2013 Fiscal Year Final Research Report
Malignant conversion of epithelial cancers through dysregulation of the p63-MYC pathway
| Project/Area Number |
23590375
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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 |
Pathological medical chemistry
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| Research Institution | National Center of Neurology and Psychiatry |
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Principal Investigator |
YUGAWA Takashi 独立行政法人国立がん研究センター, 研究所, 主任研究員 (80311372)
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| Project Period (FY) |
2011 – 2013
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| Keywords | 分子腫瘍学 / 癌 / 悪性化 / 幹細胞性 / 発現制御 / p63 / MYC |
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| Research Abstract |
Cancer cells evolve from normal cells through multiple genetic alterations. In particular, identification of a genetic cause behind the acquisition of the metastatic ability is very important for elucidating the nature of cancer.
In this study, I have found the possibility that p63, master regulator of epithelial development and stemness maintenance, acts as both an oncogene and tumor suppressor by increasing the proliferative capacity of cells while constraining metastatic tumor progression in early stages of carcinogenesis. I propose, for the first time, that up-regulation of c-MYC oncogene cancels the proliferative defect induced by p63 loss, thereby triggering malignant conversion in late stages of epithelial cancer development.
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[Journal Article] A critical role of MYC for transformation of human cells by HPV16 E6E7 and oncogenic HRAS2012
Author(s)
Narisawa-Saito M, Inagawa Y, Yoshimatsu Y, Haga K, Tanaka K, Egawa N, Ohno S, Ichikawa H, Yugawa T, Fujita M, Kiyono T
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Journal Title
Carcinogenesis
Volume: 33(4)
Pages: 910-917
DOI
Peer Reviewed
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