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Prepublished online as a Blood First Edition Paper on June 7, 2002; DOI 10.1182/blood-2002-01-0165. This Article 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 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 Social Bookmarking                   What's this? Submitted January 29, 2002 Accepted May 29, 2002 Activity of STI571 in chronic myelomonocytic leukemia with a platelet-derived growth factor ß-receptor fusion oncogene Magnus K Magnusson*, Kristin E Meade, Ryotaro Nakamura, John Barrett, and Cynthia E Dunbar Hematology Branch, National Heart, Lung,and Blood Institute, National Institutes of Health, Bethesda, MD, USA * Corresponding author; email: magnussm{at}nhlbi.nih.gov. Platelet-derived growth factor ß receptor (PDGFßR) fusion genes have been shown to be critical transforming oncogenes in a subset of patients with chronic myelomonocytic leukemia. The sensitivity of dysregulated tyrosine kinase oncogenes to the tyrosine kinase inhibitor STI571 makes it a potentially attractive treatment option in this subset of patients. We have recently cloned a novel member of the PDGFßR fusion oncogene family, rabaptin-5-PDGFßR. A patient with CMML carrying the rabaptin-5-PDGFßR fusion gene underwent allogeneic stem cell tranplantation (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 post-transplantation, 15 months post 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 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 PDGFßR fusion oncogenes. CiteULike    Connotea    Del.icio.us    Digg    Reddit    Technorati    What's this? This article has been cited by other articles: B. J. 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