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 Blood, 1 February 2008, Vol. 111, No. 3, pp. 1515-1523.
Prepublished online as a Blood First Edition Paper on October 19, 2007; DOI 10.1182/blood-2007-04-087734.

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NEOPLASIA

Constitutively activated STAT3 promotes cell proliferation and survival in the activated B-cell subtype of diffuse large B-cell lymphomas

B. Belinda Ding1, J. Jessica Yu1, Raymond Y.-L. Yu1, Lourdes M. Mendez1, Rita Shaknovich2, Yonghui Zhang3, Giorgio Cattoretti3, and B. Hilda Ye1

1 Departments of Cell Biology and 2 Pathology, Albert Einstein College of Medicine, Bronx, NY; and 3 Department of Pathology and Institute for Cancer Genetics, Columbia University Medical Center, New York, NY

Diffuse large B-cell lymphoma (DLBCL) consists of at least 2 phenotypic subtypes; that is, the germinal center B-cell–like (GCB-DLBCL) and the activated B-cell–like (ABC-DLBCL) groups. It has been shown that GCB-DLBCL responds favorably to chemotherapy and expresses high levels of BCL6, a transcription repressor known to play a causative role in lymphomagenesis. In comparison, ABC-DLBCL has lower levels of BCL6, constitutively activated nuclear factor-{kappa}B, and tends to be refractory to chemotherapy. Here, we report that the STAT3 gene is a transcriptional target of BCL6. As a result, high-level STAT3 expression and activation are preferentially detected in ABC-DLBCL and BCL6-negative normal germinal center B cells. Most importantly, inactivating STAT3 by either AG490 or small interference RNA in ABC-DLBCL cells inhibits cell proliferation and triggers apoptosis. These phenotypes are accompanied by decreased expression of several known STAT3 target genes, including c-Myc, JunB, and Mcl-1, and increased expression of the cell- cycle inhibitor p27. In addition to identifying STAT3 as a novel BCL6 target gene, our results define a second oncogenic pathway, STAT3 activation, which operates in ABC-DLBCL, suggesting that STAT3 may be a new therapeutic target in these aggressive lymphomas.


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