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

Molecular mechanism of hormone therapy resistance in cancers

Research Project

Project/Area Number 21590450
Research Category

Grant-in-Aid for Scientific Research (C)

Allocation TypeSingle-year Grants
Section一般
Research Field Experimental pathology
Research InstitutionNational Cancer Center Research Institute and Research Center for Innovative Oncology, National Cancer Center Hospital East

Principal Investigator

KUWATA Takeshi  独立行政法人国立がん研究センター, 臨床開発センター, 医長 (00327321)

Co-Investigator(Kenkyū-buntansha) OCHIAI Atsushi  独立行政法人国立がん研究センター, 臨床開発センター, 部長 (60183034)
Project Period (FY) 2009 – 2011
Project Status Completed (Fiscal Year 2011)
Budget Amount *help
¥4,550,000 (Direct Cost: ¥3,500,000、Indirect Cost: ¥1,050,000)
Fiscal Year 2011: ¥1,300,000 (Direct Cost: ¥1,000,000、Indirect Cost: ¥300,000)
Fiscal Year 2010: ¥1,430,000 (Direct Cost: ¥1,100,000、Indirect Cost: ¥330,000)
Fiscal Year 2009: ¥1,820,000 (Direct Cost: ¥1,400,000、Indirect Cost: ¥420,000)
Keywords腫瘍 / 前立腺 / アンドロゲン / 核内受容体 / 病理学 / 前立腺癌 / ホルモン依存性癌
Research Abstract

Molecular mechanism of hormone therapy resistance, especially in prostate cancer, was investigated. Interleukin(IL)-1beta showed tumor inhibitory effect in several prostate cancer cell lines including LNCap, while a previous report suggested possible involvement of IL-1beta in the resistance. Constitutive expression of these enzymes support tumor cell growth in castrated nude mice. Thus we concluded that these results suggested expression of androgenic enzymes may be involved in acquired resistant against hormone therapy in cancer.

Report

(4 results)
  • 2011 Annual Research Report   Final Research Report ( PDF )
  • 2010 Annual Research Report
  • 2009 Annual Research Report
  • Research Products

    (9 results)

All 2011 2010

All Journal Article (4 results) (of which Peer Reviewed: 4 results) Presentation (5 results)

  • [Journal Article] Targeting of bone-derived insulin-like growth factor-II by a humanizing antibody suppresses the growth of prostate cancer cells in a human bone environment2010

    • Author(s)
      Kimura T, Kuwata T, Ashimine S, Yamazaki M, Yamauchi C, Nagai K, Ikehara A, Feng Y, Dimitrov DS, Saito S, Ochiai A
    • Journal Title

      Clinical Cancer Research

      Volume: 16巻 Issue: 1 Pages: 121-129

    • DOI

      10.1158/1078-0432.ccr-09-0982

    • Related Report
      2011 Final Research Report
    • Peer Reviewed
  • [Journal Article] Pin1 acts as a modulator of cell proliferation through alteration in NF-κB but not β-catenin/TCF4 signalling in a subset of endometrial carcinoma cells.2010

    • Author(s)
      Saegusa S, Kuwata T, et al
    • Journal Title

      J Pathol

      Volume: 222 Pages: 410-420

    • Related Report
      2010 Annual Research Report
    • Peer Reviewed
  • [Journal Article] Transcriptional regulation of pro-apoptotic Par-4 by NF-kappaB/p65 and its function incontrolling cell kinetics during early events in endometrial tumourigenesis.2010

    • Author(s)
      Saegusa T, Kuwata T, et al
    • Journal Title

      J Pathol

      Volume: 221 Pages: 26-36

    • Related Report
      2010 Annual Research Report
    • Peer Reviewed
  • [Journal Article] Targeting of bone-derived insulin-like growth factor-II by a humanizing antibody suppresses the growth of prostate cancer cells in a human bone environment2010

    • Author(s)
      Kimura T
    • Journal Title

      Clinical Cancer Research 16

      Pages: 121-9

    • Related Report
      2009 Annual Research Report
    • Peer Reviewed
  • [Presentation] Aldo-keto reductase(AKR) 1C3 expression is frequently observed in human prostate cancer cases after androgen-therapy and promotes prostate cancer cell growth in castrated mice model AACR-EORTC-NCI Molecular Targets and Cancer2011

    • Author(s)
      Kuwata T and Ochiai A
    • Organizer
      Therapeutics Conference
    • Place of Presentation
      米国
    • Year and Date
      2011-11-14
    • Related Report
      2011 Final Research Report
  • [Presentation] Aldo-keto reductase (AKR) 1C3 expression is frequently observed in human prostate cancer cases after androgen-therapy and promotes prostate cancer cell growth in castrated mice model2011

    • Author(s)
      Takeshi Kuwata
    • Organizer
      AACR-EORTC-NCI Molecular Targets and Cancer Therapeutics Conference
    • Place of Presentation
      SanFran Cisco, USA
    • Year and Date
      2011-11-14
    • Related Report
      2011 Annual Research Report
  • [Presentation] 前立腺癌の抗アンドロゲン療法抵抗性獲得におけるアンドロゲン合成酵素発現の関与2011

    • Author(s)
      桑田健、落合淳志
    • Organizer
      日本病理学会総会
    • Place of Presentation
      横浜
    • Year and Date
      2011-04-30
    • Related Report
      2011 Final Research Report
  • [Presentation] 前立腺癌の抗アンドロゲン療法抵抗性獲得におけるアンドロゲン合成酵素発現の役割2011

    • Author(s)
      桑田健
    • Organizer
      第100回日本病理学会総会
    • Place of Presentation
      横浜
    • Year and Date
      2011-04-30
    • Related Report
      2011 Annual Research Report
  • [Presentation] 前立腺癌の抗アンドロゲン療法抵抗性におけるステロイド合成酵素発現の関与2010

    • Author(s)
      桑田健、落合淳志
    • Organizer
      日本病理学会総会
    • Place of Presentation
      東京
    • Year and Date
      2010-04-28
    • Related Report
      2011 Final Research Report 2010 Annual Research Report 2009 Annual Research Report

URL: 

Published: 2009-04-01   Modified: 2016-04-21  

Information User Guide FAQ News Terms of Use Attribution of KAKENHI

Powered by NII kakenhi