SEARCH:   Advanced

Prepublished online as a Blood First Edition Paper on June 7, 2002; DOI 10.1182/blood-2002-01-0165. This Article Full Text Full Text (PDF) All Versions of this Article: 2002-01-0165v1 100/3/1088    most recent Alert me when this article is cited Alert me if a correction is posted Citation Map Services Email this article to a friend Similar articles in this journal Similar articles in PubMed Alert me to new issues of the journal Download to citation manager Rights and Permissions Citing Articles Citing Articles via HighWire Citing Articles via CrossRef Citing Articles via Google Scholar Google Scholar Articles by Magnusson, M. K. Articles by Dunbar, C. E. Search for Related Content PubMed PubMed Citation Articles by Magnusson, M. K. Articles by Dunbar, C. E. Related Collections Neoplasia Oncogenes and Tumor Suppressors Brief Reports Clinical Trials and Observations Social Bookmarking                   What's this?  Previous Article  |  Table of Contents  |  Next Article  Blood, 1 August 2002, Vol. 100, No. 3, pp. 1088-1091 BRIEF REPORT Activity of STI571 in chronic myelomonocytic leukemia with a platelet-derived growth factor  receptor fusion oncogene Magnus K. Magnusson, Kristin E. Meade, Ryotaro Nakamura, John Barrett, and Cynthia E. Dunbar From the Hematology Branch, National Heart, Lung and Blood Institute, National Institutes of Health, Bethesda, MD. Platelet-derived growth factor  receptor (PDGFR) fusion genes have been shown to be critical transforming oncogenes in a subset of patients with chronic myelomonocytic leukemia (CMML). The sensitivity of dysregulated tyrosine kinase oncogenes to the tyrosine kinase inhibitor STI571 (imatinib mesylate) makes it a potentially attractive treatment option in this subset of patients. We have recently cloned a novel member of the PDGFR fusion oncogene family, rabaptin-5-PDGFR. A patient with CMML carrying the rabaptin-5-PDGFR fusion gene underwent allogeneic stem cell transplantation (SCT) and was monitored closely with a sensitive reverse transcriptase-polymerase chain assay to detect the novel fusion gene transcript. After achieving a molecular remission at 5 months after transplantation, 15 months after SCT the patient showed persistent and progressive evidence of molecular relapse. After demonstrating in vitro that cells transformed with this specific fusion oncogene are efficiently killed by STI571, the patient was started on STI571. The patient responded rapidly and entered molecular remission after 6 weeks of therapy, and he continues to be in remission 6 months later. These results suggest that STI571 may be an effective targeted therapy in patients with CMML related to PDGFR fusion oncogenes. CiteULike    Connotea    Del.icio.us    Digg    Reddit    Technorati    What's this? This article has been cited by other articles: B. J. Druker Translation of the Philadelphia chromosome into therapy for CML Blood, December 15, 2008; 112(13): 4808 - 4817. [Abstract] [Full Text] [PDF] R. Weichsel, C. Dix, L. Wooldridge, M. Clement, A. Fenton-May, A. K. Sewell, J. Zezula, E. Greiner, E. Gostick, D. A. Price, et al. Profound Inhibition of Antigen-Specific T-Cell Effector Functions by Dasatinib Clin. Cancer Res., April 15, 2008; 14(8): 2484 - 2491. [Abstract] [Full Text] [PDF] J. Gibbons, M. J. Egorin, R. K. Ramanathan, P. Fu, D. L. Mulkerin, S. Shibata, C. H.M. Takimoto, S. Mani, P. A. LoRusso, J. L. Grem, et al. Phase I and Pharmacokinetic Study of Imatinib Mesylate in Patients With Advanced Malignancies and Varying Degrees of Renal Dysfunction: A Study by the National Cancer Institute Organ Dysfunction Working Group J. Clin. Oncol., February 1, 2008; 26(4): 570 - 576. [Abstract] [Full Text] [PDF] M. David, N. C. P. Cross, S. Burgstaller, A. Chase, C. Curtis, R. Dang, M. Gardembas, J. M. Goldman, F. Grand, G. Hughes, et al. Durable responses to imatinib in patients with PDGFRB fusion gene-positive and BCR-ABL-negative chronic myeloproliferative disorders Blood, January 1, 2007; 109(1): 61 - 64. [Abstract] [Full Text] [PDF] R. H. Alvarez, H. M. Kantarjian, and