| Project/Area Number |
12557107
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| Research Category |
Grant-in-Aid for Scientific Research (B)
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| Allocation Type | Single-year Grants |
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| Section | 展開研究 |
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| Research Field |
Digestive surgery
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| Research Institution | Kyoto prefectural University of Medicine |
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Principal Investigator |
SAKAKURA Chouhei Kyoto Prefectural University of Medicine, Dept. of Digestive Surgery, Stuff, 医学部, 助手 (10285257)
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| Co-Investigator(Kenkyū-buntansha) |
OKUDA Tsukasa Kyoto Prefectural University of Medicine, Dept. of Hygiene, Stuff, 医学部, 講師 (30291587)
ITO Yoshiaki Kyoto University, Virus Institute, Professor, ウイルス研究所, 教授 (80004612)
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| Project Period (FY) |
2000 – 2001
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| Project Status |
Completed (Fiscal Year 2001)
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| Budget Amount *help |
¥5,200,000 (Direct Cost: ¥5,200,000)
Fiscal Year 2001: ¥2,400,000 (Direct Cost: ¥2,400,000)
Fiscal Year 2000: ¥2,800,000 (Direct Cost: ¥2,800,000)
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| Keywords | Gastric cancer / AML2 (RUNX3) |
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| Research Abstract |
The human runt-related gene AML2 (RUNX3), located on chromosome 1p36, is a major mediator of signals elicited by members of the transforming growth factor-β (TGF-β) super family. Here we show that 45 - 60 % of gastric cancer cell lines and surgically resected specimens do not significantly express AML2 (RUNX3) due to a combination of hemizygous deletion and hypermethylation of the AML2 (RUNX3) promoter region. Tumorigenicity of gastric cancer cell lines in nude mice was inversely related to their level of AML2 (RUNX3) expression, and one gastric tumor associated mutation (R122C), occurring within the conserved Runt domain completely abolished the tumor suppressive effect of AML2 (RUNX3). The results suggest that a lack of AML2 (RUNX3) function is causally related to the genesis and progression of human gastric cancer.
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