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Journal of Virology, December 2008, p. 11958-11963, Vol. 82, No. 23
0022-538X/08/$08.00+0 doi:10.1128/JVI.01149-08
Copyright © 2008, American Society for Microbiology. All Rights Reserved.

Naofumi Takamatsu,3
Tomonori Hidaka,4
Kinta Hatakeyama,5
Shingo Nakahata,3
Jun-ichi Fujisawa,6
Harutaka Katano,7
Naoki Yamamoto,1,2* and
Kazuhiro Morishita3*
Department of Molecular Virology, Graduate School, Tokyo Medical and Dental University, 1-5-45 Yushima, Bunkyo-ku, Tokyo 113-8519, Japan,1 AIDS Research Center, National Institute of Infectious Disease, 1-23-1 Toyama, Shinjuku-ku, Tokyo 162-8640, Japan,2 Department of Medical Sciences,3 Department of Internal Medicine,4 Department of Pathology, Faculty of Medicine, University of Miyazaki, Kiyotake, Miyazaki, Japan,5 Department of Microbiology, Kansai Medical University, Moriguchi, Osaka, Japan,6 Department of Pathology, National Institute of Infectious Diseases, 1-23-1 Toyama, Shinjuku-ku, Tokyo 162-8640, Japan7
Received 2 June 2008/ Accepted 15 September 2008
Adult T-cell leukemia (ATL) is associated with human T-cell leukemia virus type 1 infection. The tumor suppressor lung cancer 1 (TSLC1) gene was previously identified as a novel cell surface marker for ATL, and this study demonstrated the involvement of TSLC1 expression in tumor growth and organ infiltration of ATL cells. In experiments using NOD/SCID/
cnull mice, both leukemia cell lines and primary ATL cells with high TSLC1 expression caused more tumor formation and aggressive infiltration of various organs of mice. Our results suggest that TSLC1 expression in ATL cells plays an important role in the growth and organ infiltration of ATL cells.
Published ahead of print on 15 October 2008.
Present address: Department of Pathology, New York University School of Medicine, 550 First Avenue, New York, NY 10016.
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