121
Views
24
CrossRef citations to date
0
Altmetric
Review

Prospect of JAK2 inhibitor therapy in myeloproliferative neoplasms

&
Pages 663-670 | Published online: 10 Jan 2014

References

  • Liu CB, Itoh T, Arai K, Watanabe S. Constitutive activation of JAK2 confers murine interleukin-3-independent survival and proliferation of BA/F3 cells. J. Biol. Chem.274(10), 6342–6349 (1999).
  • Liu RY, Fan C, Garcia R, Jove R, Zuckerman KS. Constitutive activation of the JAK2/STAT5 signal transduction pathway correlates with growth factor independence of megakaryocytic leukemic cell lines. Blood93(7), 2369–2379 (1999).
  • Takemoto S, Mulloy JC, Cereseto A et al. Proliferation of adult T cell leukemia/lymphoma cells is associated with the constitutive activation of JAK/STAT proteins. Proc. Natl Acad. Sci. USA94(25), 13897–13902 (1997).
  • Baxter EJ, Scott LM, Campbell PJ et al. Acquired mutation of the tyrosine kinase JAK2 in human myeloproliferative disorders. Lancet365(9464), 1054–1061 (2005).
  • James C, Ugo V, Le Couedic JP et al. A unique clonal JAK2 mutation leading to constitutive signalling causes polycythaemia vera. Nature434(7037), 1144–1148 (2005).
  • Kralovics R, Passamonti F, Buser AS et al. A gain-of-function mutation of JAK2 in myeloproliferative disorders. N. Engl. J. Med.352(17), 1779–1790 (2005).
  • Levine RL, Wadleigh M, Cools J et al. Activating mutation in the tyrosine kinase JAK2 in polycythemia vera, essential thrombocythemia, and myeloid metaplasia with myelofibrosis. Cancer Cell7(4), 387–397 (2005).
  • Zhao R, Xing S, Li Z et al. Identification of an acquired JAK2 mutation in polycythemia vera. J. Biol. Chem.280(24), 22788–22792 (2005).
  • Tefferi A. Classification, diagnosis and management of myeloproliferative disorders in the JAK2V617F era. Hematology Am. Soc. Hematol. Educ. Program240–245 (2006).
  • Passamonti F, Rumi E, Pungolino E et al. Life expectancy and prognostic factors for survival in patients with polycythemia vera and essential thrombocythemia. Am. J. Med.117(10), 755–761 (2004).
  • Mesa RA, Elliott MA, Schroeder G, Tefferi A. Durable responses to thalidomide-based drug therapy for myelofibrosis with myeloid metaplasia. Mayo Clin. Proc.79(7), 883–889 (2004).
  • Thomas DA, Giles FJ, Albitar M et al. Thalidomide therapy for myelofibrosis with myeloid metaplasia. Cancer106(9), 1974–1984 (2006).
  • Tefferi A, Cortes J, Verstovsek S et al. Lenalidomide therapy in myelofibrosis with myeloid metaplasia. Blood108(4), 1158–1164 (2006).
  • Deeg HJ, Gooley TA, Flowers MED et al. Allogeneic hematopoietic stem cell transplantation for myelofibrosis. Blood102(12), 3912–3918 (2003).
  • Cervantes F, Dupriez B, Pereira A et al. A new prognostic scoring system for primary myelofibrosis based on a study of the International Working Group for Myelofibrosis Research and Treatment. Blood113(13), 2895–2901 (2008).
  • Yamaoka K, Saharinen P, Pesu M, Holt VE 3rd, Silvennoinen O, O’Shea JJ. The Janus kinases (Jaks). Genome Biol.5(12), 253 (2004).
  • Bittorf T, Jaster R, Ludtke B, Kamper B, Brock J. Requirement for JAK2 in erythropoietin-induced signalling pathways. Cell Signal.9(1), 85–89 (1997).
  • Sattler M, Durstin MA, Frank DA et al. The thrombopoietin receptor c-MPL activates JAK2 and TYK2 tyrosine kinases. Exp. Hematol.23(9), 1040–1048 (1995).
  • Brizzi MF, Aronica MG, Rosso A, Bagnara GP, Yarden Y, Pegoraro L. Granulocyte–macrophage colony-stimulating factor stimulates JAK2 signaling pathway and rapidly activates p93fes, STAT1 p91, and STAT3 p92 in polymorphonuclear leukocytes. J. Biol. Chem.271(7), 3562–3567 (1996).
