• Search Research Projects
  • Search Researchers
  • How to Use
  1. Back to previous page

Glucocorticoids induce G1cell cycle arrest in human neoplastic thymic epithelial cells

Research Project

Project/Area Number 17591470
Research Category

Grant-in-Aid for Scientific Research (C)

Allocation TypeSingle-year Grants
Section一般
Research Field Thoracic surgery
Research InstitutionOsaka University

Principal Investigator

SHIONO Hiroyuki  Osaka University, Hospital, Specially Appointed Associate Professor (20346216)

Co-Investigator(Kenkyū-buntansha) OKUMURA Meinoshin  Osaka University, Graduate School of Medicine, Associate Professor (40252647)
MINAMI Masato  Osaka University, Graduate School of Medicine, Associate Professor (10240847)
INOUE Masayoshi  Osaka University, Graduate School of Medicine, Assistant Professor (10379232)
MATSUDA Hikaru  Osaka University, Graduate School of Medicine, Professor Emeritus (00028614)
Project Period (FY) 2005 – 2006
Project Status Completed (Fiscal Year 2006)
Budget Amount *help
¥2,300,000 (Direct Cost: ¥2,300,000)
Fiscal Year 2006: ¥1,100,000 (Direct Cost: ¥1,100,000)
Fiscal Year 2005: ¥1,200,000 (Direct Cost: ¥1,200,000)
Keywordsthymoma / thymic epithelial cell / glucocorticoid / glucocorticoid receptor / apoptosis
Research Abstract

Purpose: Glucocorticoids exert anti-proliferative effects in various cell types and have long been known to induce apoptosis in thymocytes. Although a few reports have described the regression of human thymoma with glucocorticoid therapy, its effects on neoplastic thymic epithelial cells (TECs) have not been reported. In the present study, we investigated glucocorticoid receptor (GR) expression on neoplastic TECs and the effects of glucocorticoids in vitro on the cell cycle progression of tumor cells.
Patients and methods : Thymoma specimens were obtained during surgery from 21 patients. Three of the specimens with glucocorticoid therapy were examined using the TdT-mediated dUTP-biotin nick-end labeling method. Primary tumor specimens from ten untreated thymomas were examined for GR expression by immunohistochemistry. Isolated neoplastic TECs from the remaining eight untreated thymomas were examined using immunohistochemistry, flow cytometric and cell cycle analysis.
Results: GR are expressed on neoplastic TECs as well as on non-neoplastic thymocytes in thymomas, regardless of WHO histological classification. Glucocorticoids caused an accumulation of TEC in GO/G1 phase in all cases examined (n=6), and also induced apoptosis in the three with the lowest levels of Bcl-2 expression.
Conclusions : Our results indicate that neoplastic TECs express GR and that glucocorticoids directly suppress their in vitro proliferation.

Report

(3 results)
  • 2006 Annual Research Report   Final Research Report Summary
  • 2005 Annual Research Report
  • Research Products

    (2 results)

All 2006 2005

All Journal Article (2 results)

  • [Journal Article] 縦隔疾患に対する外科的アプローチ 2. 胸腺上皮性腫瘍のWHO病理分類2006

    • Author(s)
      奥村明之進, 塩野裕之, 井上匡美, 澤 芳樹
    • Journal Title

      日本外科学会雑誌 107

      Pages: 257-261

    • Related Report
      2006 Annual Research Report
  • [Journal Article] Glucocorticoids induce 01 cell cycle arrest in human neoplastic thymic epithelial cells2005

    • Author(s)
      Yasunobu Funakoshi Y, Shiono H, Inoue M, Kadota Y, Ohta M, Matsuda H, Okumura M, Eimoto T
    • Journal Title

      J Cancer Res Clin Oncol 131

      Pages: 314-322

    • Description
      「研究成果報告書概要(欧文)」より
    • Related Report
      2006 Final Research Report Summary

URL: 

Published: 2005-04-01   Modified: 2016-04-21  

Information User Guide FAQ News Terms of Use Attribution of KAKENHI

Powered by NII kakenhi