We strive to better understand how diverse members of the non-coding RNA family and their RNA binding protein partners, through their ability to modulate gene expression in the nucleus, contribute to immune pathologies in mouse models of colitis, multiple sclerosis, and cancers. Deeper understanding of how immune gene expression programs are controlled will facilitate development of new intervention strategies against inflammatory diseases.
Epigenomics and Gene Expression Control
The main objective of the Chavez laboratory is the molecular characterization of malignant childhood cancers in order to identify drug targets and improve treatment options. Our focus is mainly on pediatric brain tumors such as medulloblastoma, glioblastoma, and ependymoma. Recently, we have demonstrated how to leverage epigenetic information such as DNA methylation and enhancer profiling in pediatric brain tumors and normal human tissues to identify clinically relevant tumor subgroups, oncogenic enhancers, transcription factors, and pathways amenable to pharmacologic targeting. To reveal regulatory circuitries disturbed in childhood brain tumors, we generate and integrate public high-dimensional data from primary tumors and patient-derived cell lines. We are specifically interested in the analysis of somatic and germline DNA mutations, chromatin and DNA modifications, transcription factor binding, and gene expression.
Our lab applies our expertise in human pluripotent stem cell research and genomics to understand the molecular mechanisms underlying normal and abnormal human development, in order to improve the health of mothers and babies.
We are interested in the analysis and modeling of the three-dimensional chromatin structure from high-throughput sequencing experiments. We develop methods that are based in statistics, machine learning, optimization and graph theory to understand how changes in the 3D genome affect cellular outcome such as development, differentiation and gene expression. We have ongoing interests in the systems level analysis and reconstruction of regulatory networks, inference of enhancer-promoter contacts, predictive models of gene expression and integration of three-dimensional chromatin structure with one-dimensional epigenetic measurements in the context of cancer, malaria, asthma and several autoimmune diseases.