| Project/Area Number |
13671744
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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 | Keio University |
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Principal Investigator |
SUZUKI Nao Keio University, School of Medicine, Assistant, 医学部, 助手 (90246356)
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| Co-Investigator(Kenkyū-buntansha) |
AOKI Daisuke Keio University, School of Medicine, Assistant Professor, 医学部, 講師 (30167788)
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| Project Period (FY) |
2001 – 2002
|
| Project Status |
Completed (Fiscal Year 2002)
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| Budget Amount *help |
¥3,500,000 (Direct Cost: ¥3,500,000)
Fiscal Year 2002: ¥1,100,000 (Direct Cost: ¥1,100,000)
Fiscal Year 2001: ¥2,400,000 (Direct Cost: ¥2,400,000)
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| Keywords | Uterine Cervical Cancer / Differentiation / M-CSF / c-fms / HCG / hCG |
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| Research Abstract |
Human chorionic gonadotoropin (HCG) is a glycoprotein hormone normally produced by placenta during pregnancy. It is also well known that HCG is produced ectopicafly by many nontrophoblastic neoplasms including uterine cervical carcinoma. On the other hand, we have reported that macrophage colony-stimulating factor (M-CSF), and c-fms, a receptor tyrosine kinase for M-CSF play important functional roles in the differentiation of a human embryonal carcinoma cell line, NCR-G3 (G3) cells into trophoectoderm which produce HCG retinoic acid (RA) treatment. In this study, we investigated the relationship between ectopic production of HCG and signal transduction pathway of MCF and c-fms in uterine cervical carcinoma using uterine carcinoma cell lines (SKG-I, SKG-II, SKG-IIIa, SKG-IIIb) established in our laboratory. As a result, unfortunately we could not find out the mechanism of ectopic production of HCG in relation to the signal transduction of M-CSF and c-fms in uterine cervical carcinoma
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