  • Neubauer H, Cumano A, Muller M, Wu H, Huffstadt U, Pfeffer K. Jak2 deficiency defines an essential developmental checkpoint in definitive hematopoiesis. Cell93(3), 397–409 (1998).
  • Parganas E, Wang D, Stravopodis D et al. Jak2 is essential for signaling through a variety of cytokine receptors. Cell93(3), 385–395 (1998).
  • Harpur AG, Andres AC, Ziemiecki A, Aston RR, Wilks AF. JAK2, a third member of the JAK family of protein tyrosine kinases. Oncogene7(7), 1347–1353 (1992).
  • Saharinen P, Silvennoinen O. The pseudokinase domain is required for suppression of basal activity of Jak2 and Jak3 tyrosine kinases and for cytokine-inducible activation of signal transduction. J. Biol. Chem.277(49), 47954–47963 (2002).
  • Wernig G, Kharas MG, Okabe R et al. Efficacy of TG101348, a selective JAK2 inhibitor, in treatment of a murine model of JAK2V617F-induced polycythemia vera. Cancer Cell13(4), 311–320 (2008).
  • Pardanani AD, Gotlib J, Jamieson C et al. A Phase I study of TG101348, an orally bioavailable JAK2-selective inhibitor, in patients with myelofibrosis. ASH Annual Meeting Abstracts112(11) (2008) (Abstract 97).
  • Verstovsek S, Kantarjian HM, Pardanani AD et al. The JAK inhibitor, INCB018424, demonstrates durable and marked clinical responses in primary myelofibrosis (PMF) and post-polycythemia/essential thrombocythemia myelofibrosis (Post PV/ETMF). ASH Annual Meeting Abstracts112(11) (2008) (Abstract 1762).
  • Mesa RA, Schwager S, Radia D et al. Assessment and monitoring of constitutional symptoms in patients with myelofibrosis: a proposed new instrument the myelofibrosis symptom assessment form (MFSAF). ASH Annual Meeting Abstracts112(11) (2008) (Abstract 1754).
  • Tefferi A, Kantarjian HM, Pardanani AD et al. The clinical phenotype of myelofibrosis encompasses a chronic inflammatory state that is favorably altered by INCB018424, a selective inhibitor of JAK1/2. ASH Annual Meeting Abstracts112(11) (2008) (Abstract 2804).
  • Verstovsek S, Kantarjian HM, Pardanani AD et al. 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. ASH Annual Meeting Abstracts112(11) (2008) (Abstract 2802).
  • Paquette R, Sokol L, Shah NP et al. A Phase I study of XL019, a selective JAK2 inhibitor, in patients with polycythemia vera. ASH Annual Meeting Abstracts112(11) (2008) (Abstract 2810).
  • Shah NP, Olszynski P, Sokol L et al. A Phase I study of XL019, a selective JAK2 inhibitor, in patients with primary myelofibrosis, post-polycythemia vera, or post-essential thrombocythemia myelofibrosis. ASH Annual Meeting Abstracts112(11) (2008) (Abstract 98).
  • Guerini V, Barbui V, Spinelli O et al. Selective targeting of the JAK2V617F mutation in polycythemia vera and essential thrombocythemia by ITF2357, a novel histone deacetylase inhibitor. ASH Annual Meeting Abstracts,110(11) (2007) (Abstract 555).
  • Rambaldi A, Dellacasa CM, Salmoiraghi S et al. A Phase 2A study of the histone-deacetylase inhibitor ITF2357 in patients with Jak2V617F positive chronic myeloproliferative neoplasms. ASH Annual Meeting Abstracts112(11) (2008)(Abstract 100).
  • Giles F, Bergstrom DA, Garcia-Manero G et al. MK-0457 is a novel aurora kinase and janus kinase 2 (JAK2) inhibitor with activity in transformed JAK2-positive myeloproliferative disease (MPD). ASH Annual Meeting Abstracts108(11) (2006) (Abstract 4893).
