@article{oai:u-ryukyu.repo.nii.ac.jp:02004904,
 author = {Nakazato, Tetsuro and Okudaira, Taeko and Ishikawa, Chie and Nakama, Shinji and Sawada, Shigeki and Tomita, Mariko and Uchihara, Jun-nosuke and Taira, Naoya and Masuda, Masato and Tanaka, Yuetsu and Ohshiro, Kazuiku and Takasu, Nobuyuki and Mori, Naoki},
 issue = {11},
 journal = {Cancer Science},
 month = {Nov},
 note = {Clinical trials for treatment of adult T-cell leukemia (ATL) caused by human T-cell leukemia virus type I (HTLV-I) using all-trans-retinoic acid (ATRA) have shown satisfactory therapeutic responses, although efficacies were limited. Recently, many synthetic retinoids have been developed and among them, a novel synthetic retinoid, Am80 (Tamibarotene) is an RARα- and RARβ-specific retinoid expected to overcome ATRA resistance. The present study examined the inhibitory effects of Am80 on HTLV-I-infected T-cell lines and ATL cells. Am80 had negligible growth inhibition of peripheral blood mononuclear cells but marked growth inhibition of both HTLV-I-infected T-cell lines and ATL cells. Am80 arrested cells in the G1 phase of the cell cycle and induced apoptosis in HTLV-I-infected T-cell lines. It inhibited also the phosphorylation of IκBα and NF-κB-DNA binding, in conjunction with reduction of expression of proteins involved in the G1/S cell cycle transition and apoptosis. Am80 also inhibited the expression of JunD, resulting in suppression of AP-1-DNA binding. Furthermore, severe combined immunodeficient mice with tumors induced by subcutaneous inoculation of HTLV-I-infected T cells, responded to Am80 treatment with partial regression of tumors and no side-effects. These findings demonstrate that Am80 is a potential inhibitor of NF-κB and AP-1, and is a potentially useful therapeutic agent against ATL. (Cancer Sci 2008; 99: 2286–2294), 論文},
 pages = {2286--2294},
 title = {Anti-adult T-cell leukemia effects of a novel synthetic retinoid, Am80 (Tamibarotene)},
 volume = {99},
 year = {2008}
}