Recent breakthroughs in the understanding and management of chronic eosinophilic leukemia

References

• Hardy WR, Anderson RE. The hypereosinophilic syndromes. Ann. Intern. Med.68(6), 1220–1229 (1968).
   PubMed Web of Science ®Google Scholar
• Chusid MJ, Dale DC, West BC, Wolff SM. The hypereosinophilic syndrome: analysis of fourteen cases with review of the literature. Medicine (Baltimore)54(1), 1–27 (1975).
   PubMed Web of Science ®Google Scholar
• Gleich GJ, Leiferman KM. The hypereosinophilic syndromes: current concepts and treatments. Br. J. Haematol.145(3), 271–285 (2009).
   PubMed Web of Science ®Google Scholar
• Jaffe ES, Harris NL, Stein H, Vardiman JW. WHO Classification of Tumours of Haematopoietic and Lymphoid Tissues. IARC Press, Lyon, France (2001).
   Google Scholar
• Roufosse F, Cogan E, Goldman M. Recent advances in pathogenesis and management of hypereosinophilic syndromes. Allergy59(7), 673–689 (2004).
   PubMed Web of Science ®Google Scholar
• Swerdlow SH, Campo E, Harris NL et al.WHO Classification of Tumours of Haematopoietic and Lymphoid Tissues (4th Edition). IARC Press, Lyon, France (2008).
   Google Scholar
• Vardiman JW, Thiele J, Arber DA et al. The 2008 revision of the WHO classification of myeloid neoplasms and acute leukemia: rationale and important changes. Blood114(5), 937–951 (2009).
   PubMed Web of Science ®Google Scholar
• Gotlib J, Cools J. Five years since the discovery of FIP1L1–PDGFRA: what we have learned about the fusion and other molecularly defined eosinophilias. Leukemia22(11), 1999–2010 (2008).
   PubMed Web of Science ®Google Scholar
• Reiter A, Grimwade D, Cross NC. Diagnostic and therapeutic management of eosinophilia-associated chronic myeloproliferative disorders. Haematologica92(9), 1153–1158 (2007).
   PubMed Web of Science ®Google Scholar
• Golub TR, Barker GF, Lovett M, Gilliland DG. Fusion of PDGF receptor β to a novel ets-like gene, tel, in chronic myelomonocytic leukemia with t(5;12) chromosomal translocation. Cell77(2), 307–316 (1994).
   PubMed Web of Science ®Google Scholar
• Lierman E, Cools J. ETV6 and PDGFRB: a license to fuse. Haematologica92(2), 145–147 (2007).
   PubMed Web of Science ®Google Scholar
• Cross NC, Reiter A. Fibroblast growth factor receptor and platelet-derived growth factor receptor abnormalities in eosinophilic myeloproliferative disorders. Acta Haematol.119(4), 199–206 (2008).
   PubMed Web of Science ®Google Scholar
• Lahortiga I, Akin C, Cools J et al. Activity of imatinib in systemic mastocytosis with chronic basophilic leukemia and a PRKG2–PDGFRB fusion. Haematologica93(1), 49–56 (2008).
   PubMed Web of Science ®Google Scholar
• Walz C, Haferlach C, Hanel A et al. Identification of a MYO18A–PDGFRB fusion gene in an eosinophilia-associated atypical myeloproliferative neoplasm with a t(5;17)(q33–34;q11.2). Genes Chromosomes Cancer48(2), 179–183 (2009).
   PubMed Web of Science ®Google Scholar
• Baxter EJ, Hochhaus A, Bolufer P et al. The t(4;22)(q12;q11) in atypical chronic myeloid leukaemia fuses BCR to PDGFRA. Hum. Mol. Genet.11(12), 1391–1397 (2002).
   PubMed Web of Science ®Google Scholar
• Cools J, DeAngelo DJ, Gotlib J et al. A tyrosine kinase created by fusion of the PDGFRA and FIP1L1 genes as a therapeutic target of imatinib in idiopathic hypereosinophilic syndrome. N. Engl. J. Med.348(13), 1201–1214 (2003).
   PubMed Web of Science ®Google Scholar
• Vandenberghe P, Wlodarska I, Michaux L et al. Clinical and molecular features of FIP1L1–PDFGRA (+) chronic eosinophilic leukemias. Leukemia18(4), 734–742 (2004).
   PubMed Web of Science ®Google Scholar
• Kaufmann I, Martin G, Friedlein A, Langen H, Keller W. Human Fip1 is a subunit of CPSF that binds to U-rich RNA elements and stimulates poly(A) polymerase. EMBO J.23(3), 616–626 (2004).
