| Project/Area Number |
10671156
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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 |
Digestive surgery
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| Research Institution | Chiba University |
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Principal Investigator |
MIYAZAKI Masaru The First Department of Surgery, School of Medicine, Chiba University, Lecturer, 医学部, 講師 (70166156)
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| Co-Investigator(Kenkyū-buntansha) |
SEINO Susumu Molecular Medicine, Higher Functions in Biochemical Science, Graduate School of Medicine, Chiba University, Professor, 大学院・医学研究科, 教授 (80236067)
AMBIRU Satoshi The First Department of Surgery, School of Medicine, Chiba University, Assistant, 医学部・付属病院, 助手 (30251200)
ITO Hiroshi The First Department of Surgery, School of Medicine, Chiba University, Lecturer, 医学部・付属病院, 講師 (00232463)
吉富 秀幸 千葉大学, 医学部・第一外科, 医員
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| Project Period (FY) |
1998 – 1999
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| Project Status |
Completed (Fiscal Year 1999)
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| Budget Amount *help |
¥3,800,000 (Direct Cost: ¥3,800,000)
Fiscal Year 1999: ¥1,800,000 (Direct Cost: ¥1,800,000)
Fiscal Year 1998: ¥2,000,000 (Direct Cost: ¥2,000,000)
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| Keywords | Biliary tract carcinoma / Biliary tract tumor / Somatostatin / Somatostatin receptor / Cell proliferation / 肝 臓 癌 / 胆 道 癌 / 細胞増殖抑制 |
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| Research Abstract |
To evaluate the possibility of Somatostatin therapy for hepatobiliary tumors, molecular biological approaches were performed using MIN 6-cultured tumor cells in vitro. Cell proliferation was assessed by MTT assay, and mRNA expression of c-fos and c-jun by northern blotting and expression of Somatostatin receptor of hepatobiliary tumors by RT-PCR method. Our studies revealed the expression of Somatostatin receptor in MIN6 cells. It was shown that the proliferative activity of MIN6 cells was inhibited with the addition of Somatostatin into culture media. Furthermore, the expression of c-fos in MIN6 cells stimulated by serum was significantly suppressed by the pretreatment with Somatostatin. The expression of Somatostatin receptor was investigated in hepatobiliary tumors which were obtained as surgical specimen ; bile duct cancers in three, gallbladder carcinoma in one, hepatic cholangiocarcinoma in one. All these tumors were demonstrated to express only SSTR2, a subtype of Somatostatin r
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eceptor. Somatostatin was revealed to have inhibitory effects on cell proliferation through the mechanism that Somatostatin regulates the rate of cell proliferation by G-protein mediated signal transduction in MIN6 cells. The fact that hepatobiliary tumors have been shown to prossess Somatostatin receptor subtype, SSTR2, might suggest therapeutic implication of Somatostatin for hepatobiliary malignancies in clinical practice. It should be required to clarify the clinocopathological relationship between the expression of Somatostatin receptor and the various steps of tumor growth in hepatobiliary malignancies for the clinical application of Somatostatin therapy. At present, we are investigating its relationship using enough surgical samples including metastatic lymphnodes of hepatobiliary malignancies obtained in our institution. Our analysis has been clarifying how the expression of Somatostatin receptor affects biological events at molecular level of tumor invasion and metastasis in hepatobiliary malignancies. Therefore, further extensive investigations of this project should be required. Less
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