myelocytic leukaemia,” Nature, vol. 300, no. 5894, pp. 765–767, 1982.
- C. James, V. Ugo, J. P. Le Couédic et al., “A unique clonal JAK2 mutation leading to constitutive signalling causes polycythaemia vera,” Nature, vol. 434, no. 7037, pp. 1144–1148, 2005.
- R. L. Levine, M. Wadleigh, J. Cools et al., “Activating mutation in the tyrosine kinase JAK2 in polycythemia vera, essential thrombocythemia, and myeloid metaplasia with myelofibrosis,” Cancer Cell, vol. 7, no. 4, pp. 387–397, 2005.
- J. De Vos, M. Jourdan, K. Tarte, C. Jasmin, and B. Klein, “JAK2 tyrosine kinase inhibitor tyrphostin AG490 downregulates the mitogen-activated protein kinase (MAPK) and signal transducer and activator of transcription (STAT) pathways and induces apoptosis in myeloma cells,” British Journal of Haematology, vol. 109, no. 4, pp. 823–828, 2000.
- S. Oku, K. Takenaka, T. Kuriyama et al., “JAK2V617F uses distinct signalling pathways to induce cell proliferation and neutrophil activation: research paper,” British Journal of Haematology, vol. 150, no. 3, pp. 334–344, 2010.
- M. Boissinot, C. Cleyrat, M. Vilaine, Y. Jacques, I. Corre, and S. Hermouet, “Anti-inflammatory cytokines hepatocyte growth factor and interleukin-11 are over-expressed in Polycythemia vera and contribute to the growth of clonal erythroblasts independently of JAK2V617F,” Oncogene, vol. 30, no. 8, pp. 990–1001, 2011.
- E. Parganas, D. Wang, D. Stravopodis et al., “JAK2 is essential for signaling through a variety of cytokine receptors,” Cell, vol. 93, no. 3, pp. 385–395, 1998.
- L. M. Scott, W. Tong, R. L. Levine et al., “JAK2 exon 12 mutations in polycythemia vera and idiopathic erythrocytosis,” The New England Journal of Medicine, vol. 356, no. 5, pp. 459–468, 2007.
- S. T. Oh, E. F. Simonds, C. Jones et al., “Novel mutations in the inhibitory adaptor protein LNK drive JAK-STAT signaling in patients with myeloproliferative neoplasms,” Blood, vol. 116, no. 6, pp. 988–992, 2010.
- J. A. Kennedy, F. Barabé, B. J. Patterson et al., “Expression of TEL-JAKZ in primary human hematopoietic cells drives erythropoietin-independent erythropoiesis and induces myelofibrosis in vivo,” Proceedings of the National Academy of Sciences of the United States of America, vol. 103, no. 45, pp. 16930–16935, 2006.
- P. A. Beer, P. J. Campbell, L. M. Scott et al., “MPL mutations in myeloproliferative disorders: analysis of the PT-1 cohort,” Blood, vol. 112, no. 1, pp. 141–149, 2008.
- A. Tefferi, “Novel mutations and their functional and clinical relevance in myeloproliferative neoplasms: JAK2, MPL, TET2, ASXL1, CBL, IDH and IKZF1.,” Leukemia, vol. 24, no. 6, pp. 1128–1138, 2010.
- L. Millecker, P. A. Lennon, S. Verstovsek et al., “Distinct patterns of cytogenetic and clinical progression in chronic myeloproliferative neoplasms with or without JAK2 or MPL mutations,” Cancer Genetics and Cytogenetics, vol. 197, no. 1, pp. 1–7, 2010.
- M. A. Dawson, A. J. Bannister, B. Göttgens et al., “JAK2 phosphorylates histone H3Y41 and excludes HP1α from chromatin,” Nature, vol. 461, no. 7265, pp. 819–822, 2009.
- Y. Wang, W. Fiskus, D. G. Chong 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, vol. 114, no. 24, pp. 5024–5033, 2009.
- R. Baskin, A. Majumder, and P. P. Sayeski, “The recent medicinal chemistry development of JAK2 tyrosine kinase small molecule inhibitors,” Current Medicinal Chemistry, vol. 17, no. 36, pp. 4551–4558, 2010.
- S. Verstovsek, “Therapeutic potential of JAK2 inhibitors,” American Society of Hematology: Education Program, pp. 636–642, 2009.
- S. Verstovsek, H. Kantarjian, R. A. Mesa et al., “Safety and efficacy of INCB018424, a JAK1 and JAK2 inhibitor, in myelofibrosis,” The New England Journal of Medicine, vol. 363, no. 12, pp. 1117–1127, 2010.
