| Project/Area Number |
16K19932
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| Research Category |
Grant-in-Aid for Young Scientists (B)
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| Allocation Type | Multi-year Fund |
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| Research Field |
Digestive surgery
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| Research Institution | Yamaguchi University |
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Principal Investigator |
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| Project Period (FY) |
2016-04-01 – 2018-03-31
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| Project Status |
Completed (Fiscal Year 2017)
|
| Budget Amount *help |
¥3,900,000 (Direct Cost: ¥3,000,000、Indirect Cost: ¥900,000)
Fiscal Year 2017: ¥1,690,000 (Direct Cost: ¥1,300,000、Indirect Cost: ¥390,000)
Fiscal Year 2016: ¥2,210,000 (Direct Cost: ¥1,700,000、Indirect Cost: ¥510,000)
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| Keywords | Dclk1 / Chk1 / 膵癌 / MEK / chk1 |
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| Outline of Final Research Achievements |
Recent studies have revealed that doublecortin-like kinase 1 (Dclk1) positively regulates tumor growth, invasion, metastasis, and anti-apoptosis in pancreatic cancer cells. Therefore, Dclk1 is a potential therapeutic target for pancreatic cancer. Consistent with this finding, the GEM-induced p-Chk1 expression was significantly decreased by treatment with LRRK. Combined treatment with GEM and LRRK significantly reduced cell survival compared to individual treatment with GEM. These results indicate that Dclk1 inhibition in combination with GEM treatment offers a novel approach to treat pancreatic cancer cells.
To investigate the expression of Dclk1 in resected specimens of pancreatic cancer and its prognostic significance. Patients in the high Dclk1 group exhibited significantly shorter survival times than those in the low Dclk1 group (P < 0.05). Dclk1 may be a marker for poor prognosis in patients with resected pancreatic cancer.
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