| Project/Area Number |
23591945
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| Research Category |
Grant-in-Aid for Scientific Research (C)
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| Allocation Type | Multi-year Fund |
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| Section | 一般 |
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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 |
TOMA Atsushi 京都府立医科大学, 医学(系)研究科(研究院), 助教 (30516191)
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| Co-Investigator(Kenkyū-buntansha) |
OTSUJI Eigo 京都府立医大学, 医学研究科, 教授 (20244600)
KOMATSU Shuhei 京都府立医大学, 医学研究科, 助教 (40578978)
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| Project Period (FY) |
2011 – 2013
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| Project Status |
Completed (Fiscal Year 2013)
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| Budget Amount *help |
¥5,070,000 (Direct Cost: ¥3,900,000、Indirect Cost: ¥1,170,000)
Fiscal Year 2013: ¥1,560,000 (Direct Cost: ¥1,200,000、Indirect Cost: ¥360,000)
Fiscal Year 2012: ¥1,560,000 (Direct Cost: ¥1,200,000、Indirect Cost: ¥360,000)
Fiscal Year 2011: ¥1,950,000 (Direct Cost: ¥1,500,000、Indirect Cost: ¥450,000)
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| Keywords | 分子生物学 / 増幅遺伝子 / 癌遺伝子 / 消化器外科学 / 食道外科学 / 分子標的 / DTL |
|---|
| Research Abstract |
Although previous studies have identified various amplifications and their targets in esophageal squamous cell carcinoma (ESCC), recent progress in the human genome project prompted us to identify additional targets. In this study, we tested whether DTL, located at previously reported 1q32-q41 amplicon, acts as a cancer-promoting gene in ESCC. Overexpression of DTL protein was frequently detected in primary ESCCs, and significantly correlated with pN category, and status of recurrence. Patients with DTL-overexpressing tumors had a worse overall survival than those with non-expressing tumors, and DTL was independent prognosticator in the multivariate analysis. Knockdown of DTL inhibited and ectopic overexpression of DTL promoted the growth of ESCC cells. These findings suggest that DTL plays an important role in tumor cell growth, and highlight its usefulness as a prognosticator and potential therapeutic target in ESCC.
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