J. E. Cortes Biology of Platelet-Derived Growth Factor and Its Involvement in Disease Mayo Clin. Proc., September 1, 2006; 81(9): 1241 - 1257. [Abstract] [Full Text] [PDF] A. Tefferi, M. A. Elliott, and A. Pardanani Atypical Myeloproliferative Disorders: Diagnosis and Management Mayo Clin. Proc., April 1, 2006; 81(4): 553 - 563. [Abstract] [Full Text] [PDF] D. P. Steensma and J. M. Bennett The Myelodysplastic Syndromes: Diagnosis and Treatment Mayo Clin. Proc., January 1, 2006; 81(1): 104 - 130. [Abstract] [Full Text] [PDF] D. S. Krause and R. A. Van Etten Tyrosine Kinases as Targets for Cancer Therapy N. Engl. J. Med., July 14, 2005; 353(2): 172 - 187. [Full Text] [PDF] R. Seggewiss, K. Lore, E. Greiner, M. K. Magnusson, D. A. Price, D. C. Douek, C. E. Dunbar, and A. Wiestner Imatinib inhibits T-cell receptor-mediated T-cell proliferation and activation in a dose-dependent manner Blood, March 15, 2005; 105(6): 2473 - 2479. [Abstract] [Full Text] [PDF] W. Fiedler, H. Serve, H. Dohner, M. Schwittay, O. G. Ottmann, A.-M. O'Farrell, C. L. Bello, R. Allred, W. C. Manning, J. M. Cherrington, et al. A phase 1 study of SU11248 in the treatment of patients with refractory or resistant acute myeloid leukemia (AML) or not amenable to conventional therapy for the disease Blood, February 1, 2005; 105(3): 986 - 993. [Abstract] [Full Text] [PDF] M. Wadleigh, D. J. DeAngelo, J. D. Griffin, and R. M. Stone After chronic myelogenous leukemia: tyrosine kinase inhibitors in other hematologic malignancies Blood, January 1, 2005; 105(1): 22 - 30. [Abstract] [Full Text] [PDF] A. Pardanani and A. Tefferi Imatinib targets other than bcr/abl and their clinical relevance in myeloid disorders Blood, October 1, 2004; 104(7): 1931 - 1939. [Abstract] [Full Text] [PDF] J. L. Vizmanos, F. J. Novo, J. P. Roman, E. J. Baxter, I. Lahortiga, M. J. Larrayoz, M. D. Odero, P. Giraldo, M. J. Calasanz, and N. C. P. Cross NIN, a Gene Encoding a CEP110-Like Centrosomal Protein, Is Fused to PDGFRB in a Patient with a t(5;14)(q33;q24) and an Imatinib-Responsive Myeloproliferative Disorder1 Cancer Res., April 15, 2004; 64(8): 2673 - 2676. [Abstract] [Full Text] [PDF] B. J. Druker Imatinib As a Paradigm of Targeted Therapies J. Clin. Oncol., December 1, 2003; 21(90230): 239s - 245. [Full Text] [PDF] K. Wilkinson, E. R. P. Velloso, L. F. Lopes, C. Lee, J. C. Aster, M. A. Shipp, and R. C. T. Aguiar Cloning of the t(1;5)(q23;q33) in a myeloproliferative disorder associated with eosinophilia: involvement of PDGFRB and response to imatinib Blood, December 1, 2003; 102(12): 4187 - 4190. [Abstract] [Full Text] [PDF] J. L. Garcia, J. Font de Mora, J. M. Hernandez, J. A. Queizan, N. C. Gutierrez, J. M. Hernandez, and J. F. S. Miguel Imatinib mesylate elicits positive clinical response in atypical chronic myeloid leukemia involving the platelet-derived growth factor receptor beta Blood, October 1, 2003; 102(7): 2699 - 2700. [Full Text] [PDF] F. Cruz III, B. P. Rubin, D. Wilson, A. Town, A. Schroeder, A. Haley, T. Bainbridge, M. C. Heinrich, and C. L. Corless Absence of BRAF and NRAS Mutations in Uveal Melanoma Cancer Res., September 15, 2003; 63(18): 5761 - 5766. [Abstract] [Full Text] [PDF] F. Ravandi, M. Talpaz, and Z. Estrov Modulation of Cellular Signaling Pathways: Prospects for Targeted Therapy in Hematological Malignancies Clin. Cancer Res., February 1, 2003; 9(2): 535 - 550. [Abstract] [Full Text] [PDF] J. M.L. Ebos, J. Tran, Z. Master, D. Dumont, J. V. Melo, E. Buchdunger, and R. S. Kerbel Imatinib Mesylate (STI-571) Reduces Bcr-Abl-Mediated Vascular Endothelial Growth Factor Secretion in Chronic Myelogenous Leukemia Mol. Cancer Res., December 1, 2002; 1(2): 89 - 95. [Abstract] [Full Text] [PDF] C. L. Sawyers Imatinib GIST Keeps Finding New Indications: Successful Treatment of Dermatofibrosarcoma Protuberans by Targeted Inhibition of the Platelet-Derived Growth Factor Receptor J. Clin. Oncol., September 1, 2002; 20(17): 3568 - 3569. [Full Text] [PDF]

	Copyright © 2002 by American Society of Hematology         Online ISSN: 1528-0020