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Blood, 1 April 2008, Vol. 111, No. 7, pp. 3867-3871. Prepublished online as a Blood First Edition Paper on January 30, 2008; DOI 10.1182/blood-2007-08-108654. This Article Full Text (PDF) All Versions of this Article: blood-2007-08-108654v1 111/7/3867    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 Zhao, W.-L. Articles by Chen, S.-J. Search for Related Content PubMed PubMed Citation Articles by Zhao, W.-L. Articles by Chen, S.-J. Social Bookmarking                   What's this?  Previous Article  |  Next Article  Submitted August 22, 2007 Accepted January 19, 2008 PRDM1/BLIMP-1 is involved in chemoresistance of T-cell lymphoma and downregulated by the proteasome inhibitor Wei-Li Zhao, Yan-Yan Liu, Qun-Ling Zhang, Li Wang, Christophe Leboeuf, Yi-Wen Zhang, Jie Ma, Jose-Francisco Garcia, Yong-Ping Song, Jun-Min Li, Zhi-Xiang Shen, Zhu Chen, Anne Janin, and Sai-Juan Chen* State Key Laboratory of Medical Genomics, Shanghai Institute of Hematology, Rui Jin Hospital, Shanghai Jiao Tong University School of Medicine, Shanghai, China Henan Institute of Hematology, Henan Tumor Hospital, Zhengzhou, China Laboratory of Molecular Pathology, Pole de Recherches Franco-Chinois en Science du Vivant et Genomique, Shanghai, China Inserm, U728, Institut d'Hematologie, Paris, France The Monoclonal Antibodies Unit, Biotechnology Program, Spanish National Cancer Center (CNIO), Madrid, Spain Universite Paris 7-Denis Diderot, Paris, France * Corresponding author; email: sjchen{at}stn.sh.cn. The positive regulatory domain I (PRDM1) is a master regulator of terminal B-cell differentiation. However, PRDM1 is not B-cell specific. To determine its role in T-cell lymphoma, PRDM1 expression was investigated in 60 patients. PRDM1 and PRDM1 transcripts were detected in laser-microdissected T-lymphoma cells respectively in 27 and 14 patients, mostly in cases with IRF4 expression. PRDM1 was associated with increased c-MYC expression. PRDM1-positive patients displayed advanced Ann Arbor stage, high-risk International Prognostic Index and were linked to short survival times. In vitro, PRDM1 was related to resistance to chemotherapeutic agents and could be downregulated by the proteasome inhibitor bortezomib. Kinetic studies showed that bortezomib downregulation of PRDM1 preceded decreased IRF4 and c-MYC expression. An earlier retaining of cytoplasmic IB in bortezomib-treated cells was revealed, concomitant with blockade of NF-B nuclear translocation. These results demonstrate the involvement of PRDM1 in T-cell lymphoma, with possible therapeutic interference by the proteasome inhibitor. CiteULike    Connotea    Del.icio.us    Digg    Reddit    Technorati    What's this? This article has been cited by other articles: J. Lee, C. Suh, H. J. Kang, B.-Y. Ryoo, J. Huh, Y. H. Ko, H.-S. Eom, K. Kim, K. Park, and W. S. Kim Phase I study of proteasome inhibitor bortezomib plus CHOP in patients with advanced, aggressive T-cell or NK/T-cell lymphoma Ann. Onc., December 1, 2008; 19(12): 2079 - 2083. [Abstract] [Full Text] [PDF]

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