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Hormone regulation of c-erB-2 oncogene expression in endometrial cancer

Research Project

Project/Area Number 05671400
Research Category

Grant-in-Aid for General Scientific Research (C)

Allocation TypeSingle-year Grants
Research Field Obstetrics and gynecology
Research InstitutionTeikyo University School of Medicine

Principal Investigator

OGINO Masahiro  Teikyo University School of Medicine Assistant professor, 医学部, 助教授 (80107680)

Co-Investigator(Kenkyū-buntansha) KASHIMA Atsuko  Teikyo University School of Medicine Assistant, 医学部, 助手 (00246050)
Project Period (FY) 1993 – 1994
Project Status Completed (Fiscal Year 1994)
Budget Amount *help
¥1,100,000 (Direct Cost: ¥1,100,000)
Fiscal Year 1994: ¥600,000 (Direct Cost: ¥600,000)
Fiscal Year 1993: ¥500,000 (Direct Cost: ¥500,000)
Keywordsendometrial cancer / c-erbB-2 / estorogen / cancer cell line / Ishikawa cell line / OMC-2 cel line / 子宮体癌
Research Abstract

It is known that malignant transformation is a multistep process in which damage to genes normally involved in growth regulation culminates in tumor formation.
An attempt was made to elucidate the relationship between the estradiol and c-erbB-2 oncogene in the human endometrial cancer cell line in vitro. we examined two of celline ; Ishikasa cell line (Dr.Nishida : Tukuba Univ.) having estorogen reseptor positive (ER) and progesterone receptor positive (PR), and OMC-2 (Dr.Ueda : Osaka Med) having neiter ER nor PR.The proliferation of endometrial cancer cells of Ishikawa line was more stimulated after the 7 days than the control at concentraion 10 ^<-8>M estradiol. But such the proliferation phenomenon was not observed in OMC-2. Ishikawa cell line added estradiol at a concentration of 10^<-8>M was presented the c-erbB-2 mRNA expression, but Ishikawa cell line without estrdiol stimulation was slightly decreased after 14 days culture. OMC cell line was not presnted the c-erbB-2 mRNA expression in the both conditions. The c-erbB-2 mRNA expression can play an important role in the development of cell proliferation mediated throught the hormone receptor in the human endometrial cancer.

Report

(3 results)
  • 1994 Annual Research Report   Final Research Report Summary
  • 1993 Annual Research Report

URL: 

Published: 1993-04-01   Modified: 2025-11-19  

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