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Biology subjects

Schürer, S.

Publications and source records attributed to Schürer, S..

3 recordsLinked to original sources

Drug and single-cell gene expression integration identifies sensitive and resistant glioblastoma cell populations

Glioblastoma (GBM) remains the most common and lethal adult malignant primary brain cancer with few treatment options. A significant issue hindering GBM therapeutic development is intratumor heterogeneity. GBM tumors contain neoplastic cells within a spectrum of different transcriptional states. Identifying effective therapeutics requires a platform that predicts the differential sensitivity and resistance of these states to various treatments. Here, we developed a novel framework, ISOSCELES (Inferred cell Sensitivity Operating on the integration of Single-Cell Expression and L1000 Expression Signatures), to quantify the cellular drug sensitivity and resistance landscape. Using single-cell RNA sequencing of newly diagnosed and recurrent GBM tumors, we identified compounds from the LINCS L1000 database with transcriptional response signatures selectively discordant with distinct GBM cell states. We validated the significance of these findings in vitro, ex vivo, and in vivo, and identified a novel combination of an OLIG2 inhibitor and Depatux-M for GBM. Our studies suggest that ISOSCELES identifies cell states sensitive and resistant to targeted therapies in GBM and that it can be applied to identify new synergistic combinations. HighlightsO_LIIntegration of GBM single-cell RNA sequencing data with L1000-derived drug response signatures facilitates clustering of tumor cells and small molecules on cell-drug connectivity. C_LIO_LICell-drug connectivity predicts the identities of drug-sensitive and resistant cell states. C_LIO_LIIn silico perturbation analysis using cell-drug connectivity predicts drug-induced changes in the cell-drug connectivity landscape in vivo. C_LIO_LIIn silico perturbation analysis to predict drug-induced changes in the tumor cell-drug connectivity landscape predicts drug combinations that synergize in vivo to extend survival. C_LI

cancer biology↗

Multiplex-inhibitor bead mass spectrometry reveals differential kinome signatures in newly diagnosed and recurrent glioblastoma

Glioblastoma (GBM) is the most common and aggressive adult brain tumor. Despite years of research, clinical trials have not improved the outcome for GBM. Standard of care for newly diagnosed GBM includes surgical resection, followed by radiation and chemotherapy. Tumor recurrence is inevitable and since most patients are not candidates for a second surgical resection, there is an urgent need to identify resistance mechanisms that arise in recurrent GBM. We postulated that examining the differences of activated kinases between newly diagnosed and recurrent GBM may provide insight to resistance mechanisms. To map the kinome landscape of newly diagnosed (nGBM) and recurrent GBM (rGBM) patient derived xenograft tumors, we used Multiplexed Inhibitor Beads and Mass Spectrometry (MIB-MS). We performed pathway analysis of kinases that differed in MIB-binding between nGBM and rGBM to identify kinase-driven signaling pathways. We also analyzed transcriptional profiles to determine the overlap in signaling pathways seen using proteomics or transcriptomics. Using MIB-MS kinome profiling, we found key differences in kinase-driven signaling pathways that may account for the increase in aggressive behavior seen in recurrent GBM. This included a shift in pathways driving cell invasion and proliferation, as well as upregulation of signaling pathways that drive GBM stem-cell like cell differentiation. Analysis of RNA-sequencing showed no statistically significant differences between enriched gene ontologies in nGBM and rGBM, demonstrating the importance of MIB-MS kinome profiling. Collectively, these studies suggest that kinome profiling may inform future clinical trials for kinase inhibitors in GBM.

cancer biology↗

Proteomic cellular signatures of kinase inhibitor-induced cardiotoxicity: Mount Sinai DToxS LINCS Center Dataset

The Drug Toxicity Signature Generation Center (DToxS) at the Icahn School of Medicine at Mount Sinai is one of the centers of the NIH Library of Integrated Network-Based Cellular Signatures (LINCS) program. A key aim of DToxS is to generate both proteomic and transcriptomic signatures that can predict adverse effects, especially cardiotoxicity, of kinase inhibitors approved by the Food and Drug Administration. Towards this goal, high throughput shot-gun proteomics experiments (317 cell line/drug combinations + 64 control lysates) have been conducted at the Center for Advanced Proteomics Research at Rutgers University - New Jersey Medical School. Using computational network analyses, these proteomic data can be integrated with transcriptomic signatures generated in tandem to identify cellular signatures of cardiotoxicity that may predict kinase inhibitor-induced toxicity and possible mitigation. Both raw and processed proteomics data have been carefully screened for quality and made publicly available via the PRIDE database. As such, this broad protein kinase inhibitor-stimulated cardiomyocyte proteomic data and signature set is valuable for the prediction of drug toxicities. Links to: Metadata Tables O_TBL View this table: org.highwire.dtl.DTLVardef@1cda9f8org.highwire.dtl.DTLVardef@1520e05org.highwire.dtl.DTLVardef@16a35borg.highwire.dtl.DTLVardef@3ee6e7org.highwire.dtl.DTLVardef@1a98664_HPS_FORMAT_FIGEXP M_TBL C_TBL

pharmacology and toxicology↗