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Blood, 21 May 2009, Vol. 113, No. 21, pp. 5083-5089. Prepublished online as a Blood First Edition Paper on January 8, 2009; DOI 10.1182/blood-2008-10-187351. This Article Full Text Full Text (PDF) Supplemental Tables All Versions of this Article: blood-2008-10-187351v1 113/21/5083    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 Rubnitz, J. E. Articles by Pui, C.-H. Search for Related Content PubMed PubMed Citation Articles by Rubnitz, J. E. Articles by Pui, C.-H. Related Collections Free Research Articles Myeloid Neoplasia Lymphoid Neoplasia Clinical Trials and Observations Related Article in Blood Online Social Bookmarking                   What's this?  Previous Article  |  Table of Contents  |  Next Article  CLINICAL TRIALS AND OBSERVATIONS Acute mixed lineage leukemia in children: the experience of St Jude Children's Research Hospital Jeffrey E. Rubnitz1,2,*, Mihaela Onciu3,*, Stanley Pounds4, Sheila Shurtleff3, Xueyuan Cao4, Susana C. Raimondi2,3, Frederick G. Behm3, Dario Campana13, Bassem I. Razzouk1,2, Raul C. Ribeiro1,2, James R. Downing3, and Ching-Hon Pui13 1 Department of Oncology, St Jude Children's Research Hospital, Memphis, TN; 2 Department of Pediatrics, College of Medicine, University of Tennessee Health Science Center, Memphis; and Departments of 3 Pathology and 4 Biostatistics, St Jude Children's Research Hospital, Memphis, TN To characterize the biology and optimal therapy of acute mixed-lineage leukemia in children, we reviewed the pathologic and clinical features, including response to therapy, of 35 patients with mixed-lineage leukemia. The majority of cases (91%) had blasts cells that simultaneously expressed either T-lineage plus myeloid markers (T/myeloid, n = 20) or B-lineage plus myeloid markers (B/myeloid, n = 12). Overall survival rates for the B/myeloid and T/myeloid subgroups were not significantly different from each other or from the rate for acute myeloid leukemia (AML) but were inferior to the outcome in children with acute lymphoblastic leukemia (ALL). Patients who failed to achieve complete remission with AML-directed therapy could often be induced with a regimen of prednisone, vincristine, and L-asparaginase. Analysis of gene-expression patterns identified a subset of biphenotypic leukemias that did not cluster with T-cell ALL, B-progenitor ALL, or AML. We propose that treatment for biphenotypic leukemia begin with one course of AML-type induction therapy, with a provision for a switch to lymphoid-type induction therapy with a glucocorticoid, vincristine, and L-asparaginase if the patient responds poorly. We also suggest that hematopoietic stem cell transplantation is often not required for cure of these patients. CiteULike    Connotea    Del.icio.us    Digg    Reddit    Technorati    What's this? Related Article in Blood Online: Apples and oranges: mixed lineage acute leukemia James Nachman Blood 2009 113: 5036. [Full Text] [PDF] This article has been cited by other articles: J. Nachman Apples and oranges: mixed lineage acute leukemia Blood, May 21, 2009; 113(21): 5036 - 5036. [Full Text] [PDF]

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