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Trends Cancer. 2018 Jun;4(6):408-417. doi: 10.1016/j.trecan.2018.04.007.

Epigenetic Priming in Cancer Initiation.

Author information

1
Institute of Biomedical Research of Salamanca (IBSAL), Salamanca, Spain; Equal first author.
2
Department of Pediatric Oncology, Hematology, and Clinical Immunology, Heinrich Heine University Düsseldorf, Medical Faculty, Düsseldorf, Germany; Equal first author.
3
Department of Cell Biology and Immunology, Centro de Biologia Molecular Severo Ochoa (CBMSO), CSIC/UAM, Madrid 28049, Spain; Equal senior author. Electronic address: cesar.cobaleda@csic.es.
4
Department of Pediatric Oncology, Hematology, and Clinical Immunology, Heinrich Heine University Düsseldorf, Medical Faculty, Düsseldorf, Germany; Equal senior author. Electronic address: Arndt.Borkhardt@med.uni-duesseldorf.de.
5
Institute of Biomedical Research of Salamanca (IBSAL), Salamanca, Spain; Experimental Therapeutics and Translational Oncology Program, Instituto de Biología Molecular y Celular del Cáncer, CSIC/Universidad de Salamanca, Campus M. de Unamuno s/n, 37007 Salamanca, Spain; Equal senior author. Electronic address: isg@usal.es.

Abstract

Recent evidence from hematopoietic and epithelial tumors revealed that the contribution of oncogenes to cancer development is mediated mainly through epigenetic priming of cancer-initiating cells, suggesting that genetic lesions that initiate the cancer process might be dispensable for the posterior tumor progression and maintenance. Epigenetic priming may remain latent until it is later triggered by endogenous or environmental stimuli. This Opinion article addresses the impact of epigenetic priming in cancer development and in the design of new therapeutic approaches.

KEYWORDS:

cancer; cancer stem cell; cancer therapy; oncogenes; reprogramming; stem cells

PMID:
29860985
DOI:
10.1016/j.trecan.2018.04.007
[Indexed for MEDLINE]

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