A5085139761- Neutrophil, Myeloperoxidase and Oxidative Mechanisms
- Telomeres, Telomerase, and Senescence
- Cancer Immunotherapy and Biomarkers
- Cytomegalovirus and herpesvirus research
- Immune cells in cancer
- Immunotherapy and Immune Responses
- Nanoplatforms for cancer theranostics
- RNA modifications and cancer
- Epigenetics and DNA Methylation
- interferon and immune responses
- Single-cell and spatial transcriptomics
- Cancer Cells and Metastasis
- Phagocytosis and Immune Regulation
- Cancer Genomics and Diagnostics
- Genomics and Phylogenetic Studies
- CRISPR and Genetic Engineering
- Bioinformatics and Genomic Networks
- Pluripotent Stem Cells Research
- Gene expression and cancer classification
- Genomics and Chromatin Dynamics
- RNA and protein synthesis mechanisms
- Hippo pathway signaling and YAP/TAZ
- Skin Protection and Aging
- Gene Regulatory Network Analysis
- RNA Research and Splicing
Institute for Research in Biomedicine
2016-2025
Barcelona Institute for Science and Technology
2018-2023
Institute of Science and Technology
2022
Institute for Research in Biomedicine
2020
Ludwig-Maximilians-Universität München
2014-2015
University of Warwick
2014-2015
LMU Klinikum
2015
Universitat Politècnica de Catalunya
2011
Memorial Sloan Kettering Cancer Center
2009-2010
Leipzig University
2010
The human genome encodes hundreds of transfer RNA (tRNA) genes but their individual contribution to the tRNA pool is not fully understood. Deep sequencing transcripts (tRNA-Seq) can estimate abundance at single gene resolution, structures and posttranscriptional modifications impair these analyses. Here we present a bioinformatics strategy investigate differential expression use it compare tRNA-Seq datasets from cultured cells brain. We find that caveats affect quantitation only subset...
The expression of the pluripotency factors OCT4, SOX2, KLF4, and MYC (OSKM) can convert somatic differentiated cells into pluripotent stem in a process known as reprogramming. Notably, partial reversible reprogramming does not change cell identity but reverse markers aging cells, improve capacity aged mice to repair tissue injuries, extend longevity progeroid mice. However, little is about mechanisms involved. Here, we have studied changes DNA methylome, transcriptome, metabolome naturally...
Abstract Fibrogenesis is part of a normal protective response to tissue injury that can become irreversible and progressive, leading fatal diseases. Senescent cells are main driver fibrotic diseases through their secretome, known as senescence-associated secretory phenotype (SASP). Here, we report cellular senescence, multiple types in mice humans characterized by the accumulation iron. We show vascular hemolytic injuries efficient triggering iron accumulation, which turn cause senescence...
Abstract Chemotherapy often generates intratumoral senescent cancer cells that strongly modify the tumor microenvironment, favoring immunosuppression and growth. We discovered, through an unbiased proteomics screen, immune checkpoint inhibitor programmed cell death 1 ligand 2 (PD-L2) is highly upregulated upon induction of senescence in different types cells. PD-L2 not required for to undergo senescence, but it critical evade system persist intratumorally. Indeed, after chemotherapy,...
Human cancer is caused by the accumulation of genetic alterations in cells. Of special importance are changes that occur early during malignant transformation because they may result oncogene addiction and represent promising targets for therapeutic intervention. Here we describe a computational approach, called Retracing Evolutionary Steps Cancer (RESIC), to deduce temporal sequence events tumorigenesis from cross-sectional genomic data tumors at their fully transformed stage. When applied...
The analysis of stem cell hierarchies in human cancers has been hampered by the impossibility identifying or tracking tumor populations an intact environment. To overcome this limitation, we devised a strategy based on editing genomes patient-derived organoids using CRISPR/Cas9 technology to integrate reporter cassettes at desired marker genes. As proof concept, engineered colorectal cancer (CRC) that carry EGFP and lineage-tracing knocked LGR5 locus. Analysis LGR5-EGFP+ cells isolated from...
Abstract Transient reprogramming by the expression of OCT4, SOX2, KLF4 and MYC (OSKM) is a therapeutic strategy for tissue regeneration rejuvenation, but little known about its metabolic requirements. Here we show that OSKM in mice causes global depletion vitamin B 12 molecular hallmarks methionine starvation. Supplementation with increases efficiency both cultured cells, latter indicating cell-intrinsic effect. We epigenetic mark H3K36me3, which prevents illegitimate initiation...
The escape of mitochondrial double-stranded dsRNA (mt-dsRNA) into the cytosol has been recently linked to a number inflammatory diseases. Here, we report that release mt-dsRNA is general feature senescent cells and critical driver their secretome, known as senescence-associated secretory phenotype (SASP). Inhibition RNA polymerase, sensors RIGI MDA5, or master signaling protein MAVS, all result in reduced expression SASP, while broadly preserving other hallmarks senescence. Moreover, are...
Abstract Background Surprisingly little is known about the organization and distribution of tRNA genes tRNA-related sequences on a genome-wide scale. While gene complements are usually reported in passing as part genome annotation efforts, peculiar features such tandem arrangements Entamoeba histolytica have been described some detail, systematic comparative studies rare mostly restricted to bacteria. We therefore set out survey genomic arrangement pseudogenes wide range eukaryotes identify...
Abstract The human transcriptome contains thousands of small open reading frames (sORFs) that encode microproteins whose functions remain largely unexplored. Here, we show TINCR lncRNA encodes pTINCR, an evolutionary conserved ubiquitin-like protein (UBL) expressed in many epithelia and upregulated upon differentiation under cellular stress. By gain- loss-of-function studies, demonstrate pTINCR is a key inducer epithelial vitro vivo. Interestingly, low expression associates with worse...
Resistance of melanoma to targeted therapy and immunotherapy is linked metabolic rewiring. Here, we show that increased fatty acid oxidation (FAO) during prolonged BRAF inhibitor (BRAFi) treatment contributes acquired resistance in mice. Targeting FAO using the US Food Drug Administration-approved European Medicines Agency-approved anti-anginal drug ranolazine (RANO) delays tumour recurrence with BRAFi resistance. Single-cell RNA-sequencing analysis reveals RANO diminishes abundance...