| Project/Area Number |
60440094
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| Research Category |
Grant-in-Aid for General Scientific Research (A)
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| Allocation Type | Single-year Grants |
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| Research Field |
医学一般
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| Research Institution | Hokkaido University |
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Principal Investigator |
KOBAYASHI Hiroshi Hokkaido University, School of Medicine, Professor, 医学部, 教授 (20000911)
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| Co-Investigator(Kenkyū-buntansha) |
OIKAWA Tsuneyuki Hokkaido University, School of Medicine, Instructor, 医学部, 助手 (80150241)
KUZUMAKI Noboru Hokkaido University, School of Medicine, Professor, 医学部, 教授 (80091445)
TAKEICHI Noritoshi Hokkaido University, School of Medicine, Associate Professor, 医学部, 助教授 (40002133)
HOSOKAWA Masuo Hokkaido University, School of Medicine, Associate Professor, 医学部, 助教授 (20001901)
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| Project Period (FY) |
1985 – 1986
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| Project Status |
Completed (Fiscal Year 1986)
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| Budget Amount *help |
¥29,500,000 (Direct Cost: ¥29,500,000)
Fiscal Year 1986: ¥6,500,000 (Direct Cost: ¥6,500,000)
Fiscal Year 1985: ¥23,000,000 (Direct Cost: ¥23,000,000)
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| Keywords | Tumor cells / Malignancy / Tumor progression / Tumor regression / Tumor metastasis / Cell surface modification / Oncogene / 細胞間コミュニケーション / 腫瘍原性 / 転移能 / 突然変異 / DNAメチル化阻害 / 細胞融合 / ウイルス感染 |
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| Research Abstract |
Tumor cells are composed of heterogeneous populations. The grade of tumor cell malignancy, therefore, varies from cell to cell, and certain populations of tumor cells are highly malignant when their tumorigenicity and ability to metastasize are examined, while other are not.
In this study, we attempted to investigate the factors by which tumor cells are led to become more malignant during their in vivo proliferation. In order to achieve the purpose, we selected mutagenic chemicals (quercetin, EMS and MNNG), viruses, a DNA-hypomethylating agent (5-azacystidine), anti-differentiation agents (TPA, indomethacin) and the hybridization technique for the modification of in vivo and in vitro tumorigenicity of tumor cells. We also examined natures of tumor cells such as the oncogene expression and the ability of tumor cells to communicate to normal cells and to other tumor cells in the view points of the correlation to their metastasizing ability.
As the result, we found that the tumor cell malignancy could be altered by some of the above means, and noted that an oncogene expression (c-fos) well correlated to their metastasizing ability and that the grade of communication of tumor cells to normal fibroblasts showed a reverse correlation to their metastasizing ability.
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