   PubMed Web of Science ®Google Scholar
• Stover EH, Chen J, Folens C et al. Activation of FIP1L1–PDGFRα requires disruption of the juxtamembrane domain of PDGFRα and is FIP1L1-independent. Proc. Natl Acad. Sci. USA103(21), 8078–8083 (2006).
   PubMed Web of Science ®Google Scholar
• Buitenhuis M, Verhagen LP, Cools J, Coffer PJ. Molecular mechanisms underlying FIP1L1–PDGFRA-mediated myeloproliferation. Cancer Res.67(8), 3759–3766 (2007).
   PubMed Web of Science ®Google Scholar
• Krause DS, Van Etten RA. Tyrosine kinases as targets for cancer therapy. N. Engl. J. Med.353(2), 172–187 (2005).
   PubMed Web of Science ®Google Scholar
• Druker BJ, Talpaz M, Resta DJ et al. Efficacy and safety of a specific inhibitor of the BCR–ABL tyrosine kinase in chronic myeloid leukemia. N. Engl. J. Med.344(14), 1031–1037 (2001).
   PubMed Web of Science ®Google Scholar
• Druker BJ, Tamura S, Buchdunger E et al. Effects of a selective inhibitor of the Abl tyrosine kinase on the growth of Bcr–Abl positive cells. Nat. Med.2(5), 561–566 (1996).
   PubMed Web of Science ®Google Scholar
• Apperley JF, Gardembas M, Melo JV et al. Response to imatinib mesylate in patients with chronic myeloproliferative diseases with rearrangements of the platelet-derived growth factor receptor β. N. Engl. J. Med.347(7), 481–487 (2002).
   PubMed Web of Science ®Google Scholar
• Baccarani M, Cilloni D, Rondoni M et al. The efficacy of imatinib mesylate in patients with FIP1L1–PDGFRα-positive hypereosinophilic syndrome. Results of a multicenter prospective study. Haematologica92(9), 1173–1179 (2007).
   PubMed Web of Science ®Google Scholar
• Metzgeroth G, Walz C, Erben P et al. Safety and efficacy of imatinib in chronic eosinophilic leukaemia and hypereosinophilic syndrome: a Phase II study. Br. J. Haematol.143(5), 707–715 (2008).
   PubMed Web of Science ®Google Scholar
• Jovanovic JV, Score J, Waghorn K et al. Low-dose imatinib mesylate leads to rapid induction of major molecular responses and achievement of complete molecular remission in FIP1L1–PDGFRA-positive chronic eosinophilic leukemia. Blood109(11), 4635–4640 (2007).
   PubMed Web of Science ®Google Scholar
• Helbig G, Stella-Holowiecka B, Majewski M et al. A single weekly dose of imatinib is sufficient to induce and maintain remission of chronic eosinophilic leukaemia in FIP1L1–PDGFRA-expressing patients. Br. J. Haematol.141(2), 200–204 (2008).
   PubMed Web of Science ®Google Scholar
• Pardanani A, Reeder T, Porrata LF et al. Imatinib therapy for hypereosinophilic syndrome and other eosinophilic disorders. Blood101(9), 3391–3397 (2003).
   PubMed Web of Science ®Google Scholar
• Pitini V, Arrigo C, Azzarello D et al. Serum concentration of cardiac troponin T in patients with hypereosinophilic syndrome treated with imatinib is predictive of adverse outcomes. Blood102(9), 3456–3457 (2003).
   PubMed Web of Science ®Google Scholar
• Pardanani A, Ketterling RP, Li CY et al. FIP1L1–PDGFRA in eosinophilic disorders: prevalence in routine clinical practice, long-term experience with imatinib therapy, and a critical review of the literature. Leuk. Res.30(8), 965–970 (2006).
   PubMed Web of Science ®Google Scholar
• Griffin JH, Leung J, Bruner RJ, Caligiuri MA, Briesewitz R. Discovery of a fusion kinase in EOL-1 cells and idiopathic hypereosinophilic syndrome. Proc. Natl Acad. Sci. USA100(13), 7830–7835 (2003).
   PubMed Web of Science ®Google Scholar
• von Bubnoff N, Sandherr M, Schlimok G, Andreesen R, Peschel C, Duyster J. Myeloid blast crisis evolving during imatinib treatment of an FIP1L1–PDGFR α-positive chronic myeloproliferative disease with prominent eosinophilia. Leukemia19(2), 286–287 (2005).
   PubMed Web of Science ®Google Scholar
• Lierman E, Michaux L, Beullens E et al. FIP1L1–PDGFRα D842V, a novel panresistant mutant, emerging after treatment of FIP1L1–PDGFRα T674I eosinophilic leukemia with single agent sorafenib. Leukemia23(5), 845–851 (2009).
