| Project/Area Number |
12213139
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| Research Category |
Grant-in-Aid for Scientific Research on Priority Areas
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| Allocation Type | Single-year Grants |
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| Review Section |
Biological Sciences
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| Research Institution | Juntendo University School of Medfcine (2003-2004)
Japanese Foundation For Cancer Research (2000-2002) |
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Principal Investigator |
HINO Okio Department of Pathology, Juntendo University School of Medicine, Professor, 医学部, 教授 (90127910)
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| Co-Investigator(Kenkyū-buntansha) |
KOBAYASHI Toshiyuki Department of Pathology, Juntendo University School of Medicine, Assistant Professor, 講師 (40260070)
HAMANO Yoshitomo Department of Pathology, Juntendo University School of Medicine, Assistant Professor, 講師 (10281354)
梶野 一徳 財団法人癌研究会, 癌研究所・実験病理部, 研究員 (80260066)
梅田 知幸 (財)癌研究会, 癌研究所・実験病理部, 研究員 (10286776)
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| Project Period (FY) |
2000 – 2004
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| Project Status |
Completed (Fiscal Year 2004)
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| Budget Amount *help |
¥54,100,000 (Direct Cost: ¥54,100,000)
Fiscal Year 2004: ¥10,500,000 (Direct Cost: ¥10,500,000)
Fiscal Year 2003: ¥10,700,000 (Direct Cost: ¥10,700,000)
Fiscal Year 2002: ¥11,000,000 (Direct Cost: ¥11,000,000)
Fiscal Year 2001: ¥10,900,000 (Direct Cost: ¥10,900,000)
Fiscal Year 2000: ¥11,000,000 (Direct Cost: ¥11,000,000)
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| Keywords | Eker rat / Nihon rat / Tsc 1 gene / Tsc 2 gene / Bhd gene / Niban gene / Ere gene / hereditary cancer / Bhd遺伝子 / Niban遺伝子 / ERC遺伝子 / mTOR / Rapamycin / TSC1遺伝子 / 遺伝性腎癌 / Erc遺伝子 / TSC2遺伝子 / 起始遺伝子 / 腎発がん / Tsc1遺伝子 / Tsc2遺伝子 / 多段階発がん / 疾患モデル |
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| Research Abstract |
Cancer is a heritable disorder of somatic cells. Environment and heredity both contribute to the origin of human cancer. The Eker (Tsc 2 gene mutant) rat model of hereditary renal carcinoma (RC) is an example of a Mendelian dominantly inherited predisposition to a specific cancer in an experimental animal. Carcinogenesis looks like an opened Japanese fan, because initiated cells growing in several directions will develop into tumors having many gene abnormalities, and this is suggested by the edge of the fan. To search for such genetic alterations, we identified genes (Niban and Ere) that were expressed more abundantly in renal tumors than in the normal kidney.
Recently, we discovered a new hereditary renal carcinoma in the rat in Japan, and the rat was named the "Ninon" rat and its predisposing (Bhd) gene could be a novel renal tumor suppressor gene.
We present these unique models for the study of problems in carcinogenesis; eg., multistep carcinogenesis, cancer prevention and the development of the therapeutic treatments which can be translated into human patients, as well as how environmental factors interact with cancer susceptibility gene(s) and discuss the primal force and gene networks (federal headship) in renal carcinogenesis.
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