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Prepublished online as a Blood First Edition Paper on January 16, 2003; DOI 10.1182/blood-2002-08-2405. This Article Full Text Full Text (PDF) All Versions of this Article: 2002-08-2405v1 101/10/3862    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 Relling, M. V. Articles by Pui, C.-H. Search for Related Content PubMed PubMed Citation Articles by Relling, M. V. Articles by Pui, C.-H. Related Collections Neoplasia Clinical Trials and Observations Social Bookmarking                   What's this?  Previous Article  |  Table of Contents  |  Next Article  Blood, 15 May 2003, Vol. 101, No. 10, pp. 3862-3867 CLINICAL OBSERVATIONS, INTERVENTIONS, AND THERAPEUTIC TRIALS Granulocyte colony-stimulating factor and the risk of secondary myeloid malignancy after etoposide treatment Mary V. Relling, James M. Boyett, Javier G. Blanco, Susana Raimondi, Frederick G. Behm, John T. Sandlund, Gaston K. Rivera, Larry E. Kun, William E. Evans, and Ching-Hon Pui From the Departments of Pharmaceutical Sciences, Biostatistics, Pathology, Hematology-Oncology, and Radiation Oncology, St Jude Children's Research Hospital; and Colleges of Medicine and Pharmacy, University of Tennessee, Memphis, TN. Event-free survival for children with acute lymphoblastic leukemia (ALL) now exceeds 80% in the most effective trials. Failures are due to relapse, toxicity, and second cancers such as therapy-related myeloid leukemia or myelodysplasia (t-ML). Topoisomerase II inhibitors and alkylators can induce t-ML; additional risk factors for t-ML remain poorly defined. The occurrence of t-ML among children who had received granulocyte colony-stimulating factor (G-CSF) following ALL remission induction therapy prompted us to examine this and other putative risk factors for t-ML in 412 children treated on 2 consecutive ALL protocols from 1991 to 1998. All children received etoposide and anthracyclines, 99 of whom received G-CSF; 284 also received cyclophosphamide, 58 of whom also received cranial irradiation. There were 20 children who developed t-ML at a median of 2.3 years (range, 1.0-6.0 years), including 16 cases of acute myeloid leukemia, 3 myelodysplasia, and 1 chronic myeloid leukemia. Stratifying by protocol, the cumulative incidence functions differed (P = .017) according to the use of G-CSF and irradiation: 6-year cumulative incidence (standard error) of t-ML of 12.3% (5.3%) among the 44 children who received irradiation without G-CSF, 11.0% (3.5%) among the 85 children who received G-CSF but no irradiation, 7.1% (7.2%) among the 14 children who received irradiation plus G-CSF, and 2.7% (1.3%) among the 269 children who received neither irradiation nor G-CSF. Even when children receiving irradiation were excluded, the incidence was still higher in those receiving G-CSF (P = .019). In the setting of intensive antileukemic therapy, short-term use of G-CSF may increase the risk of t-ML. © 2003 by The American Society of Hematology.   CiteULike    Connotea    Del.icio.us    Digg    Reddit    Technorati    What's this? This article has been cited by other articles: K. Schmiegelow, I. Al-Modhwahi, M. K. Andersen, M. Behrendtz, E. Forestier, H. Hasle, M. Heyman, J. 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