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Blood, 1 September 2008, Vol. 112, No. 5, pp. 1951-1959. Prepublished online as a Blood First Edition Paper on May 30, 2008; DOI 10.1182/blood-2007-11-124560. This Article Full Text Full Text (PDF) Supplemental Table and Figures All Versions of this Article: blood-2007-11-124560v1 112/5/1951    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 Ruminy, P. Articles by Bastard, C. Search for Related Content PubMed PubMed Citation Articles by Ruminy, P. Articles by Bastard, C. Related Collections Neoplasia Social Bookmarking                   What's this?  Previous Article  |  Table of Contents  |  Next Article  NEOPLASIA Sµ mutation patterns suggest different progression pathways in follicular lymphoma: early direct or late from FL progenitor cells Philippe Ruminy1, Fabrice Jardin1,2, Jean-Michel Picquenot1, Françoise Parmentier1, Nathalie Contentin1,2, Gérard Buchonnet3, Sandrine Tison1, Vinciane Rainville1, Hervé Tilly1,2, and Christian Bastard1 1 Inserm U918, Groupe d'étude des Proliférations Lymphoïdes, Institut Federatif de Recherches Multidisciplinaires sur les Peptides 23 (IFRMP23), and 2 Department of Hematology, Centre Henri Becquerel, Rouen; and 3 Laboratoire d'hématologie, Centre Hospitalier Universitaire (CHU), Rouen, France Follicular lymphoma (FL) is a B-cell malignancy characterized by the t(14;18) translocation. Although sensitive to treatment, the disease remains incurable and the reason why tumor cells invariably evade treatment, leading to clinical relapse, is still unknown. Here, we tracked the clonal history of tumor cells by studying mutations introduced by activation-induced cytidine deaminase on the switch µ region of the der(14)t(14;18) during the early phase of the class-switch recombination (CSR) process. We observed frequent intraclonal variations, suggesting that CSR often remains active after the acquisition of the fully transformed phenotype. However, mutations only rarely accumulated over time, but instead showed complex evolutionary scenarios and 2 different progression pathways. The first pathway was a direct and rapid evolution from the dominant clone. The second was indirect, arising from earlier subclones usually after years of remission. A better understanding of these mechanisms might influence the future choice of treatment strategies. CiteULike    Connotea    Del.icio.us    Digg    Reddit    Technorati    What's this? This article has been cited by other articles: E. Carlotti and J. G. Gribben Stem cell mimicry: key to transformation? Blood, October 8, 2009; 114(15): 3133 - 3134. [Abstract] [Full Text] [PDF] A. J. Gentles, A. A. Alizadeh, S.-I. Lee, J. H. Myklebust, C. M. Shachaf, B. Shahbaba, R. Levy, D. Koller, and S. K. Plevritis A pluripotency signature predicts histologic transformation and influences survival in follicular lymphoma patients Blood, October 8, 2009; 114(15): 3158 - 3166. [Abstract] [Full Text] [PDF] J. Agopian, J.-M. Navarro, A.-C. Gac, Y. Lecluse, M. Briand, P. Grenot, P. Gauduchon, P. Ruminy, P. Lebailly, B. Nadel, et al. Agricultural pesticide exposure and the molecular connection to lymphomagenesis J. Exp. Med., July 6, 2009; 206(7): 1473 - 1483. [Abstract] [Full Text] [PDF] E. Carlotti, D. Wrench, J. Matthews, S. Iqbal, A. Davies, A. Norton, J. Hart, R. Lai, S. Montoto, J. G. Gribben, et al. Transformation of follicular lymphoma to diffuse large B-cell lymphoma may occur by divergent evolution from a common progenitor cell or by direct evolution from the follicular lymphoma clone Blood, April 9, 2009; 113(15): 3553 - 3557. [Abstract] [Full Text] [PDF]

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