Results of imatinib mesylate therapy in patients with refractory or recurrent acute myeloid leukemia, high‐risk myelodysplastic syndrome, and myeloproliferative disorders

Imatinib mesylate is a selective tyrosine kinase inhibitor of c‐abl, bcr/abl, c‐kit, and platelet‐derived growth factor‐receptor (PDGF‐R). c‐kit is expressed in most patients with acute myeloid leukemia (AML) and myelodysplastic syndrome (MDS) and PDGF has been implicated in the pathogenesis of myeloproliferative disorders (MPD).

[1]  N. Harris,et al.  The World Health Organization (WHO) classification of the myeloid neoplasms. , 2002, Blood.

[2]  Sante Tura,et al.  A phase 2 study of imatinib in patients with relapsed or refractory Philadelphia chromosome-positive acute lymphoid leukemias. , 2002, Blood.

[3]  S. Pileri,et al.  Clinical efficacy and antiangiogenic activity of thalidomide in myelofibrosis with myeloid metaplasia. A pilot study , 2002, Leukemia.

[4]  A. D. Van den Abbeele,et al.  Efficacy and safety of imatinib mesylate in advanced gastrointestinal stromal tumors. , 2002, The New England journal of medicine.

[5]  B. Bain,et al.  Response to imatinib mesylate in patients with chronic myeloproliferative diseases with rearrangements of the platelet-derived growth factor receptor beta. , 2002, The New England journal of medicine.

[6]  M. K. Magnússon,et al.  Activity of STI571 in chronic myelomonocytic leukemia with a platelet-derived growth factor beta receptor fusion oncogene. , 2002, Blood.

[7]  A. Reiter,et al.  Tyrosine kinase fusion genes in chronic myeloproliferative diseases , 2002, Leukemia.

[8]  J. Issa,et al.  Treatment of philadelphia chromosome-positive, accelerated-phase chronic myelogenous leukemia with imatinib mesylate. , 2002, Clinical cancer research : an official journal of the American Association for Cancer Research.

[9]  R. Larson,et al.  Imatinib induces hematologic and cytogenetic responses in patients with chronic myelogenous leukemia in myeloid blast crisis: results of a phase II study. , 2002, Blood.

[10]  D. Steensma,et al.  Phase 2 trial of imatinib mesylate in myelofibrosis with myeloid metaplasia. , 2002, Blood.

[11]  H. Kantarjian,et al.  Imatinib mesylate (STI571) therapy for Philadelphia chromosome-positive chronic myelogenous leukemia in blast phase. , 2002, Blood.

[12]  S. Ansell,et al.  Thalidomide treatment in myelofibrosis with myeloid metaplasia , 2002, British journal of haematology.

[13]  M. Baccarani,et al.  Imatinib induces durable hematologic and cytogenetic responses in patients with accelerated phase chronic myeloid leukemia: results of a phase 2 study. , 2002, Blood.

[14]  Shan Zeng,et al.  The c-KIT mutation causing human mastocytosis is resistant to STI571 and other KIT kinase inhibitors; kinases with enzymatic site mutations show different inhibitor sensitivity profiles than wild-type kinases and those with regulatory-type mutations. , 2002, Blood.

[15]  M. Baccarani,et al.  Hematologic and cytogenetic responses to imatinib mesylate in chronic myelogenous leukemia. , 2002, The New England journal of medicine.

[16]  B. Druker,et al.  STI571: a paradigm of new agents for cancer therapeutics. , 2002, Journal of clinical oncology : official journal of the American Society of Clinical Oncology.

[17]  M. K. Magnússon,et al.  Rabaptin-5 is a novel fusion partner to platelet-derived growth factor beta receptor in chronic myelomonocytic leukemia. , 2001, Blood.

[18]  B. Cheson,et al.  Myelodysplastic syndromes standardized response criteria: further definition. , 2001, Blood.

[19]  G. Barosi,et al.  Safety and efficacy of thalidomide in patients with myelofibrosis with myeloid metaplasia , 2001, British journal of haematology.

[20]  J. Kutok,et al.  H4(D10S170), a gene frequently rearranged in papillary thyroid carcinoma, is fused to the platelet-derived growth factor receptor beta gene in atypical chronic myeloid leukemia with t(5;10)(q33;q22). , 2001, Blood.

[21]  R. Arceci,et al.  Signal transducer and activator of transcription 3 activation is required for Asp(816) mutant c-Kit-mediated cytokine-independent survival and proliferation in human leukemia cells. , 2001, Blood.