   PubMed Web of Science ®Google Scholar
• Ohnishi H, Kandabashi K, Maeda Y, Kawamura M, Watanabe T. Chronic eosinophilic leukaemia with FIP1L1–PDGFRA fusion and T6741 mutation that evolved from Langerhans cell histiocytosis with eosinophilia after chemotherapy. Br. J. Haematol.134(5), 547–549 (2006).
   PubMed Web of Science ®Google Scholar
• Gorre ME, Mohammed M, Ellwood K et al. Clinical resistance to STI-571 cancer therapy caused by BCR–ABL gene mutation or amplification. Science293(5531), 876–880 (2001).
   PubMed Web of Science ®Google Scholar
• Azam M, Seeliger MA, Gray NS, Kuriyan J, Daley GQ. Activation of tyrosine kinases by mutation of the gatekeeper threonine. Nat. Struct. Mol. Biol.15(10), 1109–1118 (2008).
   PubMed Web of Science ®Google Scholar
• Score J, Walz C, Jovanovic JV et al. Detection and molecular monitoring of FIP1L1–PDGFRA-positive disease by analysis of patient-specific genomic DNA fusion junctions. Leukemia23(2), 332–339 (2009).
   PubMed Web of Science ®Google Scholar
• Simon D, Salemi S, Yousefi S, Simon HU. Primary resistance to imatinib in Fip1-like 1-platelet-derived growth factor receptor α-positive eosinophilic leukemia. J. Allergy Clin. Immunol.121(4), 1054–1056 (2008).
   PubMedGoogle Scholar
• Lombardo LJ, Lee FY, Chen P et al. Discovery of N-(2-chloro-6-methyl-phenyl)-2-(6-(4-(2-hydroxyethyl)-piperazin-1-yl)-2-methylpyrimidin-4-ylamino)thiazole-5-carboxamide (BMS-354825), a dual Src/Abl kinase inhibitor with potent antitumor activity in preclinical assays. J. Med. Chem.47(27), 6658–6661 (2004).
   PubMed Web of Science ®Google Scholar
• Dewaele B, Wasag B, Cools J et al. Activity of dasatinib, a dual SRC/ABL kinase inhibitor, and IPI-504, a heat shock protein 90 inhibitor, against gastrointestinal stromal tumor-associated PDGFRAD842V mutation. Clin. Cancer Res.14(18), 5749–5758 (2008).
   PubMed Web of Science ®Google Scholar
• Weisberg E, Manley PW, Breitenstein W et al. Characterization of AMN107, a selective inhibitor of native and mutant Bcr–Abl. Cancer Cell7(2), 129–141 (2005).
   PubMed Web of Science ®Google Scholar
• Stover EH, Chen J, Lee BH et al. The small molecule tyrosine kinase inhibitor AMN107 inhibits TEL–PDGFRb and FIP1L1–PDGFRα in vitro and in vivo. Blood106(9), 3206–3213 (2005).
   PubMed Web of Science ®Google Scholar
• von Bubnoff N, Gorantla SP, Thone S, Peschel C, Duyster J. The FIP1L1–PDGFRA T674I mutation can be inhibited by the tyrosine kinase inhibitor AMN107 (nilotinib). Blood107(12), 4970–4971 (2006).
   PubMed Web of Science ®Google Scholar
• Weisberg E, Wright RD, Jiang J et al. Effects of PKC412, nilotinib, and imatinib against GIST-associated PDGFRA mutants with differential imatinib sensitivity. Gastroenterology131(6), 1734–1742 (2006).
   PubMed Web of Science ®Google Scholar
• Wilhelm SM, Carter C, Tang L et al. BAY 43-9006 exhibits broad spectrum oral antitumor activity and targets the RAF/MEK/ERK pathway and receptor tyrosine kinases involved in tumor progression and angiogenesis. Cancer Res.64(19), 7099–7109 (2004).
   PubMed Web of Science ®Google Scholar
• Lierman E, Folens C, Stover EH et al. Sorafenib is a potent inhibitor of FIP1L1–PDGFRα and the imatinib-resistant FIP1L1–PDGFRα T674I mutant. Blood108(4), 1374–1376 (2006).
   PubMed Web of Science ®Google Scholar
• Lierman E, Lahortiga I, Van MH, Mentens N, Marynen P, Cools J. The ability of sorafenib to inhibit oncogenic PDGFRβ and FLT3 mutants and overcome resistance to other small molecule inhibitors. Haematologica92(1), 27–34 (2007).
