Molecular analysis of etiological factors and malignant degrees for non-small cell lung cancer
| Project/Area Number |
15590327
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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 | Kanagawa Cancer Center Research Institute (2004-2005)
Research Institute for Clinical Oncology, Saitama Cancer Center (2003) |
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Principal Investigator |
TSUCHIYA Eiju kanagawa Cancer Center Research Institute, Director, 所長 (00072314)
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| Co-Investigator(Kenkyū-buntansha) |
HAYASHI Shinichi Tohoku University, Medical Faculty, Professor, 医学部, 教授 (60144862)
西田 一典 埼玉がんセンター研究所, 研究室・研究員 (60280624)
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| Project Period (FY) |
2003 – 2005
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| Project Status |
Completed (Fiscal Year 2005)
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| Budget Amount *help |
¥3,300,000 (Direct Cost: ¥3,300,000)
Fiscal Year 2005: ¥1,100,000 (Direct Cost: ¥1,100,000)
Fiscal Year 2004: ¥1,100,000 (Direct Cost: ¥1,100,000)
Fiscal Year 2003: ¥1,100,000 (Direct Cost: ¥1,100,000)
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| Keywords | Lung cancer / non-small cell carcinoma / Squamous cell carcinoma / Adenocarcinoma / malignancy / Carcinogenesis / p53 / k-ras / 扁平上皮癌 / K-ras / 非小細胞肺がん / p53遺伝子 / マイクロダイセクション / 非小細胞癌 |
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| Research Abstract |
74 resected squamous cell carcinomas (sqs) and 239 adenocarcinomas were analyzed for p53 mutation : Any relationships between tumor location of sqs or subtype of adenocarcinomas, smoking, and p53 mutation patterns were then examined focusing on varying etiological factors. Our hypothesis was, that G→T transversion of p53 gene is caused by direct action of carcinogens contained in tobacco smoke on DNA, and that G→A transition at CpG (CpG→A) sites of the gene is caused by endogenous mechanisms. The same adenocarcinoma cases were also analyzed to determine what type of combined mutation status on p53 and k-ras affects malignancy of the tumors more strongly.
Results:1) Sqs were divided into three types by location - central, intermediate and periphera l; the highest frequencies of CpG→A in the central type, G→T in the intermediate and other mutations in the peripheral, were observed. 2)Adenocarcinomas were divided into five types - hobnail, columnar, goblet, polygonal and mixed. Of these, the hobnail type showed a low p53 mutation frequency with the highest CpG→A rate, the columnar and polygonal types had a high mutation frequency with the highest G→T rates, and the mixed type showed intermediate frequency of p53 with the highest other base change. 3)Five year survival was the highest for adenocarcinomas with the combination of non-mutated p53 and k-ras, followed by the combination of mutated p53 and non-mutated k-ras, and then the combination of non-mutated p53 and mutated k-ras, with the combination of mutated p53 and k-ras having the lowest survival.
The results show that etiological factors vary depending on locations of sqs and subtype of adenocarcinomas ; the worst malignancy was adenocarcinomas with the combined status on mutated p53 and k-ras.
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Report
(4 results)
Research Products
(16 results)
