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A NOVEL IMMUNE-REGULATORY GENE EJ3AG9: ITS CORRELATION WITH IIEPATOCELLULAR CARCINOMA AND ACUTE REJECTION AFTER LIVER TRANSPLANTATION.

Research Project

Project/Area Number 14571181
Research Category

Grant-in-Aid for Scientific Research (C)

Allocation TypeSingle-year Grants
Section一般
Research Field Digestive surgery
Research InstitutionThe University of Tokyo

Principal Investigator

MIKI Kenji  The Univ. of Tokyo, Faculty of Medicine, Research Associate, 医学部附属病院, 助手 (10242059)

Co-Investigator(Kenkyū-buntansha) INOUE Satoshi  The Univ. of Tokyo, Faculty of Medicine, Lecturer, 医学部附属病院, 講師 (40251251)
IMAMURA Hiroshi  The Univ. of Tokyo, Faculty of Medicine, Lecturer, 医学部附属病院, 講師 (00283268)
Project Period (FY) 2002 – 2003
Project Status Completed (Fiscal Year 2003)
Budget Amount *help
¥3,500,000 (Direct Cost: ¥3,500,000)
Fiscal Year 2003: ¥1,700,000 (Direct Cost: ¥1,700,000)
Fiscal Year 2002: ¥1,800,000 (Direct Cost: ¥1,800,000)
KeywordsEBAG9 / HEPATOCELLULAR CARCINOMA / DEDIFFERENTIATION / TUMOR PROLIFERATION / MULTISTEP TUMOR PROGRESSION / IMMUNOHISTOCHEMISTRY / 移植免疫 / 急性拒絶反応 / 細胞増殖
Research Abstract

The estrogen-responsive gene EBAG9, whose product is identical to cancer cell surface antigen RCAS1, is reported to be associated with tumor progression and invasiveness in various carcinomas. In this study we examined the expression of EBAG9/RCAS 1 in hepatocellular carcinoma (HCC), with special reference to its relationship with the stepwise evolution of HCC. Expression was examined by immunohistochemistry and Western blot analysis in 143 HCCs, as well as in non-cancerous liver tissue. Then the association between enhanced EBAG9/RCAS1 expression and various clinicopathological parameters including Ki-67 labeling index (LI), a marker of proliferative activity, was evaluated. There was a constant low level of EBAG9/RCAS 1 expression in non-cancerous liver tissue, with a regular cytoplasmic distribution. Positive immunoreactivity for EBAG9/RCAS1 was detected on the surface and in the cytoplasm of 84 HCC tumors, with an irregular staining pattern. Enhanced EBAG9/ROASi expression was correlated with a lower degree of differentiation and Kt67 LI. Interestingly, expression was enhanced specifically in the less differentiated lesions within "nodule-in-nodule" tumours. In conclusion, EBAG9/RCAS1 was associated with HCC tumour dedifferentiation and increased proliferative activity.

Report

(3 results)
  • 2003 Annual Research Report   Final Research Report Summary
  • 2002 Annual Research Report
  • Research Products

    (6 results)

All Other

All Publications (6 results)

  • [Publications] Aoki T, et al.: "EBAG9/RCAS1 expression in hepatocellular carcinoma : correlation with tumour dedifferentiation and proliferation"European Journal of Cancer. 39. 1552-1561 (2003)

    • Description
      「研究成果報告書概要(和文)」より
    • Related Report
      2003 Final Research Report Summary
  • [Publications] Aoki T, et al.: "EBAG9/RCAS1 expression in hepatocelluilar carcinoma: correlation with tumour dedifferentiation and proliferation."Eur J Cancer. 39. 1552-1561 (2003)

    • Description
      「研究成果報告書概要(欧文)」より
    • Related Report
      2003 Final Research Report Summary
  • [Publications] Aoki T, et al.: "EBAG9/RCAS1 expression inhepatocellular carcinoma : correlation with tumour de differentiation and proliferation."European Journal of Cancer. 39・11. 1552-1561 (2003)

    • Related Report
      2003 Annual Research Report
  • [Publications] Imamura H, et al.: "One thousand fifty-six hepatectomies without mortality in 8 years."Archives of Surgery. 138・11. 1198-1206 (2003)

    • Related Report
      2003 Annual Research Report
  • [Publications] Imamura H, et al.: "Pringle's manoeuvre in living donors."Lancet. 360・9350. 2049-2050 (2002)

    • Related Report
      2002 Annual Research Report
  • [Publications] Imamura H, et al.: "Risk factors contributing to early and late phase intrahepatic recurrence of hepatocellular carcinoma after hepatectomy"Journal of Hepatology. 38・2. 200-207 (2003)

    • Related Report
      2002 Annual Research Report

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Published: 2002-04-01   Modified: 2016-04-21  

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