   PubMed Web of Science ®Google Scholar
• Safaian NN, Czibere A, Bruns I et al. Sorafenib (Nexavar®) induces molecular remission and regression of extramedullary disease in a patient with FLT3–ITD(+) acute myeloid leukemia. Leuk. Res.33(2), 348–350 (2009).
   PubMed Web of Science ®Google Scholar
• Zhang W, Konopleva M, Shi YX et al. Mutant FLT3: a direct target of sorafenib in acute myelogenous leukemia. J. Natl Cancer Inst.100(3), 184–198 (2008).
   PubMed Web of Science ®Google Scholar
• Fabbro D, Ruetz S, Bodis S et al. PKC412 – a protein kinase inhibitor with a broad therapeutic potential. Anticancer Drug Des.15(1), 17–28 (2000).
   PubMedGoogle Scholar
• Cools J, Stover EH, Boulton CL et al. PKC412 overcomes resistance to imatinib in a murine model of FIP1L1–PDGFRα-induced myeloproliferative disease. Cancer Cell3(5), 459–469 (2003).
   PubMed Web of Science ®Google Scholar
• Heidel F, Solem FK, Breitenbuecher F et al. Clinical resistance to the kinase inhibitor PKC412 in acute myeloid leukemia by mutation of Asn-676 in the FLT3 tyrosine kinase domain. Blood107(1), 293–300 (2006).
   PubMed Web of Science ®Google Scholar
• Pan J, Quintas-Cardama A, Manshouri T et al. The novel tyrosine kinase inhibitor EXEL-0862 induces apoptosis in human FIP1L1–PDGFR-α-expressing cells through caspase-3-mediated cleavage of Mcl-1. Leukemia21(7), 1395–1404 (2007).
   PubMed Web of Science ®Google Scholar
• Chen J, DeAngelo DJ, Kutok JL et al. PKC412 inhibits the zinc finger 198-fibroblast growth factor receptor 1 fusion tyrosine kinase and is active in treatment of stem cell myeloproliferative disorder. Proc. Natl Acad. Sci. USA101(40), 14479–14484 (2004).
   PubMed Web of Science ®Google Scholar
• Chase A, Grand FH, Cross NC. Activity of TKI258 against primary cells and cell lines with FGFR1 fusion genes associated with the 8p11 myeloproliferative syndrome. Blood110(10), 3729–3734 (2007).
   PubMed Web of Science ®Google Scholar
• Sarker D, Molife R, Evans TR et al. A Phase I pharmacokinetic and pharmacodynamic study of TKI258, an oral, multitargeted receptor tyrosine kinase inhibitor in patients with advanced solid tumors. Clin. Cancer Res.14(7), 2075–2081 (2008).
   PubMed Web of Science ®Google Scholar
• Rothenberg ME, Hogan SP. The eosinophil. Annu. Rev. Immunol.24, 147–174 (2006).
   PubMed Web of Science ®Google Scholar
• Simon HU, Plotz SG, Dummer R, Blaser K. Abnormal clones of T cells producing interleukin-5 in idiopathic eosinophilia. N. Engl. J. Med.341(15), 1112–1120 (1999).
   PubMed Web of Science ®Google Scholar
• Yamada Y, Rothenberg ME, Lee AW et al. The FIP1L1–PDGFRA fusion gene cooperates with IL5 to induce murine hypereosinophilic syndrome (HES)/chronic eosinophilic leukemia (CEL)-like disease. Blood107(10), 4071–4079 (2006).
   PubMed Web of Science ®Google Scholar
• Rothenberg ME, Klion AD, Roufosse FE et al. Treatment of patients with the hypereosinophilic syndrome with mepolizumab. N. Engl. J. Med.358(12), 1215–1228 (2008).
   PubMed Web of Science ®Google Scholar
• Klion AD, Law MA, Noel P, Kim YJ, Haverty TP, Nutman TB. Safety and efficacy of the monoclonal anti-interleukin-5 antibody SCH55700 in the treatment of patients with hypereosinophilic syndrome. Blood103(8), 2939–2941 (2004).
   PubMed Web of Science ®Google Scholar
• Verstovsek S, Tefferi A, Kantarjian H et al. Alemtuzumab therapy for hypereosinophilic syndrome and chronic eosinophilic leukemia. Clin. Cancer Res.15(1), 368–373 (2009).
   PubMed Web of Science ®Google Scholar
• Pitini V, Teti D, Arrigo C, Righi M. Alemtuzumab therapy for refractory idiopathic hypereosinophilic syndrome with abnormal T cells: a case report. Br. J. Haematol.127(5), 477 (2004).
