1986 Fiscal Year Final Research Report Summary
Studies on the nature of tumor cell malignancy
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 |
Research Field |
医学一般
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Research Institution | Hokkaido University |
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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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 |
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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