| Project/Area Number |
13576001
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| Research Category |
Grant-in-Aid for Scientific Research (B)
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| Allocation Type | Single-year Grants |
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| Section | 海外学術 |
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| Research Field |
General anatomy (including Histology/Embryology)
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| Research Institution | Nagasaki University |
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Principal Investigator |
KOJI Takehiko Nagasaki University, Graduate School of Biomedical Sciences, Department of Developmental and Reconstructive Medicine, Professor, 大学院・医歯薬学総合研究科, 教授 (30170179)
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| Co-Investigator(Kenkyū-buntansha) |
IZUMI Shinichi Nagasaki University, Graduate School of Biomedical Sciences, Department of Developmental and Reconstructive Medicine, Instructor, 大学院・医歯薬学総合研究科, 助手 (40264246)
EJIMA Kuniaki Nagasaki University, Graduate School of Biomedical Sciences, Department of Developmental and Reconstructive Medicine, Assistant Professor, 大学院・医歯薬学総合研究科, 講師 (30309984)
HISAKAWA Yoshitaka Nagasaki University, Graduate School of Biomedical Sciences, Department of Developmental and Reconstructive Medicine, Assistant Professor, 大学院・医歯薬学総合研究科, 講師 (60304276)
ABE Kuniko Nagasaki University Hospital of Medicine and Dentistry, Instructor, 医学部・歯学部附属病院, 助手 (00253641)
OKADA Shigeru Okayama University, Graduate School of Medicine and Dentistry, Department of Pathological Research, Professor, 大学院・医歯学総合研究科, 教授 (60135556)
進 正志 長崎大学, 大学院・医歯薬学総合研究科, 助手 (80145226)
石川 隆俊 大学評価・学位授与機, 構, 教授 (30085633)
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| Project Period (FY) |
2001 – 2003
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| Project Status |
Completed (Fiscal Year 2003)
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| Budget Amount *help |
¥13,000,000 (Direct Cost: ¥13,000,000)
Fiscal Year 2003: ¥3,700,000 (Direct Cost: ¥3,700,000)
Fiscal Year 2002: ¥3,200,000 (Direct Cost: ¥3,200,000)
Fiscal Year 2001: ¥6,100,000 (Direct Cost: ¥6,100,000)
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| Keywords | Myanmar / hepatocellular carcinoma / iron / iron-responsive element binding proteins / hepatitis viruses / apoptosis / Fas / Fas ligand / molecular histochemistry / Fasリガンド / 肝炎ウィルス |
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| Research Abstract |
The precocious development of hepatocellular carcinoma (HCC) is a crucial problem in Myanmar. As a possible cause, iron incorporated from the environment is implicated. In the present study, we investigated the deposition of iron and the expression of iron-responsive element binding protein (IREBP) in the tissue sections from Myanmar HCC, and then the correlation between these iron-related parameters and HCC cell kinetics under the intimate cooperation with Department of Medical Research (DMR). Actually, we collected cancerous and non-cancerous parts of more than 30 HCC patients at our 3-times visit to Yangon (December 18 to 24, 2001, December 19-28, 2002 and December 18-23, 2003). During our visit, we also' held not only several meetings with DMR and Medical University scientists and but workshops on TUNEL in 2002 and nonradioactive in situ hybridization in 2003 in DMR, which successfully promoted our friendships. When Myanmar HCC tissue sections were examined for iron deposition, we found significantly heavier deposition of iron in Myanmar HCC than that of Japanese one. However, we failed to analyze the expression of IREBP effectively because of the inevitable loss of structural details after microwave retrieval of reactivity. In the study on the HCC cell kinetics, the specimens with a high proliferating activity assessed by Ki-67 staining was correlated with a low frequency of TUNEL positive cells while low proliferative cases were with frequent apoptosis. In the latter case, an apparent association with Fas ligand expression was found. Moreover, when we investigated the liver regeneration kinetics after partial hepatectomy in iron-overloaded rat model, a significant precocious starting of regeneration was observed, accompanying overall increase in the rate of apoptosis. These results indicate that acceleration of hepatocyte turnover by overloaded iron may promote the development of HCC under the proliferation-induced conditions such as viral infection.
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