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Blood, 1 March 2007, Vol. 109, No. 5, pp. 2156-2164. Prepublished online as a Blood First Edition Paper on October 31, 2006; DOI 10.1182/blood-2006-06-028969. This Article Full Text Full Text (PDF) Supplemental Tables All Versions of this Article: blood-2006-06-028969v1 109/5/2156    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 Lamant, L. Articles by Delsol, G. Search for Related Content PubMed PubMed Citation Articles by Lamant, L. Articles by Delsol, G. Related Collections Oncogenes and Tumor Suppressors Gene Expression Genomics Neoplasia Social Bookmarking                   What's this?  Previous Article  |  Table of Contents  |  Next Article  NEOPLASIA Gene-expression profiling of systemic anaplastic large-cell lymphoma reveals differences based on ALK status and two distinct morphologic ALK+ subtypes Laurence Lamant1,2, Aurélien de Reyniès3, Marie-Michèle Duplantier1,2, David S. Rickman3, Frédérique Sabourdy1,2, Sylvie Giuriato1,2, Laurence Brugières4, Philippe Gaulard5, Estelle Espinos1,2, and Georges Delsol1,2 1 Institut National de la Santé et de la Recherche Médicale (INSERM) U563 Centre de physiopathologie Toulouse Purpan, Toulouse, France; 2 Université Paul-Sabatier, Toulouse, France; 3 Programme Cartes d'Identité des Tumeurs (CIT), Ligue Nationale Contre le Cancer, Paris, France; 4 Department of Pediatric Oncology, Institut Gustave Roussy, Paris, France; 5 Department of Pathology, Inserm U 617, Hôpital Henri Mondor, Créteil, France With the use of microarray gene-expression profiling, we analyzed a homogeneous series of 32 patients with systemic anaplastic large-cell lymphoma (ALCL) and 5 ALCL cell lines. Unsupervised analysis classified ALCL in 2 clusters, corresponding essentially to morphologic subgroups (ie, common type vs small cell and "mixed" variants) and clinical variables. Patients with a morphologic variant of ALCL had advanced-stage disease. This group included a significant number of patients who experienced early relapse. Supervised analysis showed that ALK+ALCL and ALK– ALCL have different gene-expression profiles, further confirming that they are different entities. Among the most significantly differentially expressed genes between ALK+ and ALK– samples, we found BCL6, PTPN12, CEBPB, and SERPINA1 genes to be overexpressed in ALK+ ALCL. This result was confirmed at the protein level for BCL-6, C/EBPß and serpinA1 through tissue microarrays. The molecular signature of ALK– ALCL included overexpression of CCR7, CNTFR, IL22, and IL21 genes but did not provide any obvious clues to the molecular mechanism underlying this tumor subtype. Once confirmed on a larger number of patients, the results of the present study could be used for clinical and therapeutic management of patients at the time of diagnosis. CiteULike    Connotea    Del.icio.us    Digg    Reddit    Technorati    What's this? This article has been cited by other articles: H. M. Amin and R. Lai Pathobiology of ALK+ anaplastic large-cell lymphoma Blood, October 1, 2007; 110(7): 2259 - 2267. [Abstract] [Full Text] [PDF] L. M. Morton, J. J. Turner, J. R. Cerhan, M. S. Linet, P. A. Treseler, C. A. Clarke, A. Jack, W. Cozen, M. Maynadie, J. J. Spinelli, et al. Proposed classification of lymphoid neoplasms for epidemiologic research from the Pathology Working Group of the International Lymphoma Epidemiology Consortium (InterLymph) Blood, July 15, 2007; 110(2): 695 - 708. [Abstract] [Full Text] [PDF]

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