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Analysis of molecular signal transduction pathway between M-CSF and c-fms involved in uterine cervical cancer

Research Project

Project/Area Number 13671744
Research Category

Grant-in-Aid for Scientific Research (C)

Allocation TypeSingle-year Grants
Section一般
Research Field Obstetrics and gynecology
Research InstitutionKeio University

Principal Investigator

SUZUKI Nao  Keio University, School of Medicine, Assistant, 医学部, 助手 (90246356)

Co-Investigator(Kenkyū-buntansha) AOKI Daisuke  Keio University, School of Medicine, Assistant Professor, 医学部, 講師 (30167788)
Project Period (FY) 2001 – 2002
Project Status Completed (Fiscal Year 2002)
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)
KeywordsUterine Cervical Cancer / Differentiation / M-CSF / c-fms / HCG / hCG
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

Report

(3 results)
  • 2002 Annual Research Report   Final Research Report Summary
  • 2001 Annual Research Report

URL: 

Published: 2001-04-01   Modified: 2016-04-21  

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