| Budget Amount *help |
¥4,550,000 (Direct Cost: ¥3,500,000、Indirect Cost: ¥1,050,000)
Fiscal Year 2010: ¥1,430,000 (Direct Cost: ¥1,100,000、Indirect Cost: ¥330,000)
Fiscal Year 2009: ¥1,560,000 (Direct Cost: ¥1,200,000、Indirect Cost: ¥360,000)
Fiscal Year 2008: ¥1,560,000 (Direct Cost: ¥1,200,000、Indirect Cost: ¥360,000)
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| Research Abstract |
Dysregulation in the pathway that control normal stem-cell self-renewal is considered a key early event in carcinogenesis. To reveal the involvement of Polycomb-group (PcG) genes in early event in pancreatic cancer development, we analyzed the function of the PcG gene Bmi1 in murine pancreatic stem/progenitor cells. As a result, overexpressed Bmi1 did not enhance the proliferation capability and differentiation capability of pancreatic stem/progenitor cells. We also examined activation of pancreatic stem/progenitor cells in pancreatic tumor formation in a pdx1-cre mediated Kras G12D expression model mouse. Histological analysis revealed that Pancreatic Intraepithelial Neoplasia (PanIN) was observed in intra/ interlobular pancreatic ducts of pancreas with high frequency. These results will enable us to better understand the process of pancreatic cancer development from pancreatic stem/progenitor cells.
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