| Project/Area Number |
09671667
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| Research Category |
Grant-in-Aid for Scientific Research (C)
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| Allocation Type | Single-year Grants |
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| Section | 一般 |
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| Research Field |
Obstetrics and gynecology
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| Research Institution | TOYAMA MEDICAL AND PHARMACEUTICAL UNIVERSITY |
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Principal Investigator |
FUJIMURA Masaki Toyama Medical and Pharmaceutical University, Hospital, Instructor, 附属病院, 講師 (80242501)
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| Co-Investigator(Kenkyū-buntansha) |
SAITO Shigeru Toyama Medical and Pharmaceutical University, Faculty of Medicine, Prof., 医学部, 教授 (30175351)
TSUDA Hiroshi Toyama Medical and Pharmaceutical University, Hospital, Assist. Prof., 附属病院, 助手 (80293314)
HIDAKA Takao Toyama Medical and Pharmaceutical University, Hospital, Assist. Prof., 附属病院, 助手 (70283083)
YAMAKAWA Yoshihiro Toyama Medical and Pharmaceutical University, Faculty of Medicine, Instructor, 医学部, 講師 (90191212)
泉 陸一 富山医科薬科大学, 医学部, 教授 (30010177)
伏木 弘 富山医科薬科大学, 医学部, 講師 (70173375)
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| Project Period (FY) |
1997 – 2000
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| Project Status |
Completed (Fiscal Year 2001)
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| Budget Amount *help |
¥2,900,000 (Direct Cost: ¥2,900,000)
Fiscal Year 2000: ¥600,000 (Direct Cost: ¥600,000)
Fiscal Year 1999: ¥1,200,000 (Direct Cost: ¥1,200,000)
Fiscal Year 1998: ¥500,000 (Direct Cost: ¥500,000)
Fiscal Year 1997: ¥600,000 (Direct Cost: ¥600,000)
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| Keywords | Ovarianclearcell adenocarcmoma / Chemo-resistant ovarian cancer / Growth Faetor / EGF-R / HER2 / neu / Monoclonal antibody / ZD1839 / HERCEPTIN / 明細胞腺癌 / 卵巣癌 / チロシンキナーゼ / サイトカイン / Clear cell adenocarcinoma / Ovarian cancer / Tyrosin Kinase / Cytokine / 薬剤耐性 / ステロイドホルモンレセプター / HRT |
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| Research Abstract |
The basic anti-caner drug for treating ovarian clear cell adenocarcinoma (CCA) was revealed to be CPT-ll. Hyperthermia and Glycerol addition which were known as enhencer of anti-cancer drug, have insufficient effect on its clinically available condition. Estrogen receptor-α (ER α), and ER β were not expressed in clinically resected Ovarian CCA specimens and cultured CCAcell lines. EOF and TGF α stimulation through EGF-R, which was thought to be located at the lower stream of ERα, stimulated the growth and invasion of CCA cell lines by autocline system. Stimulation through HER2 was also involved in the growth of ovarian CCA cell lines. Then Iressa, a specific inhibitor of EGF-R phosphorylation, inhibited the growth and invasion of CCA cell lines dose dependently. Iressa also inhibit the growth of xenografted CCA(RMG-l) on the back of SCID mice. The mice in which Iressa was administered survived more longer than the mice in control group. Herceptin which is known as humanized anti-HER2 monoclonal antibody, also inhibited the growth of CCA cell line in vitro and in vivo. Also Herceptin administered mice survived more longer than the mice in control group.
From these findings, Iressa and Herceptin were revealed to be potent inhibitors of CCA cell lines and could be a good candidate as one of clinically comprehensive treatment modality for CCA.
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