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Blood, 1 August 2007, Vol. 110, No. 3, pp. 1025-1028. Prepublished online as a Blood First Edition Paper on April 10, 2007; DOI 10.1182/blood-2006-12-061283. This Article Full Text (PDF) All Versions of this Article: blood-2006-12-061283v1 110/3/1025    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 Tamburini, J. Articles by Bouscary, D. Search for Related Content PubMed PubMed Citation Articles by Tamburini, J. Articles by Bouscary, D. Social Bookmarking                   What's this?  Previous Article  |  Next Article  Submitted December 4, 2006 Accepted March 26, 2007 Constitutive Phosphoinositide-3kinase/AKT activation represents a favourable prognostic factor in de novo AML patients Jerome Tamburini, Caroline Elie, Valerie Bardet, Nicolas Chapuis, Sophie Park, Philippe Broet, Pascale Cornillet-Lefebvre, Bruno Lioure, Valerie Ugo, Odile Blanchet, Norbert Ifrah, Francis Witz, Francois Dreyfus, Patrick Mayeux, Catherine Lacombe, and Didier Bouscary* Departement d'Hematologie, Institut Cochin, Paris, France Departement de Biostatistique, Hopital Cochin, Paris, France INSERM, U567, Paris, France CRNS, UMR8104, Paris, France Faculte de Medecine Rene Descartes, Universite Paris Descartes, UMR-S 8140, Paris, France Department de statistique, Faculte de Medecine Paris Sud, Paris, France Laboratoire d'hematologie, CHU Reims, Reims, France Departement d'hematologie et d'Oncologie, Hopitaux Universitaires, Strasbourg, France Laboratoire d'hematologie, CHU Brest, Brest, France Laboratoire d'hematologie, CHU Angers, Angers, France Service des Maladies du Sang, CHU Angers, Angers, France Service d'Hematologie, Hopital Brabois, Nancy, France Service de Medecine Interne - UF d'Hematologie, Assistance Publique - Hopital Cochin, Paris, France Laboratoire d'hematologie, Assistance Publique - Hopitaux de Paris, Hopital Cochin, Paris, France * Corresponding author; email: bouscary{at}cochin.inserm.fr. The PI3K/AKT pathway is activated in AML and is promising for targeted inhibition. Ninety-two patients with primary AML were analyzed for PI3K/AKT constitutive activation. Fifty percent of the patients presented constitutive PI3K activation (PI3K+). No difference was observed between PI3K+ and PI3K- groups concerning age, gender, WBC count, LDH level, bone marrow blast cells, FAB, cytogenetics, RAS or NPM mutations. Slightly more FLT3-ITD was detected in the PI3K- group (p=0.048). The complete remission rate was similar between the two groups. With a median follow-up of 26 months, we observed for PI3K+ and PI3K- patients respectively: 56% and 33% of overall survival (p=0.001); 72% and 41%, of relapse free survival (p=0.001). Constitutive PI3K/AKT activity is a favourable prognosis factor in AML, even after adjustment for FLT3-ITD, and may confer a particular sensitivity to chemotherapy. A better understanding of downstream effectors of the PI3K/AKT pathway is needed before targeting in AML. CiteULike    Connotea    Del.icio.us    Digg    Reddit    Technorati    What's this? This article has been cited by other articles: J. A. Powell, D. Thomas, E. F. Barry, C. H. Kok, B. J. McClure, A. Tsykin, L. B. To, A. Brown, I. D. Lewis, K. Herbert, et al. Expression profiling of a hemopoietic cell survival transcriptome implicates osteopontin as a functional prognostic factor in AML Blood, November 26, 2009; 114(23): 4859 - 4870. [Abstract] [Full Text] [PDF] J. Tamburini, A. S. Green, V. Bardet, N. Chapuis, S. Park, L. Willems, M. Uzunov, N. Ifrah, F. Dreyfus, C. Lacombe, et al. Protein synthesis is resistant to rapamycin and constitutes a promising therapeutic target in acute myeloid leukemia Blood, August 20, 2009; 114(8): 1618 - 1627. [Abstract] [Full Text] [PDF] T. R. Hercus, D. Thomas, M. A. Guthridge, P. G. Ekert, J. King-Scott, M. W. Parker, and A. F. 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