| Project/Area Number |
08457065
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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 | 一般 |
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| Research Field |
Human pathology
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| Research Institution | Nagoya City University |
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Principal Investigator |
EIMOTO Tadaaki Nagoya City University , Medical School, Professor, 医学部, 教授 (60140779)
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| Co-Investigator(Kenkyū-buntansha) |
INAGAKI Hiroshi Nagoya City University , Medical School, Assistant, 医学部, 助手 (30232507)
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| Project Period (FY) |
1996 – 1998
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| Project Status |
Completed (Fiscal Year 1998)
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| Budget Amount *help |
¥4,700,000 (Direct Cost: ¥4,700,000)
Fiscal Year 1998: ¥1,000,000 (Direct Cost: ¥1,000,000)
Fiscal Year 1997: ¥900,000 (Direct Cost: ¥900,000)
Fiscal Year 1996: ¥2,800,000 (Direct Cost: ¥2,800,000)
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| Keywords | Lung cancer / Premalignant lesion / Peripheral SCC / Large cell carcinoma / Small cell carcinoma / Tumorigenesis / Tumor-related gene / Clonality / 肺 / p53 / TUNEL法 / HUMARA遺伝子 / EBウイルス / 脱分化 / 免疫組織化学 / 腺扁平上皮癌 / 異型腺腫様過形成 / 扁平上皮化生・異形成 |
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| Research Abstract |
1. The lung tissue in peripheral squamous cell (SCC) and adenosquamous carcinomas were examined to identify the premalignant lesions. Localized interstitial fibroses were frequent, the lining cells showing hyperplasia (AH), atypical hyperplasia (AAH), or AAH with squamous metaplasia (AAHS). In some peripheral SCCs, epithelial dysplasia was seen in small bronchi. Immunohistochemistry showed surfactant apoprotein increased in AH, but decreased in AAH ; positive p53 protein in one ANHS ; and negative c-erbB-2 in all the lesions. The labeling index of PCNA or MIB-1 was increased in AH, AAH, and AAHS in this order.
2. Large cell carcinoma were examined by immunohistochemistry and in situ hybridization method for EB virus. Comparing the histology with tumor sizes, many large cell carcinomas seem to arise in preexisting SCC or adenocarcinoma as tumor progression. However, lymphoepithelioma-like large cell carcinomas may arise "de novo", and some may arise as large cell neuroendocrine carcinoma.
3. Combined type of small cell carcinoma was examined as to the clonality each of small cell carcinoma and nonsmall cell carcinoma. Sequencing study of the p53 gene showed different point mutations in small cell and nonsmall cell portions, suggesting a separate origin of the two types of carcinoma.
4. Techniques in examination of premalignant lesions were refined. Effects of prefixation and fixation times on apoptosis detection by TUNEL method were examined. The fixation times showed no effect, but prefixation times longer than two hours resulted in false positive cells. The method of the HUMARA gene analysis was revised, proving polyclonality in the lesions of bowenoid papulosis.
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