Publicaciones en colaboración con investigadores/as de Instituto de Biología Molecular y Celular del Cáncer de Salamanca / Centro de Investigación del Cáncer (13)

2023

  1. Immune stress suppresses innate immune signaling in preleukemic precursor B-cells to provoke leukemia in predisposed mice

    Nature Communications, Vol. 14, Núm. 1

2022

  1. Transient Inhibition of the JAK/STAT Pathway Prevents B-ALL Development in Genetically Predisposed Mice

    Cancer research, Vol. 82, Núm. 6, pp. 1098-1109

2020

  1. An intact gut microbiome protects genetically predisposed mice against leukemia

    Blood, Vol. 136, Núm. 18, pp. 2003-2017

  2. Inhibition of inflammatory signaling in Pax5 mutant cells mitigates B-cell leukemogenesis

    Scientific Reports, Vol. 10, Núm. 1

2019

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

    Leukemia, Vol. 33, Núm. 1, pp. 249-278

  2. Infectious stimuli promote malignant B-cell acute lymphoblastic leukemia in the absence of AID

    Nature Communications, Vol. 10, Núm. 1

2018

  1. Lmo2 expression defines tumor cell identity during T-cell leukemogenesis

    EMBO Journal, Vol. 37, Núm. 14

  2. Loss of Pax5 exploits sca1-BCR-ABLp190 susceptibility to confer the metabolic shift essential for pB-ALL

    Cancer Research, Vol. 78, Núm. 10, pp. 2669-2679

  3. Supplementary data for the biological age linked to oxidative stress modifies breast cancer aggressiveness

    Data in Brief

2017

  1. Infection exposure promotes ETV6-RUNX1 precursor B-cell leukemia via impaired H3K4 demethylases

    Cancer Research, Vol. 77, Núm. 16, pp. 4365-4377

2015

  1. Infection exposure is a causal factor in B-cell precursor acute lymphoblastic leukemia as a result of Pax5-inherited susceptibility

    Cancer Discovery, Vol. 5, Núm. 12, pp. 1328-1343

2012

  1. A novel molecular mechanism involved in multiple myeloma development revealed by targeting MafB to haematopoietic progenitors

    EMBO Journal, Vol. 31, Núm. 18, pp. 3704-3717

2010

  1. Cancer as a reprogramming-like disease: Implications in tumor development and treatment

    Seminars in Cancer Biology, Vol. 20, Núm. 2, pp. 93-97