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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 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 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 Tamburini, J. Articles by Bouscary, D. Search for Related Content PubMed PubMed Citation Articles by Tamburini, J. Articles by Bouscary, D. Related Collections Signal Transduction Brief Reports Clinical Trials and Observations Neoplasia Social Bookmarking                   What's this?  Previous Article  |  Table of Contents  |  Next Article  NEOPLASIA Brief Report Constitutive phosphoinositide 3-kinase/Akt activation represents a favorable prognostic factor in de novo acute myelogenous leukemia patients Jerome Tamburini1,4,6, Caroline Elie4,7, Valérie Bardet1,5, Nicolas Chapuis1,4, Sophie Park1,4,6, Philippe Broët8, Pascale Cornillet-Lefebvre9, Bruno Lioure10, Valérie Ugo11, Odile Blanchet12, Norbert Ifrah13, Francis Witz14, François Dreyfus1,4,6, Patrick Mayeux1,4, Catherine Lacombe1,5, and Didier Bouscary1,4,6 1 Institut Cochin, Département d'Hématologie, Paris; 2 Institut National de la Santé et de la Recherche Médicale (INSERM), U567, Paris; 3 Centre National de la Recherche Scientifique (CNRS), Unité Mixte de Recherche (UMR) 8104, Paris; 4 Université Paris Descartes, Faculté de Médecine René Descartes, Unité Mixte de Recherche (UMR)-S 8104, Paris; 5 Laboratoire d'Hématologie, Assistance Publique–Hôpitaux de Paris, Hôpital Cochin, Paris; 6 Service de Médecine Interne–Hématologie, Assistance Publique–Hôpitaux de Paris, Hôpital Cochin, Paris; 7 Département de Biostatistique, Hôpital Cochin, Paris; 8 JE 2492, Faculté de Médecine Paris Sud; 9 Laboratoire d'Hématologie, Centre Hospitalo–Universitaire (CHU) Reims; 10 Département d'Hématologie et d'Oncologie, Hôpitaux Universitaires, Strasbourg; 11 Laboratoire d'Hématologie, CHU Brest; 12 Laboratoire d'Hématologie, CHU Angers; 13 Service des Maladies du Sang, CHU Angers; 14 Service d'Hématologie, Hôpital Brabois, Nancy, France The phosphoinositide 3-kinase (PI3K/Akt) pathway is activated in acute myelogenous leukemia (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 with constitutive PI3K activation (PI3K +). No difference was observed between PI3K + and PI3K – groups concerning age, sex, white blood cell count, lactate dehydrogenase (LDH) level, bone marrow blast cells, French-American-British (FAB) classification, cytogenetics, RAS or nucleophosmin (NPM) mutations. Slightly more FLT3-ITD was detected in the PI3K – group (P = .048). The complete remission rate was similar between the 2 groups. With a median follow-up of 26 months, we observed for PI3K + and PI3K – patients, respectively, 56% and 33% overall survival (P = .001) and 72% and 41% relapse-free survival (P = .001). Constitutive PI3K/Akt activity is a favorable prognosis factor in AML, even after adjustment for FLT3-ITD, and may confer a particular sensitivity to chemotherapy. A better understanding of the 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: P. Ramirez and J. F. DiPersio Therapy Options in Imatinib Failures Oncologist, April 1, 2008; 13(4): 424 - 434. [Abstract] [Full Text] [PDF] J. Tamburini, N. Chapuis, V. Bardet, S. Park, P. Sujobert, L. Willems, N. Ifrah, F. Dreyfus, P. Mayeux, C. Lacombe, et al. Mammalian target of rapamycin (mTOR) inhibition activates phosphatidylinositol 3-kinase/Akt by up-regulating insulin-like growth factor-1 receptor signaling in acute myeloid leukemia: rationale for therapeutic inhibition of both pathways Blood, January 1, 2008; 111(1): 379 - 382. [Abstract] [Full Text] [PDF] B. A. Babbin, A. J. Jesaitis, A. I. Ivanov, D. Kelly, M. Laukoetter, P. Nava, C. A. Parkos, and A. Nusrat Formyl Peptide Receptor-1 Activation Enhances Intestinal Epithelial Cell Restitution through Phosphatidylinositol 3-Kinase-Dependent Activation of Rac1 and Cdc42 J. Immunol., December 15, 2007; 179(12): 8112 - 8121. [Abstract] [Full Text] [PDF]

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