| Project/Area Number |
13671239
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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 |
General surgery
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| Research Institution | TFE University of Tokushima |
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Principal Investigator |
KOMAKI Kansei University of Tokushima, university hospital, Assistant Professor, 医学部附属病院, 講師 (60215382)
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| Co-Investigator(Kenkyū-buntansha) |
MASUDA Eitarou University of Tokushima, university hospital, Assistant, 医学部附属病院, 助手 (50314860)
KONDO Kazuya University of Tokushima, school of medicine, Assistant Professor, 医学部, 講師 (10263815)
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| Project Period (FY) |
2001 – 2002
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| Project Status |
Completed (Fiscal Year 2002)
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| Budget Amount *help |
¥3,500,000 (Direct Cost: ¥3,500,000)
Fiscal Year 2002: ¥1,500,000 (Direct Cost: ¥1,500,000)
Fiscal Year 2001: ¥2,000,000 (Direct Cost: ¥2,000,000)
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| Keywords | Rho A / Rho B / Rac-1 / estrogen receptor / DMBA induced breast cancer / breast cancer |
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| Research Abstract |
[Expression of Rho family proteins in human breast concer-relation to ER status and histologic grade pf malignancy] Generally, Rho family proteins were weakly expressed in human invasive ductal carcinoma of the bresst. Ns Though ER prote expression inversely related to Rac-1 expression, which had no related to Rho B expressions. Between Rho family protein expression, there was significant relation in Rac-1 and Rho A, and expression of Rho A protein related to the degree of tubular formation of the tumors.
[Relationship between expression of Rho family and ability of tumor in DMBA induced rat breast cancer] Concerning with the expression of Rho family proteins in DMBA induced rat brest cancer, Rho A protein and Rac-1 protein showed strong ex pression at the time that began to palpate tumors, and these proteins expression decreased at 16 weeks later from that time. However, a statistical significance was not able to confirm in the changes of these protains expression. There was no constant tendency in the expresson of Rho B during the growing in DMBA induced rat tumor. In addition, as for the expression of estrogen receptor, a decreasing tendency inclued expression same as a conventional examination result. With Rho A, Rac-1, expression was similar and paralleled in DMBA rat breast cancer. Tumor invasiveness at 16 weeks was significantly strong in comparison with the beginning of tumor palpable. In conclusion, Rho A and Rac-1 proteins expression was decreased same as estrogen receptor expression according as the tumor growing, where the ability of invasivness was increased.
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