ABSTRACT: WGBS files accompanying the paper titled "Identification of Therapeutic Targets in Rhabdomyosarcoma Through Integrated Genomic, Epigenomic, and Proteomic Analyses".
Project description:ChIP-Seq files accompanying the paper titled "Identification of Therapeutic Targets in Rhabdomyosarcoma Through Integrated Genomic, Epigenomic, and Proteomic Analyses".
Project description:ChIP-Seq files accompanying the paper titled "Identification of Therapeutic Targets in Rhabdomyosarcoma Through Integrated Genomic, Epigenomic, and Proteomic Analyses".
Project description:Whole Genome Sequencing files accompanying the paper titled "Structure and evolution of double minutes in diagnosis and relapse brain tumors". Please read the paper for more details.
Project description:Our paper presents the results of a study in which we used whole genome bisulfite sequencing (WGBS) and RNA-Seq (i.e. transcriptomics) to examine the long-term epigenomic dynamics of an experimenta evolution study under high CO2 in the marine cyanobacterium Trichodesmium. We identify m5C methylated sites that rapidly change in response to short-term high CO2 exposure, which are then maintained for 4.5 years even after adaptation (i.e. trait canalization). After 7 years of CO2 selection, high-CO2 triggered methylation levels return to ancestral, low-CO2 levels, consistent with genetic assimilation theory and observations in eukaryotic model systems. These data suggest a potential role for m5C methylation in prokaryotic trait canalization and identify genetic assimilation as an evolutionary mechanism of potential biogeochemical importance under global change factors.
Project description:RNA-Seq files accompanying the paper titled "Somatic Histone H3 Mutations in Diffuse Intrinsic Pontine Gliomas and Non-Brainstem Paediatric Glioblastomas".
Project description:Our paper presents the results of a study in which we used whole genome bisulfite sequencing (WGBS), RNA-Seq (i.e. transcriptomics), high-CO2 physiology experiments, and spatiotemporally separated samples isolated in situ (i.e. directly from the ocean) to examine the metabolic potential of genome-wide cytosine (5mC) methylation (i.e. epigenomics), its potential impacts to transcriptional dynamics under both present-day and future ocean acidification conditions, and its biogeographic conservation in the globally-significant, biogeochemically-critical marine cyanobacterium Trichodesmium.
Project description:WXS files for Zhang PanNBL paper titled "Pan-neuroblastoma analysis reveals age- and ROS-associated drivers and novel therapeutic targets"
Project description:Personalized cancer therapy based on the somatic mutations identified in patient tumors is becoming an increasingly emphasized approach to improve outcomes of patients with cancer. There are also examples of therapeutic vulnerabilities in cancer that result from changes in gene expression that are a direct or indirect result of tumor specific epigenetic perturbations. These genomic and epigenomic changes are ultimately manifest in the tumor proteome and phosphoproteome. In this study, we integrated genomic, epigenomic and proteomic data for rhabdomyosarcoma (RMS) to identify therapeutic vulnerabilities. RMS was selected for this analysis because RAS pathway mutations in rhabdomyosarcoma (RMS) are the most common potentially actionable lesions across pediatric solid tumors. The epigenomic data was useful for identifying deregulated developmental pathways in RMS including the WNT, HH, BMP, adenyl cyclase, p38/MAPK and PI3K pathways. Perturbations in those 6 myogenic signal transduction pathways were also evident in the proteome and phosphoteome data. In addition, the proteomic/phosphoproteomic data revealed that the cell cycle checkpoint, unfolded protein response and RB/E2F pathways were deregulated in RMS relative to normal muscle. Recent success targeting CDK4/6 and MEK in adult cancers with RAS mutations led us to test the value of these targets in RMS tumors. We also targeted the unfolded protein response pathway and cell cycle checkpoint pathway using molecular targeted therapeutics in orthotopic patient derived xenografts. Taken together, these data demonstrate the value of integrating epigenomic and proteomic data to identify tumor vulnerabilities that extend beyond somatic mutations identified in the genome.
