help button home button Am J Pathol Epitomics, Inc.
HOME HELP FEEDBACK SUBSCRIPTIONS ARCHIVE SEARCH TABLE OF CONTENTS

This Article
Right arrow Full Text
Right arrow Full Text (PDF)
Right arrow Purchase Article
Right arrow View Shopping Cart
Services
Right arrow Similar articles in this journal
Right arrow Similar articles in PubMed
Right arrow Alert me to new issues of the journal
Right arrow Download to citation manager
Right arrow reprints & permissions
Citing Articles
Right arrow Citing Articles via HighWire
Right arrow Citing Articles via Google Scholar
Google Scholar
Right arrow Articles by Takakuwa, T.
Right arrow Articles by Aozasa, K.
Right arrow Search for Related Content
PubMed
Right arrow PubMed Citation
Right arrow Articles by Takakuwa, T.
Right arrow Articles by Aozasa, K.
(American Journal of Pathology. 2004;164:967-974.)
© 2004 American Society for Investigative Pathology

Integration of Epstein-Barr Virus into Chromosome 6q15 of Burkitt Lymphoma Cell Line (Raji) Induces Loss of BACH2 Expression

Tetsuya Takakuwa, Wen-Juan Luo, Maria Francisca Ham, Femiko Sakane-Ishikawa, Naoki Wada and Katsuyuki Aozasa

From the Department of Pathology, Osaka University Graduate School of Medicine, Suita, Osaka, Japan

Epstein-Barr virus (EBV) initially isolated from cultured Burkitt lymphoma (BL) cells, is a well-known oncogenic virus. The Raji cell line was established from BL tissue and used for research worldwide. Previous study showed that each Raji cell contains an average of 50–60 EBV genome equivalents, and a significant proportion of the EBV genome is linearly integrated into host genome through BamHI-W close to the BamHI-Y fragment. However, a definitive EBV integration site in the chromosome has not been identified as yet. In this study, direct evidence that EBV DNA is integrated into the host genome was provided through cloning of the fragments containing nucleotide sequence of Raji integration sites. Integrated EBV DNA consisted of the BamHI-W fragment at one end and BamHI-D fragment at another end. Both junction sites were highly guanine/cytosine-rich. The BamHI-W fragment and the adjacent part of chromosome 6 showed 70% homology, while no homology was found between the BamHI-D and adjacent host sequences. EBV was present at intron 1 of the BACH2 gene located on chromosome 6q15. BACH2 was not expressed in the Raji cell line. Because BACH2 is a putative tumor suppressor gene, loss of its expression through EBV integration might contribute to lymphomagenesis.





This article has been cited by other articles:


Home page
J BiochemHome page
H. Hoshino, T. G. Nishino, S. Tashiro, M. Miyazaki, Y. Ohmiya, K. Igarashi, S. Horinouchi, and M. Yoshida
Co-repressor SMRT and Class II Histone Deacetylases Promote Bach2 Nuclear Retention and Formation of Nuclear Foci that are Responsible for Local Transcriptional Repression
J. Biochem., May 1, 2007; 141(5): 719 - 727.
[Abstract] [Full Text] [PDF]


Home page
JCOHome page
E. Sakane-Ishikawa, S.-i. Nakatsuka, Y. Tomita, S. Fujita, I. Nakamichi, T. Takakuwa, H. Sugiyama, S. Fukuhara, M. Hino, A. Kanamaru, et al.
Prognostic Significance of BACH2 Expression in Diffuse Large B-Cell Lymphoma: A Study of the Osaka Lymphoma Study Group
J. Clin. Oncol., November 1, 2005; 23(31): 8012 - 8017.
[Abstract] [Full Text] [PDF]




HOME HELP FEEDBACK SUBSCRIPTIONS ARCHIVE SEARCH TABLE OF CONTENTS
Copyright © 2004 by the American Society for Investigative Pathology.