| Project/Area Number |
04671490
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| Research Category |
Grant-in-Aid for General Scientific Research (C)
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| Allocation Type | Single-year Grants |
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| Research Field |
内分泌・代謝学
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| Research Institution | Nagasaki University |
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Principal Investigator |
NAMBA Hiroyuki University School of Medicine, Sub Professor, 医学部, 助教授 (80237635)
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| Co-Investigator(Kenkyū-buntansha) |
YAMASHITA Shunichi Nagasaki University School of Medicine, Professor, 医学部, 教授 (30200679)
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| Project Period (FY) |
1992 – 1993
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| Project Status |
Completed (Fiscal Year 1993)
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| Budget Amount *help |
¥2,100,000 (Direct Cost: ¥2,100,000)
Fiscal Year 1993: ¥700,000 (Direct Cost: ¥700,000)
Fiscal Year 1992: ¥1,400,000 (Direct Cost: ¥1,400,000)
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| Keywords | Thyroid / cancer / signal transduction / 甲状腺癌 |
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| Research Abstract |
It is well known that the alternations of signal transduction system are occurred in cancer cell. TSH is a major differentiation and growth promoting factor to thyroid cells. The action of TSH is mainly mediated through G-protein and c-AMP as a second messenger in the cell.
A response to the TSH is impaired in thyroid cancer. The establishment of an aberrant signal transduction system may lead to a selective growth advantage and change the rate of cell growth in malignancy.
In order to examine the impaired signal transduction in thyroid cancer cell, we have investigated the signaling path-way. The TSH signal transduction system in the carcinoma cells was compared with that in normal thyroid cells. Although unresponsiveness to bovine and human TSH was demonstrated by measurement of c-AMP production and [^<-3>H] thymidine incorporation after treatment of TSH, c-AMP production was induced after stimulation of these cells by forskolin, Cholera toxin, and isoproterenol. Intact TSH-R overexpression in the thyroid carcinoma cell revealed that specific binding to ^<125>I-TSH was increased, but the signal transduction was still impaired.
These findings suggest that the unresponsiveness to TSH in the thyroid carcinoma cells may be due to an abnormality of TSH receptor-G-protein coupling or defect of third factor(s).
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