| Project/Area Number |
61480339
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| Research Category |
Grant-in-Aid for General Scientific Research (B)
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| Allocation Type | Single-year Grants |
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| Research Field |
Urology
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| Research Institution | Tokyo Medical and Dental University |
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Principal Investigator |
OSHIMA Hiroyuki Professor, Tokyo Medical and Dental University, 医学部, 教授 (60013934)
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| Co-Investigator(Kenkyū-buntansha) |
KIHARA Kazunori Assistant, Tokyo Medical and Dental University, 医学部, 助手 (40161541)
HIGASHI Yotsuo Lecturer, Tokyo Medical and Dental University, 医学部, 講師 (50092432)
FUKUI Iwao Assistant Professor, Tokyo Medical and Dental University, 医学部, 助教授 (90014232)
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| Project Period (FY) |
1986 – 1988
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| Project Status |
Completed (Fiscal Year 1988)
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| Budget Amount *help |
¥5,000,000 (Direct Cost: ¥5,000,000)
Fiscal Year 1988: ¥1,000,000 (Direct Cost: ¥1,000,000)
Fiscal Year 1987: ¥1,000,000 (Direct Cost: ¥1,000,000)
Fiscal Year 1986: ¥3,000,000 (Direct Cost: ¥3,000,000)
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| Keywords | Urogenital Tumors / 細胞間相互作用 |
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| Research Abstract |
Intercellular communication (IC) was investigated by dye transfer method in the human urogenital epithelia. 1) In transitional cell carcinoma (TCC) cells, high and low IC was observed in differenciated and undifferenciated TCCs, respectively. High or lack of IC was observed between various combination of different TCC cells. Fibroblasts showed apparent IC with none of TCC cells.
2) In prostatic epithelium, the extent of IC among prostatic carcinoma cells was lower than that of benign prostatic diseases. IC of prostatic carcinoma cells cultured from metastatic lesions of bone (PC-3) and lymph nodes was very limited. IC between benign prostatic epithelium and PC-3 was almost absent. No IC was present between prostatic epithelium and interstitial cells.
3) Testosterone inhibites IC of TCC cell lines. This inhibition was time- and dose-dependent and recovered rapidly after deprivation of testosterone. In contrast, neither estradiol-17 nor cortisol inhibites IC of these TCC cells. IC of fibroblasts was not influenced by testosterone.
4) To detect malignant transformation of the urothelium, cytokeration and cell surface antigens were investigated. (1) In normal urothelium, keratin fibers are thin, straight, constant in diameter and are distributed evenly in the cytoplasm. In TCC cells, they vary in diameter, wind their ways through and are distributed unevenly in the cytoplasm. The changes of ketatin fibers in bladder carcinoma cells appeared to be parallel to the grade of malignancy.
5) Three monoclonal antibodies (MoAb) generated against a TCC cell line (JTC-30) appeared to be related to blood group A antigen but have different reaction patterns with anti-blood group A MoAb. These anti-JTC-30 MoAbs recognize a blood group A related epitope(s), which is unstable in the process of malignant degeneration.
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