2017 Fiscal Year Final Research Report
Role of dedifferentiation on cancer development
| Project/Area Number |
15H04721
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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 |
Experimental pathology
|
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| Research Institution | The University of Tokyo (2017)
Kyoto University (2015-2016) |
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Principal Investigator |
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| Project Period (FY) |
2015-04-01 – 2018-03-31
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| Keywords | dedifferentiation / cancer / iPS cell / reprogramming |
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| Outline of Final Research Achievements |
The faithful shutdown of the somatic program occurs in the early stage of reprogramming. Here, we examined the effect of in vivo reprogramming on Kras-induced cancer development. We show that the transient expression of reprogramming factors in pancreatic acinar cells results in the transient repression of acinar cell enhancers. Notably, the transient expression of reprogramming factors in Kras mutant mice is sufficient to induce the rapid formation of pancreatic ductal adenocarcinoma. These results underscore a crucial role of dedifferentiation-associated epigenetic regulations in the initiation of pancreatic cancers.
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| Free Research Field |
腫瘍病理学
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