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welcomeWelcome to GliomalabWelcome to our Glioblastoma research laboratory
contactContact with GliomalabDo you want to contact us? Find where and how to contact
neurooncology/peopleWelcome to GliomalabKnow the people who is collaborating in our Glioblastoma research laboratory
neurooncology/publicationsPublications of Glioblastoma laboratoryList of publications produced by Gliomalab
neurooncology/fundingFunding of Glioblastoma Research laboratoryKnow who is financing Gliomalab research work
neurooncology/projectsProjects which Gliomablastoma laboratory is working onList of projects which Gliomalab have been working on along last years.
neurooncology/projects/targeting-egfrin-in-glioblastomaTargeting EGFR in gliomasEGFR is one of the most commonly amplifed and/or mutated genes in GB. Nevertheless, the attempts to cure this cancer targeting EGFR kinase activity have not been successful. As an example, we have tested the efficiency of dacomitinib (Pfizer), which has a strong inhibitory effect on the growth of EGFR-depending gliomas in mice (Zahonero et al., 2015). However, only few recurrent GB patients have benefited from dacomitinib treatment (SepĂșlveda et al., 2017).
neurooncology/projects/neuro-degenerative-genes-in-gliomasNeurodegenerative genes in gliomasThe global genomic analysis of different neurodegenerative diseases has evidenced the relevance of several common biological process like mitochondrial alterations, inflammation and transcriptional or proteosomal malfunctioning in pathologies like Alzheimer, Parkinson and ALS (Amyotrophic lateral sclerosis). In addition, it has been recently described a co-morbidity of Alzheimer disease and GB, which has also been associated with common mitochondrial modifications. In this line of thought, we have performed a comprehensive study of the expression in gliomas of several genes associated with Alzheimer (APP, Tau (MAPT), PSEN1, PSEN2, APOE4 y GSK3B), Parkinson (GBA, LRRK2, PARK2, PARK7, PINK1, SNCA (alpha-Synuclein) y UCHL1), and ALS (C90RF72, TARDBP, SOD1, APB, FUS, UBQLN2, y HNRNPA2B1). From all these genes, TAU (MAPT) is the most significantly deregulated genes in the three parameters: tumor expression, histological grade and survival.
neurooncology/projects/glioma-genotype-neo-vascular-fitnessGlioma genotype determines neo-vascular fitnessThe tumor microenvironment (TME) contains endothelial cells, pericytes, fibroblasts, and immune cells, which can contribute to the growth and to the resistance to therapies of different cancers. The TME in gliomas is particularly different from other cancers, both at the molecular level (the extracellular matrix, the glucose content), as well as at the cellular level, with the presence of microglia, astrocytes, neurons. Another important feature of glioma TME is the presence of the blood-brain-barrier (BBB), which impedes the entrance of many anti-tumor drugs. High grade gliomas are characterized by their abundant and aberrant vasculature, with disruption of the BBB and the appearance of frequent hemorrhages. Using several PDXs and mouse glioma cell lines, we have recently described that the status of EGFR determines the degree of vascular disruption and BBB leakage, which influences glioma growth and possibly the response of the tumors to different therapies.
neurooncology/projects/glioma-pericytes-tumor-progressionGlioma-derived pericytes in tumor progression and therapy resistanceGlioma-derived pericytes in tumor progression and therapy resistance.
neurooncology/projects/bioinformatics-applied-to-gliomasBioinformatics applied to gliomasWe have used a series of bioinformatics tools to stratify the pathology of gliomas. We are currently analyzing the global genomic expression using Bioconductor and Biostars in R, CIBERSORT for signature; cBioportal and xena-UCSC to identify mutations, deletions and CNV, in correlation with signature of expression or prominent genes in the pathology of gliomas. We are also studying that biological processes that are associated with different tumor markers or the tumor microenvironment, using the enriched biological processes. For this we use David 6.8 and GSEA analysis and Overlap analysis between sDEGs, then we combine these analyses in IVYGAP for Gene Selection and Anatomic Structures ISH for Enriched Genes, based on the specificity of their expression patterns in the 5 major anatomic structures of glioblastoma. Our final goal is to use different markers to establish cellular subpopulations within the heterogeneity of gliomas, to understand their biology, poor prognosis and therapeutic resistance.
hospital-12-de-octubre/umnoUMNO, Hospital 12 de OctubreThe Neurooncology Multidisciplinary Unit (UMNO), at Hospital 12 de Octubre, is formed by all the clinicians involved in the diagnosis and the treatment of brain tumors.
hospital-12-de-octubre/umno/peoplePeople, UMNO Hospital 12 de OctubrePeople, UMNO Hospital 12 de Octubre
hospital-12-de-octubre/umno/fundingFunding, UMNO, Hospital 12 de OctubreKnow who is financing Gliomalab research work in UMNO, Hospital 12 de Octubre