| Project/Area Number |
01480392
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| Research Category |
Grant-in-Aid for General Scientific Research (B)
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| Allocation Type | Single-year Grants |
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| Research Field |
Obstetrics and gynecology
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| Research Institution | Osaka University |
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Principal Investigator |
MIYAKE Akira Osaka University, Obstetrics & Gynecology, Associate Professor, 医学部, 講師 (90093468)
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| Co-Investigator(Kenkyū-buntansha) |
寺川 直樹 大阪大学, 医学部, 講師 (90135690)
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| Project Period (FY) |
1989 – 1991
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| Project Status |
Completed (Fiscal Year 1991)
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| Budget Amount *help |
¥6,400,000 (Direct Cost: ¥6,400,000)
Fiscal Year 1991: ¥700,000 (Direct Cost: ¥700,000)
Fiscal Year 1990: ¥1,800,000 (Direct Cost: ¥1,800,000)
Fiscal Year 1989: ¥3,900,000 (Direct Cost: ¥3,900,000)
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| Keywords | ovarian cancer / cell growth / autocrine mechanism / growth factors / transforming growth factor alpha / epidermal growth factor / epidermal growth factor receptor / cell culture / ovarian cancer / cellーline / transforming growth factorα / epidermal growth factor / epidermal growth factor receptor / mRNA / northern blot analysis / immunocytochemistry / EGF受容体 / メッセンジャ-RNA |
|---|
| Research Abstract |
Autocrine mechanisms by transforming growth factors (TGF), insulin like growth factor are reported to be expressed in many kinds of cancers and cancer cell-lines. We studied the expression of epidermal growth factor (EGF) receptor in 35 cases of ovarian cancers and 20 of them expressed EGF receptor and found the biological significance of TGFalpha/EGFR autocrine growth mechanism in primary o, vSSL, ria c cer cells and in an ovarian cancer cell-line, in vitro and in vivo. We-examined the expression of the growth factor and its receptor by Northern blot analysis, immunocytochemistry, binding studies. We also observed-that this autocrine mechanism was more commonly expressed in serous cystadenocarcinomas than in mucinous cancers. It is known that serous type ovarian cancers are more aggressive in their progression than mucinous cystadenocarcinomas. We might propose a possibility that the aggressive growth of serous cystadenocarinomas are, at least in part, due to TGFA/EGF autocrine growth mechanism, and that there might be a possibility of treatments by blocking the autocrine mechanism.
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