Journal
TRENDS IN CANCER
Volume 4, Issue 6, Pages 408-417Publisher
CELL PRESS
DOI: 10.1016/j.trecan.2018.04.007
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Funding
- FEDER
- Miguel Servet grant from the Instituto de Salud Carlos III (Ministerio de Economia y Competitividad) [CP14/00082]
- Fondo de Investigaciones Sanitarias/Instituto de Salud Carlos III [PI17/00167, PI14/00025]
- Lady Tata International Award for Research in Leukaemia 2016-2017
- German Children's Cancer Foundation [DJCLS 02R/2016, KKS A2016/07]
- Forschungskommission of the Medical Faculty of Heinrich Heine University
- MINECO [SAF2017-83061, SAF2012-32810, SAF2015-64420-R]
- Fundacion Ramon Areces
- Banco de Santander
- German Children's Cancer Foundation
- Federal Ministry of Education and Research, Bonn, Germany
- Red de Excelencia Consolider [OncoBIOSAF2014-57791-REDC]
- Instituto de Salud Carlos III [PIE14/00066]
- ISCIII Plan de Ayudas IBSAL 2015 Proyectos Integrados [IBY15/00003]
- Junta de Castilla y Leon [BIO/SA51/15, CSI001U14, UIC-017, CSI001U16]
- Fundacion Inocente Inocente
- EU
- German Carreras Foundation [DJCLS R13/26]
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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.
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