  • Levis M, Smith BD, Beran M et al. 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. ASH Annual Meeting Abstracts106(11) (2005) (Abstract 403).
  • Dobrzanski P, Hexner E, Serdikoff C et al. CEP-701 is a JAK2 inhibitor which attenuates jak2/stat5 signaling pathway and the proliferation of primary cells from patients with myeloproliferative disorders. ASH Annual Meeting Abstracts108(11) (2006) (Abstract 3594).
  • Moliterno AR, Roboz GJ, Carroll M, Luger S, Hexner E, Bensen-Kennedy DM. An open-label study of cep-701 in patients with JAK2 V617F-positive polycythemia vera and essential thrombocytosis. ASH Annual Meeting Abstracts112(11) (2008) (Abstract 99).
  • Fukuoka M, Yano S, Giaccone G et al. Multi-institutional randomized Phase II trial of gefitinib for previously treated patients with advanced non-small-cell lung cancer (The IDEAL 1 Trial) [corrected]. J. Clin. Oncol.21(12), 2237–2246 (2003).
  • Lynch TJ, Bell DW, Sordella R et al. Activating mutations in the epidermal growth factor receptor underlying responsiveness of non-small-cell lung cancer to gefitinib. N. Engl. J. Med.350(21), 2129–2139 (2004).
  • Li Z, Xu M, Xing S et al. Erlotinib effectively inhibits JAK2V617F activity and polycythemia vera cell growth. J. Biol. Chem.282(6), 3428–3432 (2007).
  • Albrightson-Winslow CR, Brickson B, King A et al. Beneficial effects of long-term treatment with SK&F 105685 in murine lupus nephritis. J. Pharmacol. Exp. Ther.255(1), 382–387 (1990).
  • Amit-Vazina M, Shishodia S, Harris D et al. Atiprimod blocks STAT3 phosphorylation and induces apoptosis in multiple myeloma cells. Br. J. Cancer93(1), 70–80 (2005).
  • Faderl S, Ferrajoli A, Harris D, Van Q, Kantarjian HM, Estrov Z. Atiprimod blocks phosphorylation of JAK–STAT and inhibits proliferation of acute myeloid leukemia (AML) cells. Leuk. Res.31(1), 91–95 (2007).
  • Duan Z, Bradner J, Greenberg E et al. 8-benzyl-4-oxo-8-azabicyclo[3.2.1]oct-2-ene-6,7-dicarboxylic acid (SD-1008), a novel janus kinase 2 inhibitor, increases chemotherapy sensitivity in human ovarian cancer cells. Mol. Pharmacol.72(5), 1137–1145 (2007).
  • Lucet IS, Fantino E, Styles M et al. The structural basis of Janus kinase 2 inhibition by a potent and specific pan-Janus kinase inhibitor. Blood107(1), 176–183 (2006).
  • Thompson JE, Cubbon RM, Cummings RT et al. Photochemical preparation of a pyridone containing tetracycle: a Jak protein kinase inhibitor. Bioorg. Med. Chem. Lett.12(8), 1219–1223 (2002).
  • Sayyah J, Magis A, Ostrov DA, Allan RW, Braylan RC, Sayeski PP. Z3, a novel Jak2 tyrosine kinase small-molecule inhibitor that suppresses Jak2-mediated pathologic cell growth. Mol. Cancer Ther.7(8), 2308–2318 (2008).
  • Grandage VL, Everington T, Linch DC, Khwaja A. Go6976 is a potent inhibitor of the JAK 2 and FLT3 tyrosine kinases with significant activity in primary acute myeloid leukaemia cells. Br. J. Haematol.135(3), 303–316 (2006).
  • Muto A, Hori M, Sasaki Y et al. Emodin has a cytotoxic activity against human multiple myeloma as a Janus-activated kinase 2 inhibitor. Mol. Cancer Ther.6(3), 987–994 (2007).
  • Meydan N, Grunberger T, Dadi H et al. Inhibition of acute lymphoblastic leukaemia by a Jak-2 inhibitor. Nature379(6566), 645–648 (1996).
  • Duek A, Lichman I, Shtalrid M, Berrebi A. The Jak2-inhibitor AG409 affects survival of BFU-E and CFU-GM of myeloproliferative disorder cells carrying the JAK2 V617F mutation. ASH Annual Meeting Abstracts,108(11) (2006) (Abstract 4907).
