Líneas de investigación

  • 1-Cancer Stem Cells and Cell Plasticity in Cancer

    Cell plasticity predisposes cells to malignant transformation. Tumor cells lose their previously normal identity and function and, through a cellular plasticity program, acquire a dedifferentiated phenotype. Our group investigates the regulation of gene expression in cancer stem and somatic cells in the tumor and in immune cells of the microenvironment during tumor initiation and progression.

  • 2-Stem Cells, Cell Differentiation and Tissue Regeneration

    Normal cells and tissues are continuously adapting themselves to exogenous challenges. Stem cell plasticity is central to the adaptation and regeneration responses to pathophysiological conditions and injury. Our group investigates the regulation of gene expression in response to stress (muscle atrophy) and tissue damage (muscular dystrophies) with the goal of identifying new approaches to promote tissue adaptation and regeneration by normal stem cells.

  • 3-Cell Plasticity in Immune Cells during Inflammation in Tissue Regeneration and Cancer

    Inflammation has positive and negative functions. On the one hand, inflammation is a normal response of the body to infections and injury. The migration of immune cells into the inflamed tissue is a requisite for the subsequent regeneration of injured tissues. Our group investigates how the acquisition of a cell plasticity program endows macrophages with an anti-inflammatory and pro-regenerative phenotype in acutely and chronically (muscular dystrophies) injured tissues. On the other hand, chronic inflammation is at the root of many diseases, including cancer.

    Our group investigates the role of cell plasticity in linking chronic inflammation and cancer. We investigate the mechanisms by which chronic inflammation induces lesions in the DNA of cells and, at the same time, inhibits our own body's self-repair mechanisms. In addition, we also investigate how cues from immune cells in the tumor microenvironment can either reinforce or revert the dedifferentiated phenotype of tumor cells.