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Viral manipulation of the host epigenome for oncogenic transformation

Abstract

The cancerous cellular state is associated with multiple epigenetic alterations, but elucidating the precise order of such alterations during tumorigenic progression and their contributions to the transformed phenotype remains a significant challenge in cancer biology. Here we discuss recent findings on how viral oncoproteins exploit specific epigenetic processes to coerce normal cells to replicate when they should remain quiescent — a hallmark of cancer. These findings may highlight roles of epigenetic processes in normal biology and shed light on epigenetic events occurring along the path of non-viral neoplastic transformation.

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Figure 1: Schematic structure of small e1a and its interactions with cellular proteins required for induction of cell cycling.
Figure 2: A model for e1a-induced epigenetic reprogramming in primary human fibroblasts.

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Acknowledgements

This work is supported by National Institutes of Health grant R37CA25235 to A.J.B. and an American Cancer Society grant and a Howard Hughes Medical Institute early career award to S.K.K. We thank members of the University of California Los Angeles Gene Affinity Regulation Group for providing a stimulating environment.

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Correspondence to Arnold J. Berk or Siavash K. Kurdistani.

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Ferrari, R., Berk, A. & Kurdistani, S. Viral manipulation of the host epigenome for oncogenic transformation. Nat Rev Genet 10, 290–294 (2009). https://doi.org/10.1038/nrg2539

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