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The Causal Relationship Between Epigenetic Abnormality and Cancer Development: in Vivo Reprogramming and Its Future Application

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Specialties Biology
Science
Date 2018 Jun 12
PMID 29887568
Citations 7
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Abstract

There is increasing evidence that cancer cells acquire epigenetic abnormalities as well as genetic mutations during cancer initiation, maintenance, and progression. However, the role of epigenetic regulation in cancer development, especially at the organismal level, remains to be elucidated. Here, we describe the causative role of epigenetic abnormalities in cancer, referring to our in vivo studies using induced pluripotent stem cell technology. We first summarize epigenetic reorganization during cellular reprogramming and introduce our in vivo reprogramming system for investigating the impact of dedifferentiation-driven epigenetic disruption in cancer development. Accordingly, we propose that particular types of cancer, in which causative mutations are not often detectable, such as pediatric cancers like Wilms' tumor, may develop mainly through alterations in epigenetic regulation triggered by dedifferentiation. Finally, we discuss issues that still remain to be resolved, and propose possible future applications of in vivo reprogramming to study cancer and other biological phenomena including organismal aging.

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References
1.
Molenaar J, Koster J, Zwijnenburg D, van Sluis P, Valentijn L, van der Ploeg I . Sequencing of neuroblastoma identifies chromothripsis and defects in neuritogenesis genes. Nature. 2012; 483(7391):589-93. DOI: 10.1038/nature10910. View

2.
Yamada Y, Jackson-Grusby L, Linhart H, Meissner A, Eden A, Lin H . Opposing effects of DNA hypomethylation on intestinal and liver carcinogenesis. Proc Natl Acad Sci U S A. 2005; 102(38):13580-5. PMC: 1224663. DOI: 10.1073/pnas.0506612102. View

3.
Hong H, Takahashi K, Ichisaka T, Aoi T, Kanagawa O, Nakagawa M . Suppression of induced pluripotent stem cell generation by the p53-p21 pathway. Nature. 2009; 460(7259):1132-5. PMC: 2917235. DOI: 10.1038/nature08235. View

4.
Cobaleda C, Jochum W, Busslinger M . Conversion of mature B cells into T cells by dedifferentiation to uncommitted progenitors. Nature. 2007; 449(7161):473-7. DOI: 10.1038/nature06159. View

5.
Yagi M, Kishigami S, Tanaka A, Semi K, Mizutani E, Wakayama S . Derivation of ground-state female ES cells maintaining gamete-derived DNA methylation. Nature. 2017; 548(7666):224-227. DOI: 10.1038/nature23286. View