The efficacy of imatinib mesylate in patients with FIP1L1-PDGFRα-positive hypereosinophilic syndrome. Results of a multicenter prospective study
暂无分享,去创建一个
M. Baccarani | M. Rondoni | S. Paolini | G. Rosti | G. Martinelli | I. Iacobucci | D. Cilloni | F. Messa | G. Saglio | E. Ottaviani | E. Giugliano | S. Soverini | F. Pane | F. Buccisano | N. Testoni | M. Tiribelli | E. Gottardi | A. de Vivo | S. Merante | F. Rancati | C. Astolfi | Francesca Rancati
[1] M. Baccarani,et al. FIP1L1-PDGFRalpha Positive Hypereosinophilic Syndrome (HES). The Response to Imatinib (IM) Is Durable. A Report of 21 Patients with a Follow-Up of 12 to 67 Months. , 2006 .
[2] A. Tefferi,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. , 2006, Leukemia research.
[3] Brian Walters,et al. Cardiotoxicity of the cancer therapeutic agent imatinib mesylate , 2006, Nature Medicine.
[4] A. Reiter,et al. The results of imatinib therapy for patients with primary eosinophilic disorders , 2006, European journal of haematology.
[5] Glenn Heller,et al. Altered bone and mineral metabolism in patients receiving imatinib mesylate. , 2006, The New England journal of medicine.
[6] M. Baccarani,et al. Imatinib Mesylate Can Induce Molecular Complete Remission in Idiopathic Hypereosinophilic Syndrome (HES). A Phase II Multicentric Italian Clinical Trial. , 2005 .
[7] B. Quesnel,et al. Molecular characterization of the idiopathic hypereosinophilic syndrome (HES) in 35 French patients with normal conventional cytogenetics , 2005, Leukemia.
[8] A. Tefferi,et al. FIP1L1-PDGFRA fusion: prevalence and clinicopathologic correlates in 89 consecutive patients with moderate to severe eosinophilia. , 2004, Blood.
[9] G. Webersinke,et al. p53-Binding Protein 1 Is Fused to the Platelet-Derived Growth Factor Receptor β in a Patient with a t(5;15)(q33;q22) and an Imatinib-Responsive Eosinophilic Myeloproliferative Disorder , 2004, Cancer Research.
[10] Ayalew Tefferi,et al. Imatinib targets other than bcr/abl and their clinical relevance in myeloid disorders. , 2004, Blood.
[11] S. Gottschalk,et al. Imatinib (STI571)-Mediated Changes in Glucose Metabolism in Human Leukemia BCR-ABL-Positive Cells , 2004, Clinical Cancer Research.
[12] A. la Sala,et al. Heterogeneity of Response to Imatinib-Mesylate (Glivec) in Patients with Hypereosinophilic Syndrome: Implications for Dosing and Pathogenesis , 2004, Leukemia & lymphoma.
[13] D. Gary Gilliland,et al. The FIP1L1-PDGFRα fusion tyrosine kinase in hypereosinophilic syndrome and chronic eosinophilic leukemia: implications for diagnosis, classification, and management , 2004 .
[14] D. Gilliland,et al. Clinical and molecular features of FIP1L1-PDFGRA (+) chronic eosinophilic leukemias , 2004, Leukemia.
[15] M. Baccarani,et al. Molecular response to imatinib in late chronic-phase chronic myeloid leukemia. , 2004, Blood.
[16] C. Preudhomme,et al. Sustained molecular response with imatinib in a leukemic form of idiopathic hypereosinophilic syndrome in relapse after allograft , 2004, Leukemia.
[17] D. Metcalfe,et al. Molecular remission and reversal of myelofibrosis in response to imatinib mesylate treatment in patients with the myeloproliferative variant of hypereosinophilic syndrome. , 2004, Blood.
[18] D. Gilliland,et al. CHIC2 deletion, a surrogate for FIP1L1-PDGFRA fusion, occurs in systemic mastocytosis associated with eosinophilia and predicts response to imatinib mesylate therapy. , 2003, Blood.
[19] D. Gilliland,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. , 2003, Blood.
[20] H. Kantarjian,et al. Efficacy of imatinib mesylate in the treatment of idiopathic hypereosinophilic syndrome. , 2003, Blood.
[21] Peter Marynen,et al. A tyrosine kinase created by fusion of the PDGFRA and FIP1L1 genes as a therapeutic target of imatinib in idiopathic hypereosinophilic syndrome. , 2003, The New England journal of medicine.
[22] Francisco Cervantes,et al. Imatinib compared with interferon and low-dose cytarabine for newly diagnosed chronic-phase chronic myeloid leukemia. , 2003, The New England journal of medicine.
[23] S. Kulkarni,et al. Novel translocations that disrupt the platelet‐derived growth factor receptor β (PDGFRB) gene in BCR–ABL‐negative chronic myeloproliferative disorders , 2003, British journal of haematology.
[24] H. Kantarjian,et al. Response of idiopathic hypereosinophilic syndrome to treatment with imatinib mesylate. , 2002, Leukemia research.
[25] 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.
[26] A. Reiter,et al. Tyrosine kinase fusion genes in chronic myeloproliferative diseases , 2002, Leukemia.
[27] Nicholas C P Cross,et al. The t(4;22)(q12;q11) in atypical chronic myeloid leukaemia fuses BCR to PDGFRA. , 2002, Human molecular genetics.
[28] A. Tefferi,et al. Treatment of hypereosinophilic syndrome with imatinib mesilate , 2002, The Lancet.
[29] E. Macintyre,et al. Standardized RT-PCR analysis of fusion gene transcripts from chromosome aberrations in acute leukemia for detection of minimal residual disease , 1999, Leukemia.
[30] 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.
[31] J. Melo,et al. Durable responses to imatinib in patients with PDGFRB fusion gene-positive and BCR-ABL-negative chronic myeloproliferative disorders. , 2007, Blood.
[32] R. Piazza,et al. In reply to 'Cardiotoxicity of the cancer therapeutic agent imatinib mesylate' , 2007, Nature Medicine.
[33] H. Kantarjian,et al. In reply to 'Cardiotoxicity of the cancer therapeutic agent imatinib mesylate' , 2007, Nature Medicine.
[34] U. Martens,et al. Imatinib mesylate as a novel treatment option for hypereosinophilic syndrome: two case reports and a comprehensive review of the literature , 2005, Annals of Hematology.
[35] P. Marynen,et al. The hypereosinophilic syndrome: fluorescence in situ hybridization detects the del(4)(q12)-FIP1L1/PDGFRA but not genomic rearrangements of other tyrosine kinases. , 2005, Haematologica.
[36] B. Bain. The idiopathic hypereosinophilic syndrome and eosinophilic leukemias. , 2004, Haematologica.
[37] M. Baccarani,et al. Imatinib mesylate can induce complete molecular remission in FIP1L1-PDGFR-a positive idiopathic hypereosinophilic syndrome. , 2004, Haematologica.
[38] P. Zalloua,et al. Effective treatment of hypereosinophilic syndrome with imatinib mesylate. , 2003, The hematology journal : the official journal of the European Haematology Association.
[39] E. Baxter,et al. Imatinib therapy for hypereosinophilic syndrome and other eosinophilic , 2003 .
[40] T. Meyer,et al. Inhibition of the Abl protein-tyrosine kinase in vitro and in vivo by a 2-phenylaminopyrimidine derivative. , 1996, Cancer research.
[41] A. Hagenbeek,et al. Minimal Residual Disease in Acute Leukemia , 1984, Developments in Oncology.
[42] Iscn. International System for Human Cytogenetic Nomenclature , 1978 .