|
|
Blood, 15 March 2006, Vol. 107, No. 6, pp. 2536-2539.
Prepublished online as a Blood First Edition Paper on November 1, 2005; DOI 10.1182/blood-2005-07-2694.
 Previous Article | Next Article 
Submitted July 11, 2005
Accepted October 1, 2005
Classical Hodgkin lymphoma is characterized by high constitutive expression of activating transcription factor 3 (ATF3) which promotes viability of Hodgkin/Reed-Sternberg cells
Martin Janz*, Michael Hummel, Matthias Truss, Brigitte Wollert-Wulf, Stephan Mathas, Korinna Johrens, Christian Hagemeier, Kurt Bommert, Harald Stein, Bernd Dorken, and Ralf C Bargou
Max Delbruck Center for Molecular Medicine, Berlin, Germany; Hematology, Oncology, and Tumorimmunology, Charite, University Medicine Berlin, Campus Buch and Campus Virchow-Klinikum, Berlin, Germany
Institute of Pathology, Charite, University Medicine Berlin, Campus Benjamin Franklin, Berlin, Germany
Department of Pediatrics, Laboratory for Molecular Biology, Charite, University Medicine Berlin, Berlin, Germany
* Corresponding author; email: mjanz{at}mdc-berlin.de.
Hodgkin/Reed-Sternberg (HRS) cells of classical Hodgkin lymphoma (cHL) display unique characteristics that discriminate cHL from other B cell lymphomas and normal B cells. Therefore, comparative gene expression profiling of Hodgkin and non-Hodgkin B cells could lead to the identification of candidate genes that are critical for the pathogenesis of cHL. We performed microarray analysis of Hodgkin and non-Hodgkin cell lines and identified the transcription factor ATF3, a member of the CREB/ATF family, as a differentially expressed candidate gene. Extensive analysis of a large panel of cell lines, primary tumor samples, and normal tissues revealed that high expression of ATF3 is found in nearly all cases of cHL and is almost exclusively restricted to it. Selective knock-down of ATF3 by RNA interference suppressed proliferation and strongly reduced viability of Hodgkin cells. Thus, overexpression of ATF3 is a molecular hallmark of cHL that contributes to the malignant growth of HRS cells.
 CiteULike  Connotea  Del.icio.us  Digg  Reddit  Technorati What's this?
This article has been cited by other articles:
|
|
|
|
 
S. Mathas, S. Kreher, K. J. Meaburn, K. Johrens, B. Lamprecht, C. Assaf, W. Sterry, M. E. Kadin, M. Daibata, S. Joos, et al.
Gene deregulation and spatial genome reorganization near breakpoints prior to formation of translocations in anaplastic large cell lymphoma
PNAS,
April 7, 2009;
106(14):
5831 - 5836.
[Abstract]
[Full Text]
[PDF]
|
|
|
|
|
|
|
K. Miyazaki, S. Inoue, K. Yamada, M. Watanabe, Q. Liu, T. Watanabe, M. T. Adachi, Y. Tanaka, and S. Kitajima
Differential usage of alternate promoters of the human stress response gene ATF3 in stress response and cancer cells
Nucleic Acids Res.,
April 1, 2009;
37(5):
1438 - 1451.
[Abstract]
[Full Text]
[PDF]
|
|
|
|
|
|
|
K. Weidenfeld-Baranboim, T. Hasin, I. Darlyuk, R. Heinrich, O. Elhanani, J. Pan, K. K. Yokoyama, and A. Aronheim
The ubiquitously expressed bZIP inhibitor, JDP2, suppresses the transcription of its homologue immediate early gene counterpart, ATF3
Nucleic Acids Res.,
April 1, 2009;
37(7):
2194 - 2203.
[Abstract]
[Full Text]
[PDF]
|
|
|
|
|
|
|
B. Hirsch, M. Hummel, S. Bentink, F. Fouladi, R. Spang, R. Zollinger, H. Stein, and H. Durkop
CD30-Induced Signaling Is Absent in Hodgkin's Cells but Present in Anaplastic Large Cell Lymphoma Cells
Am. J. Pathol.,
February 1, 2008;
172(2):
510 - 520.
[Abstract]
[Full Text]
[PDF]
|
|
|
|
|
|
|
S. Bandyopadhyay, Y. Wang, R. Zhan, S. K. Pai, M. Watabe, M. Iiizumi, E. Furuta, S. Mohinta, W. Liu, S. Hirota, et al.
The Tumor Metastasis Suppressor Gene Drg-1 Down-regulates the Expression of Activating Transcription Factor 3 in Prostate Cancer
Cancer Res.,
December 15, 2006;
66(24):
11983 - 11990.
[Abstract]
[Full Text]
[PDF]
|
|
|
|
|
