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Blood, 15 January 2006, Vol. 107, No. 2, pp. 716-724. Prepublished online as a Blood First Edition Paper on September 20, 2005; DOI 10.1182/blood-2005-02-0735.
NEOPLASIA Efficient intervention of growth and infiltration of primary adult T-cell leukemia cells by an HIV protease inhibitor, ritonavirFrom the Department of Molecular Virology, Graduate School of Medicine, Tokyo Medical and Dental University, Tokyo, Japan; the AIDS Research Center, National Institute of Infectious Diseases, Tokyo, Japan; the Division of Molecular Virology and Oncology, Graduate School of Medicine, University of the Ryukyus, Okinawa, Japan; the Department of Pathology, National Institute of Infectious Diseases, Tokyo, Japan; the Central Institute for Experimental Animals, Kanagawa, Japan; the Department of Bioorganic Medical Chemistry, Graduate School of Pharmaceutical Sciences, Kyoto University, Kyoto, Japan; the Department of Epidemiology and Preventive Medicine, Kagoshima University Graduate School of Medical and Dental Sciences, Kagoshima, Japan; the Department of Hematology, Molecular Medicine Unit, Atomic Bomb Disease Institute, Nagasaki University Graduate School of Biomedical Sciences, Nagasaki, Japan; the Second Department of Internal Medicine, Miyazaki Medical College, University of Miyazaki, Miyazaki, Japan; the Department of Laboratory Medicine, Miyazaki Medical College, University of Miyazaki, Miyazaki, Japan; and the Division of Clinical Trials and Research, Breast Cancer Research and Treatment Program, Tokyo Metropolitan Komagome Hospital, Tokyo Medical Center for Cancer and Infectious Disease, Tokyo, Japan.
Adult T-cell leukemia (ATL), an aggressive malignancy of CD4+ T cells associated with human T-cell leukemia virus type I (HTLV-I) infection, carries a very poor prognosis because of the resistance of leukemic cells to any conventional regimen, including chemotherapy. We examined the effect of ritonavir, an HIV protease inhibitor, on HTLV-I-infected T-cell lines and primary ATL cells and found that it induced apoptosis and inhibited transcriptional activation of NF-
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