  • Kapuria V, Bartholomeusz G, Kong L-Y et al. A novel small-molecule approach to inhibit Jak2 tyrosine kinase signaling. ASH Annual Meeting Abstracts110(11) (2007) (Abstract 1556).
  • Manshouri T, Estrov Z, Quintas-Cardama A et al. WP1066 inhibits growth of human cells carrying the JAK2 V617F mutation. ASH Annual Meeting Abstracts108(11) (2006) (Abstract 4885).
  • Ferrajoli A, Faderl S, Wang T et al. WP1066: a novel PI-3K inhibitor with antileukemic activity in philadelphia chromosome-positive ALL. ASH Annual Meeting Abstracts106(11) (2005) (Abstract 850).
  • Mesa RA, Powell H, Lasho T, Dewald G, McClure R, Tefferi A. JAK2(V617F) and leukemic transformation in myelofibrosis with myeloid metaplasia. Leuk. Res.30(11), 1457–1460 (2006).
  • Theocharides A, Boissinot M, Girodon F et al. Leukemic blasts in transformed JAK2-V617F-positive myeloproliferative disorders are frequently negative for the JAK2-V617F mutation. Blood110(1), 375–379 (2007).
  • Vannucchi AM, Antonioli E, Guglielmelli P, Pardanani A, Tefferi A. Clinical correlates of JAK2V617F presence or allele burden in myeloproliferative neoplasms: a critical reappraisal. Leukemia22(7), 1299–1307 (2008).
  • Epling-Burnette PK, Liu JH, Catlett-Falcone R et al. Inhibition of STAT3 signaling leads to apoptosis of leukemic large granular lymphocytes and decreased Mcl-1 expression. J. Clin. Invest.107(3), 351–362 (2001).
  • Dohner K, Du J, Corbacioglu A, Scholl C, Schlenk RF, Dohner H. JAK2V617F mutations as cooperative genetic lesions in t(8;21)-positive acute myeloid leukemia. Haematologica91(11), 1569–1570 (2006).
  • Lo M-C, Peterson LF, Yan M et al. Identification of the JAK/STAT signaling pathway as a valid therapeutic target of t(8;21) acute myeloid leukemia using combined gene expression and promoter occupancy profiling. ASH Annual Meeting Abstracts112(11) (2008) (Abstract 3336).
  • Schnittger S, Bacher U, Kern W, Haferlach C, Haferlach T. JAK2 seems to be a typical cooperating mutation in therapy-related t(8;21)/ AML1-ETO-positive AML. Leukemia21(1), 183–184 (2007).
  • Samanta AK, Lin H, Sun T, Kantarjian H, Arlinghaus RB. Jak2: a potential therapeutic target for chronic myelogenous leukemia (CML). ASH Annual Meeting Abstracts108(11) (2006) (Abstract 2121).
  • Sun X, Layton JE, Elefanty A, Lieschke GJ. Comparison of effects of the tyrosine kinase inhibitors AG957, AG490, and STI571 on BCR-ABL – expressing cells, demonstrating synergy between AG490 and STI571. Blood97(7), 2008–2015 (2001).
  • Fridman J, Nussenzveig R, Liu P et al. Discovery and preclinical characterization of INCB018424, a selective JAK2 inhibitor for the treatment of myeloproliferative disorders. ASH Annual Meeting Abstracts110(11) (2007) (Abstract 3538).

Website

Reprints and Corporate Permissions

Please note: Selecting permissions does not provide access to the full text of the article, please see our help page How do I view content?

To request a reprint or corporate permissions for this article, please click on the relevant link below:

Academic Permissions

Please note: Selecting permissions does not provide access to the full text of the article, please see our help page How do I view content?

Obtain permissions instantly via Rightslink by clicking on the button below:

If you are unable to obtain permissions via Rightslink, please complete and submit this Permissions form. For more information, please visit our Permissions help page.