|
|
 Previous Article | Table of Contents | Next Article 
Expression of the Epstein-Barr Virus Protein LMP1 Mediates Tumor
Regression In Vivo
Barry W. Cherney,
Cecilia Sgadari,
Chiharu Kanegane,
Frederick Wang, and
Giovanna Tosato
4From the Division of Hematologic Products, Center for Biologics
Evaluation and Research, Food and Drug Administration, Bethesda, MD;
and the Infectious Disease Division, Brigham and Women's Hospital,
Harvard Medical School, Boston, MA.
By stimulating the expression of murine IP-10 and Mig, CXC
chemokines that inhibit neovascularization and cause damage to established tumor vasculature, human B cells immortalized with Epstein-Barr virus (EBV) can promote an effective antitumor response in
athymic mice. In the present study, we examined the potential role of
EBV in the induction of this antitumor response. Using a panel of
EBV+ and EBV Burkitt lymphoma (BL) cell
lines, a significant correlation was detected between the expression of
the EBV latency gene LMP1 and the occurrence of spontaneous tumor
regression in athymic mice. Inoculation of LMP1+ and
LMP1 BL cells in the same subcutaneous site resulted in
tumors that completely regressed in a manner indistinguishable from
that induced by EBV-immortalized B cells. EBV-converted BL30 and BL41
sublines infected with B95-8 virus expressed LMP1, generated tumors
that frequently regressed spontaneously, and promoted an effective antitumor response against progressively growing tumors. In contrast, the EBV BL30 and BL41 cell lines and the EBV-converted
BL30 and BL41 infected with P3HR-1 virus did not express LMP1 protein,
and generated progressively growing tumors in nude mice. When
transfected with the LMP1 gene, BL41 cells produced tumors that
regressed spontaneously in most cases, and could induce the regression
of tumors derived from BL41 cells transfected with vector alone. Tumors
induced by LMP1-expressing cells expressed murine IP-10 and Mig and
displayed histological evidence of extensive tumor tissue necrosis and
vascular damage. We conclude that the EBV protein LMP1 is likely
responsible for the antitumor response elicited by EBV-immortalized
cells in athymic mice.
Blood, Vol. 91 No. 7 (April 1), 1998:
pp. 2491-2500
© 1998 by The American Society of Hematology.
 CiteULike  Connotea  Del.icio.us  Digg  Reddit  Technorati What's this?
This article has been cited by other articles:
|
|
|
|
 
J.-H. Lin, C.-H. Tsai, J.-S. Chu, J.-Y. Chen, K. Takada, and J.-Y. Shew
Dysregulation of HER2/HER3 Signaling Axis in Epstein-Barr Virus-Infected Breast Carcinoma Cells
J. Virol.,
June 1, 2007;
81(11):
5705 - 5713.
[Abstract]
[Full Text]
[PDF]
|
|
|
|
|
|
|
S. Pai, B. J. O'Sullivan, L. Cooper, R. Thomas, and R. Khanna
RelB Nuclear Translocation Mediated by C-Terminal Activator Regions of Epstein-Barr Virus-Encoded Latent Membrane Protein 1 and Its Effect on Antigen-Presenting Function in B Cells
J. Virol.,
February 15, 2002;
76(4):
1914 - 1921.
[Abstract]
[Full Text]
[PDF]
|
|
|
|
|
|
|
L. Yao, J. Setsuda, C. Sgadari, B. Cherney, and G. Tosato
Interleukin-18 expression induced by Epstein-Barr virus-infected cells
J. Leukoc. Biol.,
May 1, 2001;
69(5):
779 - 784.
[Abstract]
[Full Text]
|
|
|
|
|
|
|
L. Guedez, A. J. McMarlin, D. W. Kingma, T. A. Bennett, M. Stetler-Stevenson, and W. G. Stetler-Stevenson
Tissue Inhibitor of Metalloproteinase-1 Alters the Tumorigenicity of Burkitt's Lymphoma via Divergent Effects on Tumor Growth and Angiogenesis
Am. J. Pathol.,
April 1, 2001;
158(4):
1207 - 1215.
[Abstract]
[Full Text]
[PDF]
|
|
|
|
|
|
|
J. Xu, A. Ahmad, M. D'Addario, L. Knafo, J. F. Jones, U. Prasad, R. Dolcetti, E. Vaccher, and J. Menezes
Analysis and Significance of Anti-Latent Membrane Protein-1 Antibodies in the Sera of Patients with EBV-Associated Diseases
J. Immunol.,
March 1, 2000;
164(5):
2815 - 2822.
[Abstract]
[Full Text]
[PDF]
|
|
|
|
|
|
|
J. Teruya-Feldstein, E. S. Jaffe, P. R. Burd, D. W. Kingma, J. E. Setsuda, and G. Tosato
Differential Chemokine Expression in Tissues Involved by Hodgkin's Disease: Direct Correlation of Eotaxin Expression and Tissue Eosinophilia
Blood,
April 15, 1999;
93(8):
2463 - 2470.
[Abstract]
[Full Text]
[PDF]
|
|
|
|
|
|
|
M. I. Gutierrez, B. Cherney, A. Hussain, H. Mostowski, G. Tosato, I. Magrath, and K. Bhatia
Bax Is Frequently Compromised in Burkitt's Lymphomas with Irreversible Resistance to Fas-induced Apoptosis
Cancer Res.,
February 1, 1999;
59(3):
696 - 703.
[Abstract]
[Full Text]
[PDF]
|
|
|
|
|
