| Project/Area Number |
11670162
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| Research Category |
Grant-in-Aid for Scientific Research (C)
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| Allocation Type | Single-year Grants |
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| Section | 一般 |
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| Research Field |
Human pathology
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| Research Institution | Chiba University |
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Principal Investigator |
ISHIKURA Hiroshi Chiba University, School of Medicine, Professor, 医学部, 教授 (70222982)
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| Co-Investigator(Kenkyū-buntansha) |
OZAKI Daisuke Chiba University, University Hospital, Lecturer, 医学部・附属病院, 講師 (20272312)
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| Project Period (FY) |
1999 – 2000
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| Project Status |
Completed (Fiscal Year 2000)
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| Budget Amount *help |
¥2,900,000 (Direct Cost: ¥2,900,000)
Fiscal Year 2000: ¥1,600,000 (Direct Cost: ¥1,600,000)
Fiscal Year 1999: ¥1,300,000 (Direct Cost: ¥1,300,000)
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| Keywords | hepatoid adenocarcinoma / hepatocyte nuclear factor / hepatocyte nuclear factor / AFP / HNF |
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| Research Abstract |
Hepatoid adenocarcinomas arise from a variety of endodermal and genito-urinary organs, and hepatocellular phenotypes of these tumors have been supported primarily by morphology and immunohistochemistry. The genesis of hepatoid adenocarcinoma in these organs may involve aberrant transcriptional controls for liver-specific proteins. We studied mRNA expression of liver-enriched nuclear factors, hepatocyte nuclear factor (HNF)-1 and HNF-4α, in hepatoid adenocarcinoma tissues from the stomach, lung, pancreas, and uterus. The hepatoid adenocarcinoma tissues expressed mRNA for liver-specific proteins such as alpha-fetoprotein (AFP), transferrin (TF), and albumin (ALB). All of the examined hepatoid adenocarcinomas expressed HNF-4α mRNA.Quantitative analysis revealed that HNF-4α mRNA in hepatoid adenocarcinomas of the lung was expressed to the order of several hundred fold more than in pulmonary non-hepatoid carcinomas and normal lung tissues. RT-PCR for HNF-1 mRNA demonstrated that virtually all tissues and tumors examined expressed similar amounts except for non-hepatoid carcinomas of the pancreas and lung, and normal lung tissues. Results suggest a possible integral role of HNFs in the genesis of carcinomas with an aberrant hepatocellular phenotype, especially in the lungs.
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