2000 Fiscal Year Final Research Report Summary
Study of Genomic Aberrations Using CGH Method and Cell Death of Oral Cancer
| Project/Area Number |
10671882
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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 |
Surgical dentistry
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| Research Institution | Yamaguchi University |
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Principal Investigator |
ITA Masamichi Yamaguchi University School of Medicine, Research Associate, 医学部, 助手 (60176279)
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| Co-Investigator(Kenkyū-buntansha) |
MATSUO Akira Yamaguchi University Hospital, Clinical Fellow, 医学部・附属病院, 医員(臨床)
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| Project Period (FY) |
1998 – 2000
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| Keywords | CGH / oral canncer / cell lines / chromosome / apoptosis / cisplatin / KRN5500 |
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| Research Abstract |
The Aberration of DNA copy number in 14 oral squamous cell lines and 11 oral cancers were investigated using comparative genomic hybridization (CGH) method. Cell lines had more aberrations of DNA copy number than oral cancer. It was considered that culture cells must change DNA copy number in order to adapt to in vitro which is different from in vivo. Common regions of gain between them were 5p, 8q, and 5q, on the other hand, those of loss were 18q and 19q. The results suggested that those aberrations involve in carcinogenesis and tumor proliferation in oral cancer. There are relationships among DNA copy number, DNA ploidy pattern, and tumor size ; aberrations of DNA copy number tend to increase in DNA aneuploid tumors and advanced tumors. In this point, DNA aneuploid and tumor advance represent chromosomal instability.
Cell death induced by cisplatin was examined on oral squamous cell carcinoma cell line, KM-1. Cells treated with cisplatin died in population to drug concentration. All of cells treated with 100μM of cisplatin died within 48 hours showing shrinkage, on the other hand, some of cells treated with 10μM began to die 24 hours after treatment. Both groups did not show typical apoptotic morphology and ladder formation using agarose gel electrophoresis, but DNA-strand breaks were detected by flow cytometry. Those cells increased uptake of FITC, suggesting that treated cell might produce some kinds of proteins in order to survive or die. On the other hand, HL-60, leukemia cells, were induced apoptosis in short time by cisplatin. It was suggested that cispaltin could not induced typical apoptosis to oral squamous cell carcinoma cells.
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