Analysis of the mechanism for invasive ability by MUC16 and mesothelin in the pancreatic cancer.
| Project/Area Number |
24890208
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| Research Category |
Grant-in-Aid for Research Activity Start-up
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| Allocation Type | Single-year Grants |
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| Research Field |
Digestive surgery
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| Research Institution | Wakayama Medical University |
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Principal Investigator |
SHIMIZU Atsushi 和歌山県立医科大学, 医学部, 学内助教 (00637910)
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| Project Period (FY) |
2012-08-31 – 2014-03-31
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| Project Status |
Completed (Fiscal Year 2013)
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| Budget Amount *help |
¥3,120,000 (Direct Cost: ¥2,400,000、Indirect Cost: ¥720,000)
Fiscal Year 2013: ¥1,430,000 (Direct Cost: ¥1,100,000、Indirect Cost: ¥330,000)
Fiscal Year 2012: ¥1,690,000 (Direct Cost: ¥1,300,000、Indirect Cost: ¥390,000)
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| Keywords | 膵癌浸潤規定遺伝子 / MUC16 / mesothelin / 膵癌 / 浸潤能規定因子 / 新規膵癌治療標的分子 / 膵癌新規治療標的分子 |
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| Research Abstract |
We have identified two specific genes, MUC16 and mesothelin, associated with the invasion process in patients with pancreatic cancer using genome-wide expression profiling (Cancer Sci, 2012). In this study, it was intended to elucidate the mechanism of the invasion and metastasis, associated with EMT, induced by MUC16/mesothelin. By in vitro examination using pancreatic cancer cell line, it was suggested that the presence (and binding) of MUC16 and mesothelin in pancreatic cancer might affect the acquisition of high invasion and metastasis ability through the EMT. MUC16 and mesothelin clinically represent new prognostic biomarkers for PDAC and might be new therapeutic targets for patients with PDAC.
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Report
(3 results)
Research Products
(7 results)
