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Blood, 15 November 2006, Vol. 108, No. 10, pp. 3484-3493. Prepublished online as a Blood First Edition Paper on July 20, 2006; DOI 10.1182/blood-2005-09-009977. This Article Full Text Full Text (PDF) Supplemental Tables and Figure All Versions of this Article: blood-2005-09-009977v1 108/10/3484    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 CrossRef Citing Articles via Google Scholar Google Scholar Articles by Chapiro, E. Articles by Macintyre, E. A. Search for Related Content PubMed PubMed Citation Articles by Chapiro, E. Articles by Macintyre, E. A. Related Collections Immunobiology Neoplasia Oncogenes and Tumor Suppressors Related Article in Blood Online Social Bookmarking                   What's this?  Previous Article  |  Table of Contents  |  Next Article  NEOPLASIA Expression of T-lineage-affiliated transcripts and TCR rearrangements in acute promyelocytic leukemia: implications for the cellular target of t(15;17) Elise Chapiro, Eric Delabesse, Vahid Asnafi, Corinne Millien, Frederic Davi, Elizabeth Nugent, Kheira Beldjord, Torsten Haferlach, David Grimwade, and Elizabeth A. Macintyre From the Department of Hematology, Université Paris-Descartes, Faculté de Médecine, and Institut National de la Santé et de la Recherche Médicale (INSERM) EMI0210, Assistance Publique-Hôpitaux de Paris (AP-HP) Necker-Enfants Malades, Paris, France; Department of Hematology, AP-HP La Pitié-Salpêtrière, Paris, France; MLL Munich Leukemia Laboratory, Munich, Germany; and King's College London School of Medicine, Division of Genetics and Molecular Medicine, Guy's Hospital, London, United Kingdom. Acute promyelocytic leukemia (APL) is the most differentiated form of acute myeloid leukemia (AML) and has generally been considered to result from transformation of a committed myeloid progenitor. Paradoxically, APL has long been known to express the T-cell lymphoid marker, CD2. We searched for other parameters indicative of T-cell lymphoid specification in a cohort of 36 APL cases, revealing a frequent but asynchronous T-cell lymphoid program most marked in the hypogranular variant (M3v) subtype, with expression of PTCRA, sterile TCRA, and TCRG transcripts and TCRG rearrangement in association with sporadic cytoplasmic expression of CD3 or TdT proteins. Gene-expression profiling identified differentially expressed transcription factors that have been implicated in lymphopoiesis. These data carry implications for the hematopoietic progenitor targeted by the PML-RARA oncoprotein in APL and are suggestive of a different cellular origin for classic hypergranular (M3) and variant forms of the disease. They are also consistent with the existence and subsequent transformation of progenitor populations with lymphoid/myeloid potential. CiteULike    Connotea    Del.icio.us    Digg    Reddit    Technorati    What's this? Related Article in Blood Online: CEBPA dosage in leukemogenesis Thomas Mercher and D. Gary Gilliland Blood 2006 108: 3234. [Full Text] [PDF]

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