| Project/Area Number |
16590275
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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 | Shiga University of Medical Science |
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Principal Investigator |
HATTORI Takanori Shiga Univ. of Medical Science, Pathology, professor, 医学部, 教授 (70079721)
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| Co-Investigator(Kenkyū-buntansha) |
SUGIHARA Hiroyuki Shiga Univ. of Medical Science, Pathology, associate professor, 医学部, 助教授 (30171169)
MUKAISHO Ken-ichi Shiga Univ. of Medical Science, Pathology, research assistant, 医学部, 助手 (50343223)
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| Project Period (FY) |
2004 – 2005
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| Project Status |
Completed (Fiscal Year 2005)
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| Budget Amount *help |
¥2,700,000 (Direct Cost: ¥2,700,000)
Fiscal Year 2005: ¥1,300,000 (Direct Cost: ¥1,300,000)
Fiscal Year 2004: ¥1,400,000 (Direct Cost: ¥1,400,000)
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| Keywords | genetic analysis / gastric carcinoma / CGH / p53 / mucin phenotype / マイクロダイセクション / 未分化型胃癌 / 分化型胃癌 / 混合型胃癌 / FISH |
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| Research Abstract |
The present study aims to clarify whether the tumors that have been classified as the same series on the basis of morphology and mucin phenotype are of common genetic lineage by applying a comparative genomic hybridization (CGH)-based lineage analysis to various gastric carcinomas (GCs). Consequently, we demonstrated (1) signet ring cell carcinoma (SIG) and tubular adenocarcinoma that have common gastric-type mucin phenotype were of different genetic lineages ; (2) early SIG that often had mixed gastric/intestinal phenotype was proved to be genetically continuous to poorly differentiated, advanced GC that had predominantly gastric phenotype, suggesting that the mucin phenotype may alter through subclonal selection or changes in cellular gene expression during progression of diffuse GC ; (3) tubular early GC was not always genetically continuous to advanced poorly differentiated GC ; (4) two thirds of poorly differentiated GC with tubular component (TC) derived from the TC through dedifferentiation, whereas the TC was genetically discontinuous to tubular early GC as far as CGH results and p53 inactivation are concerned. These findings suggest that the progression of tubular early GC of gastric phenotype to poorly differentiated GC may be less frequent phenomenon than many Japanese gastrointestinal pathologists have assumed.
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