| Project/Area Number |
13470239
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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 | 一般 |
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| Research Field |
General surgery
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| Research Institution | Kyushu University |
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Principal Investigator |
MIMORI Koshi Medical Institute of Bioregulation Kyushu Univ. Research Associate, 生体防御医学研究所, 助手 (50322748)
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| Co-Investigator(Kenkyū-buntansha) |
INOUE Hiroshi Medical Institute of Bioregulation Kyushu Univ. Associate Profesor, 生体防御医学研究所, 助教授 (90203249)
MORI Masaki Medical Institute of Bioregulation Kyushu Univ. Profesor, 生体防御医学研究所, 教授 (70190999)
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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 |
¥14,500,000 (Direct Cost: ¥14,500,000)
Fiscal Year 2002: ¥6,300,000 (Direct Cost: ¥6,300,000)
Fiscal Year 2001: ¥8,200,000 (Direct Cost: ¥8,200,000)
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| Keywords | fragile histidine triad / common fragile site / precancerrous lesion / cancer susceptible gene / mismatch repair gene / apoptosis / cDNA microarray / adenovirus vector / Ponasteron A / MAR / Msh2 |
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| Research Abstract |
1) Identification of the FHIT related genes in esophageal cancer: First of all we have already established the expression vector of FHIT regulated by the admininistration of Ecdyson. Now we are identifying genes expressing along with FHIT expression by cDNA microarray analysis. We obtained several intriguing genes, and preparing papers to be published.
2) Recent studies have suggested that FHIT inactivation can be a consequence of defects in mismatch repair proteins, particularly Msh2. Interestingly, alteration of the fragile FHIT locus and loss of Fhit protein expression was significantly more frequent in sporadic CRCs lacking Msh2 protein, suggesting that this mismatch repair protein may be important in maintaining the integrity of the common fragile locus within the FHIT gene.
3) Reintroduction of a tumor suppressor gene product in cancer cells is a promising strategy for cancer gene therapy. We have studied the biological effects of adenoviral-FHIT transduction in esophageal cancer cell lines. Adenoviral-FHIT expression induced caspase-dependent apoptosis in two esophageal cancer cell lines. The adenoviral-FHIT expression can inhibit the growth of esophageal cancer cells, at least in part through caspase-dependent apoptosis.
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