[22]  C. Sawyers,et al.  Efficacy and safety of a specific inhibitor of the BCR-ABL tyrosine kinase in chronic myeloid leukemia. , 2001, The New England journal of medicine.

[23]  C. Sawyers,et al.  Activity of a specific inhibitor of the BCR-ABL tyrosine kinase in the blast crisis of chronic myeloid leukemia and acute lymphoblastic leukemia with the Philadelphia chromosome. , 2001, The New England journal of medicine.

[24]  B. Druker,et al.  Inhibition of c-kit receptor tyrosine kinase activity by STI 571, a selective tyrosine kinase inhibitor. , 2000, Blood.

[25]  L. Ashman,et al.  Effects of mutant c-Kit in early myeloid cells. , 1999, Leukemia & lymphoma.

[26]  E. Thiel,et al.  Expression of the C-kit receptor (CD117) is a feature of almost all subtypes of de novo acute myeloblastic leukemia (AML), including cytogenetically good-risk AML, and lacks prognostic significance. , 1999, Leukemia & lymphoma.

[27]  Y. Ma,et al.  Clustering of activating mutations in c-KIT's juxtamembrane coding region in canine mast cell neoplasms. , 1999, The Journal of investigative dermatology.

[28]  J. Reilly 3 Pathogenesis and management of idiopathic myelofibrosis , 1998 .

[29]  A. Órfão,et al.  The reliability and specificity of c-kit for the diagnosis of acute myeloid leukemias and undifferentiated leukemias. The European Group for the Immunological Classification of Leukemias (EGIL). , 1998, Blood.

[30]  Z. Estrov,et al.  Selective inhibition of cell proliferation and BCR-ABL phosphorylation in acute lymphoblastic leukemia cells expressing Mr 190,000 BCR-ABL protein by a tyrosine kinase inhibitor (CGP-57148). , 1998, Clinical cancer research : an official journal of the American Association for Cancer Research.

[31]  R. Berger,et al.  Fusion of Huntingtin Interacting Protein 1 to Platelet-Derived Growth Factor β Receptor (PDGFβR) in Chronic Myelomonocytic Leukemia With t(5;7)(q33;q11.2) , 1998 .

[32]  H. Kawasaki,et al.  Serum soluble c‐kit receptor and expression of c‐kit protein and mRNA in acute myeloid leukemia , 1998, European journal of haematology.

[33]  S. Hirota,et al.  Gain-of-function mutations of c-kit in human gastrointestinal stromal tumors. , 1998, Science.

[34]  J. Reilly Pathogenesis and management of idiopathic myelofibrosis. , 1998, Bailliere's clinical haematology.

[35]  R. Berger,et al.  Fusion of Huntingtin interacting protein 1 to platelet-derived growth factor beta receptor (PDGFbetaR) in chronic myelomonocytic leukemia with t(5;7)(q33;q11.2). , 1998, Blood.

[36]  M. Carroll,et al.  CGP 57148, a tyrosine kinase inhibitor, inhibits the growth of cells expressing BCR-ABL, TEL-ABL, and TEL-PDGFR fusion proteins. , 1997, Blood.

[37]  L. Stempora,et al.  CD117/CD34 expression in leukemic blasts. , 1996, American journal of clinical pathology.

[38]  Jürg Zimmermann,et al.  Effects of a selective inhibitor of the Abl tyrosine kinase on the growth of Bcr–Abl positive cells , 1996, Nature Medicine.

[39]  Todd R. Golub,et al.  Fusion of PDGF receptor β to a novel ets-like gene, tel, in chronic myelomonocytic leukemia with t(5;12) chromosomal translocation , 1994, Cell.

[40]  I. Bernstein,et al.  Blasts from patients with acute myelogenous leukemia express functional receptors for stem cell factor. , 1992, Blood.

[41]  F. Rueda,et al.  Abnormal levels of platelet-specific proteins and mitogenic activity in myeloproliferative disease. , 1991, Acta haematologica.

[42]  C. Bloomfield,et al.  Report of the National Cancer Institute-sponsored workshop on definitions of diagnosis and response in acute myeloid leukemia. , 1990, Journal of clinical oncology : official journal of the American Society of Clinical Oncology.

[43]  R. Carmel,et al.  Platelet-derived growth factor concentrations in platelet-poor plasma and urine from patients with myeloproliferative disorders. , 1989, Blood.