Editorial:epigenetic reprogramming and cancer development

Editorial on the Research Topic: Epigenetic Reprogramming and Cancer Development.Research in the CV-D group was 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). Research in IS-G group was partially supported by SAF2015-64420-R MINECO/FEDER, UE, RTI2018-093314-B-I00 MCIU/AEI/FEDER, UE, by Junta de Castilla y León (UIC-017, CSI001U16, and CSI234P18), and by the German Carreras Foundation (DJCLS R13/26 and DJCLS 02R/2016). IS-G lab is a member of the EuroSyStem and the DECIDE Network funded by the European Union under the FP7 program. IS-G and CV-D have been supported by the German Federal Office for Radiation Protection (BfS) (FKZ: 3618S32274). GB lab is a member of the DECIDE Network funded by the European Union under the FP7 program.Peer reviewe

Hit-and-run lymphomagenesis by the Bcl6 Oncogene

Editorials: Cell Cycle FeaturesPeer Reviewe

Cancer Stem Cells as a Result of a Reprogramming-Like Mechanism

Open Access: under CC BY-NCSA 3.0 license.Research in our groups is partially supported by FEDER and by MICINN (SAF2009-08803 to ISG), by Junta de Castilla y León (Proyecto Biomedicina 2009-2010 to ISG, and Proyecto Biomedicina 2010-2011 to CVD), by MEC OncoBIO Consolider-Ingenio 2010 (Ref. CSD2007- 0017) to ISG, by NIH grant (R01 CA109335-04A1) to ISG, by Sandra Ibarra Foundation to ISG, and by Group of Excellence Grant (GR15) from Junta de Castilla y Leon to ISG and JJC.Peer reviewe

Essential role for telomerase in chronic myeloid leukemia induced by BCR-ABL in mice

This work is licensed under a Creative Commons Attribution 3.0 License.The telomerase protein is constitutively activated in malignant cells from many patients with cancer, including the chronic myeloid leukemia (CML), but whether telomerase is essential for the pathogenesis of this disease is not known. Here, we used telomerase deficient mice to determine the requirement for telomerase in CML induced by BCR-ABL in mouse models of CML. Loss of one telomerase allele or complete deletion of telomerase prevented the development of leukemia induced by BCR-ABL. However, BCR-ABL was expressed and active in telomerase heterozygous and null leukemic hematopoietic stem cells. These results demonstrate that telomerase is essential for oncogene-induced reprogramming of hematopoietic stem cells in CML development and validate telomerase and the genes it regulates as targets for therapy in CML.Research in ISG group was partially supported by FEDER and by MICINN (SAF2009-08803 to ISG), by Junta de Castilla y León (REF. CSI007A11-2 and Proyecto Biomedicina 2009-2010), by MEC OncoBIO Consolider-Ingenio 2010 (Ref. CSD2007-0017), by NIH grant (R01 CA109335-04A1), by Sandra Ibarra Foundation, and the ARIMMORA project (FP7-ENV-2011, European Union Seventh Framework Program) and by Proyecto en Red de Investigación en Celulas Madre Tumorales en Cancer de Mama, supported by Obra Social Kutxa y Conserjería de Sanidad de la Junta de Castilla y Leon. All Spanish funding is co-sponsored by the European Union FEDER program. ISG is an API lab of the EuroSyStem project.Peer Reviewe

Fat-specific FUS-DDIT3-transgenic mice establish PPARgamma inactivation is required to liposarcoma development.

Peer reviewe

Early epigenetic cancer decisions

A cancer dogma states that inactivation of oncogene(s) can cause cancer remission, implying that oncogenes are the Achilles' heel of cancers. This current model of cancer has kept oncogenes firmly in focus as therapeutic targets and is in agreement with the fact that in human cancers all cancerous cells, with independence of the cellular heterogeneity existing within the tumour, carry the same oncogenic genetic lesions. However, recent studies of the interactions between an oncogene and its target cell have shown that oncogenes contribute to cancer development via developmental reprogramming of the epigenome within the target cell. These results provide the first evidence that carcinogenesis can be initiated by epigenetic stem cell reprogramming, and uncover a new role for oncogenes in the origin of cancer. Here we analyse these evidences and discuss how this vision offers new avenues for developing novel anti-cancer interventions.Research in our group is partially supported by FEDER and by MICINN (SAF2012-32810), by NIH grant (R01 CA109335-04A1), by the ARIMMORA project (FP7-ENV-2011, European Union Seventh Framework Program), by Junta de Castilla y Leon (BIO/SA06/13), and by the Deutsche José Carreras Leukämie-Stiftung (DJCLS project 13/26). All Spanish funding is co-sponsored by the European Union FEDER program. ISG is an API lab of the EuroSyStem project and a partner within the Marie Curie Initial Training Network DECIDE (Decision-making within cells and differentiation entity therapies) funded by the European Union’s Seventh Programme under grant agreement n° 315902.Peer Reviewe

Childhood B-Cell Preleukemia Mouse Modeling

Leukemia is the most usual childhood cancer, and B-cell acute lymphoblastic leukemia (B-ALL) is its most common presentation. It has been proposed that pediatric leukemogenesis occurs through a “multi-step” or “multi-hit” mechanism that includes both in utero and postnatal steps. Many childhood leukemia-initiating events, such as chromosomal translocations, originate in utero, and studies so far suggest that these “first-hits” occur at a far higher frequency than the incidence of childhood leukemia itself. The reason why only a small percentage of the children born with such preleukemic “hits” will develop full-blown leukemia is still a mystery. In order to better understand childhood leukemia, mouse modeling is essential, but only if the multistage process of leukemia can be recapitulated in the model. Therefore, mouse models naturally reproducing the “multi-step” process of childhood B-ALL will be essential to identify environmental or other factors that are directly linked to increased risk of disease.Research in CV-D group has been funded by Instituto de Salud Carlos III (ISCIII), through a “Miguel Servet Grant” (CPII19/00024-AES 2017–2020); co-funded by the European Union. Research in IS-G group is partially supported by FEDER and by SAF2015-64420-R MINECO/FEDER, UE, RTI2018-093314-B-I00 MCIU/AEI/FEDER, UE, by PID2021-122185OB-I00 MCIU/AEI/FEDER, UE, and by Junta de Castilla y León (UIC-017, CSI001U16, CSI234P18, and CSI144P20). IS-G have been supported by the Fundacion Unoentrecienmil (CUNINA project). CC and IS-G have been supported by the Fundación Científica de la Asociación Española contra el Cáncer (PRYCO211305SANC). Research at CC’s laboratory was partially supported by Ministerio de Ciencia e Innovación/AEI/FEDER (PID2021-122787OB-I00), FEDER MINECO (SAF2017-83061-R), the “Fundación Ramón Areces” and a Research Contract with the “Fundación Síndrome de Wolf-Hirschhorn o 4p-”. Institutional grants from the “Fundación Ramón Areces” and “Banco de Santander” to the CBMSO are also acknowledged. J.M.-C. is the recipient of a UAM FPU fellowship. AC-G (CSI067-18) and MI-H (CSI021-19) are supported by FSE-Conserjería de Educación de la Junta de Castilla y León 2019 and 2020 (ESF—European Social Fund) fellowship, respectively. SA-A is supported by an Ayuda para Contratos predoctorales para la formación de doctores (PRE2019-088887). L.S. is supported by a scholarship from University of Salamanca co-financed by Banco Santander and ESF