   PubMedGoogle Scholar
• Sefcick A, Sowter D, DasGupta E, Russell NH, Byrne JL. Alemtuzumab therapy for refractory idiopathic hypereosinophilic syndrome. Br. J. Haematol.124(4), 558–559 (2004).
   PubMed Web of Science ®Google Scholar
• Taverna JA, Lerner A, Goldberg L, Werth S, Demierre MF. Infliximab as a therapy for idiopathic hypereosinophilic syndrome. Arch. Dermatol.143(9), 1110–1112 (2007).
   PubMed Web of Science ®Google Scholar
• Berger SL. Histone modifications in transcriptional regulation. Curr. Opin. Genet. Dev.12(2), 142–148 (2002).
   PubMed Web of Science ®Google Scholar
• Glaser KB. HDAC inhibitors: clinical update and mechanism-based potential. Biochem. Pharmacol.74(5), 659–671 (2007).
   PubMed Web of Science ®Google Scholar
• Cools J, Quentmeier H, Huntly BJ et al. The EOL-1 cell line as an in vitro model for the study of FIP1L1–PDGFRA-positive chronic eosinophilic leukemia. Blood103(7), 2802–2805 (2004).
   PubMed Web of Science ®Google Scholar
• Ishihara K, Kaneko M, Kitamura H et al. Mechanism for the decrease in the FIP1L1–PDGFRα protein level in EoL-1 cells by histone deacetylase inhibitors. Int. Arch. Allergy Immunol.146(Suppl. 1), 7–10 (2008).
   PubMedGoogle Scholar
• Workman P, Burrows F, Neckers L, Rosen N. Drugging the cancer chaperone HSP90: combinatorial therapeutic exploitation of oncogene addiction and tumor stress. Ann. NY Acad. Sci.1113, 202–216 (2007).
   PubMed Web of Science ®Google Scholar
• Peng C, Li D, Li S. Heat shock protein 90: a potential therapeutic target in leukemic progenitor and stem cells harboring mutant BCR–ABL resistant to kinase inhibitors. Cell Cycle6(18), 2227–2231 (2007).
   PubMed Web of Science ®Google Scholar
• Gleich GJ, Leiferman KM, Pardanani A, Tefferi A, Butterfield JH. Treatment of hypereosinophilic syndrome with imatinib mesilate. Lancet359(9317), 1577–1578 (2002).
   PubMed Web of Science ®Google Scholar
• Klion AD, Noel P, Akin C et al. Elevated serum tryptase levels identify a subset of patients with a myeloproliferative variant of idiopathic hypereosinophilic syndrome associated with tissue fibrosis, poor prognosis, and imatinib responsiveness. Blood101(12), 4660–4666 (2003).
   PubMed Web of Science ®Google Scholar
• Pardanani A, Ketterling RP, Brockman SR et al.CHIC2 deletion, a surrogate for FIP1L1–PDGFRA fusion, occurs in systemic mastocytosis associated with eosinophilia and predicts response to imatinib mesylate therapy. Blood102(9), 3093–3096 (2003).
   PubMed Web of Science ®Google Scholar
• Klion AD, Robyn J, Akin C et al. Molecular remission and reversal of myelofibrosis in response to imatinib mesylate treatment in patients with the myeloproliferative variant of hypereosinophilic syndrome. Blood103(2), 473–478 (2004).
   PubMed Web of Science ®Google Scholar
• Pardanani A, Brockman SR, Paternoster SF et al.FIP1L1–PDGFRA fusion: prevalence and clinicopathologic correlates in 89 consecutive patients with moderate to severe eosinophilia. Blood104(10), 3038–3045 (2004).
   PubMed Web of Science ®Google Scholar
• Roche-Lestienne C, Lepers S, Soenen-Cornu V et al. Molecular characterization of the idiopathic hypereosinophilic syndrome (HES) in 35 French patients with normal conventional cytogenetics. Leukemia19(5), 792–798 (2005).
   PubMed Web of Science ®Google Scholar
• La Starza R., Specchia G, Cuneo A et al. The hypereosinophilic syndrome: fluorescence in situ hybridization detects the del(4)(q12)-FIP1L1/PDGFRA but not genomic rearrangements of other tyrosine kinases. Haematologica90(5), 596–601 (2005).
   PubMed Web of Science ®Google Scholar
• David M, Cross NC, Burgstaller S et al. Durable responses to imatinib in patients with PDGFRB fusion gene-positive and BCR–ABL-negative chronic myeloproliferative disorders. Blood109(1), 61–64 (2007).
   PubMed Web of Science ®Google Scholar