- A. Quintás-Cardama, K. Vaddi, P. Liu et al., “Preclinical characterization of the selective JAK1/2 inhibitor INCB018424: therapeutic implications for the treatment of myeloproliferative neoplasms,” Blood, vol. 115, no. 15, pp. 3109–3117, 2010.
- T. L. Lasho, A. Tefferi, J. D. Hood, S. Verstovsek, D. G. Gilliland, and A. Pardanani, “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, vol. 22, no. 9, pp. 1790–1792, 2008.
- G. Wernig, M. G. Kharas, R. Okabe et al., “Efficacy of TG101348, a selective JAK2 inhibitor, in treatment of a murine model of JAK2V617F-induced polycythemia vera,” Cancer Cell, vol. 13, no. 4, pp. 311–320, 2008.
- A. Tefferi, G. Barosi, R. A. Mesa et al., “International Working Group (IWG) consensus criteria for treatment response in myelofibrosis with myeloid metaplasia, for the IWG for Myelofibrosis Research and Treatment (IWG-MRT),” Blood, vol. 108, no. 5, pp. 1497–1503, 2006.
- A. Pardanani, J. R. Gotlib, C. Jamieson et al., “Safety and efficacy of TG101348, a selective JAK2 inhibitor, in myelofibrosis,” Journal of Clinical Oncology, vol. 29, no. 7, pp. 789–796, 2011.
- J. W. Tyner, T. G. Bumm, J. Deininger et al., “CYT387, a novel JAK2 inhibitor, induces hematologic responses and normalizes inflammatory cytokines in murine myeloproliferative neoplasms,” Blood, vol. 115, no. 25, pp. 5232–5240, 2010.
- E. O. Hexner, C. Serdikoff, M. Jan et al., “Lestaurtinib (CEP701) is a JAK2 inhibitor that suppresses JAK2/STAT5 signaling and the proliferation of primary erythroid cells from patients with myeloproliferative disorders,” Blood, vol. 111, no. 12, pp. 5663–5671, 2008.
- F. P. S. Santos, H. M. Kantarjian, N. Jain et al., “Phase 2 study of CEP-701, an orally available JAK2 inhibitor, in patients with primary or post-polycythemia vera/essential thrombocythemia myelofibrosis,” Blood, vol. 115, no. 6, pp. 1131–1136, 2010.
- J. M. Goldman and J. V. Melo, “Targeting the BCR-ABL tyrosine kinase in chronic myeloid leukemia,” The New England Journal of Medicine, vol. 344, no. 14, pp. 1084–1086, 2001.
- R. A. Mesa, “Ruxolitinib, a selective JAK1 and JAK2 inhibitor for the treatment of myeloproliferative neoplasms and psoriasis,” IDrugs, vol. 13, no. 6, pp. 394–403, 2010.
- D. J. Barnes and J. V. Melo, “Primitive, quiescent and difficult to kill: the role of non-proliferating stem cells in chronic myeloid leukemia,” Cell Cycle, vol. 5, no. 24, pp. 2862–2866, 2006.
- A. Mullally, S. W. Lane, B. Ball et al., “Physiological JAK2V617F expression causes a lethal myeloproliferative neoplasm with differential effects on hematopoietic stem and progenitor cells,” Cancer Cell, vol. 17, no. 6, pp. 584–596, 2010.
- M. Lu, W. Zhang, Y. Li et al., “Interferon-α targets JAK2V617F-positive hematopoietic progenitor cells and acts through the p38 MAPK pathway,” Experimental Hematology, vol. 38, no. 6, pp. 472–480, 2010.
- J.-J. Kiladjian, R. A. Mesa, and R. Hoffman, “The renaissance of interferon therapy for the treatment of myeloid malignancies,” Blood, vol. 117, no. 18, pp. 4706–4715, 2011.
- T. Manshouri, Z. Estrov, A. Quintás-Cardama et al., “Bone marrow stroma-secreted cytokines protect JAK2V617F-mutated cells from the effects of a JAK2 inhibitor,” Cancer Research, vol. 71, no. 11, pp. 3831–3840, 2011.
- E. Jabbour, D. Thomas, H. Kantarjian et al., “Comparison of thalidomide and lenalidomide as therapy for myelofibrosis,” Blood, vol. 118, no. 4, pp. 899–902, 2011.
- K. H. Begna, R. A. Mesa, A. Pardanani et al., “A phase-2 trial of low-dose pomalidomide in myelofibrosis,” Leukemia, vol. 25, no. 2, pp. 301–304, 2011.
- C. Besses, A. Álvarez-Larrán, L. Martínez-Avilés et al., “Modulation of JAK2V617F allele burden dynamics by hydroxycarbamide in polycythaemia vera and essential thrombocythaemia patients,” British Journal of Haematology, vol. 152, no. 4, pp. 413–419, 2011.