Dnmt1 links BCR-ABLp210 to epigenetic tumor stem cell priming in myeloid leukemia

The clonal nature of cancer evolution dictates that all tumor cells carry the same cancer-initiating genetic lesions. However, the latest findings have shown that the mode of action of oncogenes is not homogeneous throughout the developmental history of the tumor. Studies on different types of hematopoietic and solid tumors have shown that the contribution of some oncogenes to cancer development is mediated through the epigenetic reprogramming of the cancer-initiating target cell [1,2,3,4]. Epigenetic reprogramming is therefore a new type of interaction between oncogenes and tumor cells, in which the oncogene primes for cancer development by establishing a new pathological tumor cell identity. The current challenge is to test whether epigenetic remodeling in the absence of the driver oncogene is sufficient for tumorigenesis.
Research in CVD group is partially supported by FEDER, “Miguel Servet” Grant (CP14/00082 - AES 2013-2016) from the Instituto de Salud Carlos III (Ministerio de Economía y Competitividad), “Fondo de Investigaciones Sanitarias/Instituto de Salud Carlos III” (PI17/00167), and by the Lady Tata International Award for Research in Leukaemia 2016–2017. Research in ISG group is partially supported by FEDER and by MINECO (SAF2012-32810, SAF2015-64420-R and Red de Excelencia Consolider OncoBIO SAF2014-57791- REDC), Instituto de Salud Carlos III (PIE14/00066), ISCIII- Plan de Ayudas IBSAL 2015 Proyectos Integrados (IBY15/00003), by Junta de Castilla y León (BIO/SA51/15, CSI001U14, UIC-017, and CSI001U16), and by the German Carreras Foundation (DJCLS R13/26). ISG lab is a member of the EuroSyStem and the DECIDE Network funded by the European Union under the FP7 program. IGR was supported by BES-Ministerio de Economía y Competitividad (BES2013-063789). GRH was supported by FSE-Conserjería de Educación de la Junta de Castilla y León (CSI001-15).