A5030213661- Acute Lymphoblastic Leukemia research
- Epigenetics and DNA Methylation
- Chronic Myeloid Leukemia Treatments
- Acute Myeloid Leukemia Research
- Chronic Lymphocytic Leukemia Research
- CAR-T cell therapy research
- Cancer-related gene regulation
- Pluripotent Stem Cells Research
- Lymphoma Diagnosis and Treatment
- Cancer Cells and Metastasis
- Histone Deacetylase Inhibitors Research
- Genomic variations and chromosomal abnormalities
- Childhood Cancer Survivors' Quality of Life
- Neuroblastoma Research and Treatments
- Cancer therapeutics and mechanisms
Universidad de Salamanca
2014-2021
Centro de Investigación del Cáncer
2014-2021
Instituto de Investigación Biomédica de Salamanca
2014-2021
Consejo Superior de Investigaciones Científicas
2021
Biblioteca Nacional de España
2014
Abstract ETV6-RUNX1 is associated with the most common subtype of childhood leukemia. As few carriers develop precursor B-cell acute lymphocytic leukemia (pB-ALL), underlying genetic basis for development full-blown remains to be identified, but appearance cases in time-space clusters keeps infection as a potential causal factor. Here, we present vivo evidence mechanistically connecting preleukemic expression hematopoetic stem cells/precursor cells (HSC/PC) and postnatal infections...
Preleukemic clones carrying
ETV6-RUNX1 is almost exclusively associated with childhood B-cell acute lymphoblastic leukemia (B-ALL), but the consequences of expression on cell lineage decisions during leukemogenesis are completely unknown. Clinically silent preleukemic clones frequently found in neonatal cord blood, few carriers develop B-ALL as a result secondary genetic alterations. The understanding mechanisms underlying first transforming steps could greatly advance development non-toxic prophylactic interventions....
Abstract The prerequisite to prevent childhood B-cell acute lymphoblastic leukemia (B-ALL) is decipher its etiology. current model suggests that infection triggers B-ALL development through induction of activation-induced cytidine deaminase (AID; also known as AICDA) in precursor B-cells. This evidence has been largely acquired the use ex vivo functional studies. However, whether this mechanism governs native non-transplant unknown. Here we show that, surprisingly, AID genetic deletion does...
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 Economia y Competitividad), “Fondo Investigaciones Sanitarias/Instituto III” (PI17/00167), and Lady Tata International Award for Leukaemia 2016–2017. ISG FEDER MINECO (SAF2012-32810, SAF2015-64420-R Red Excelencia Consolider OncoBIO SAF2014-57791- REDC), (PIE14/00066), ISCIII- Plan Ayudas IBSAL 2015 Proyectos Integrados (IBY15/00003),...
Genetic lineage tracing in cell type-specific mouse models of T-cell acute lymphoblastic leukemia (T-ALL) have revealed that tumor identity is imposed by expression the oncogene Lim Domain Only 2 (LMO2), rather than target phenotype. This approach allowed to identify secondary genomic alterations, like Notch1 mutations, appeared late and only took place within thymus during T-ALL development. These concepts are therefore critical for development modern therapies aimed at curing T-ALL.
<div>Abstract<p>Preleukemic clones carrying <i>BCR-ABL</i><sup><i>p190</i></sup> oncogenic lesions are found in neonatal cord blood, where the majority of preleukemic carriers do not convert into precursor B-cell acute lymphoblastic leukemia (pB-ALL). However, critical question how these cells transform pB-ALL remains undefined. Here, we model a BCR-ABL<sup>p190</sup> state and show that limiting expression to hematopoietic...