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Publications

  • Exploiting combinatorial patterns in cancer genomic data for personalized therapy and new target discovery
  • Comprehensive pharmacogenomic profiling of malignant pleural mesothelioma identifies a subgroup sensitive to FGFR inhibition.
  • Multilevel models improve precision and speed of IC50 estimates.
  • Integrated transcriptomic and proteomic analysis identifies protein kinase CK2 as a key signaling node in an inflammatory cytokine network in ovarian cancer cells.
  • Unravelling druggable signalling networks that control F508del-CFTR proteostasis.
  • A Landscape of Pharmacogenomic Interactions in Cancer.
  • E-MTAB-3610 - Transcriptional Profiling of 1,000 human cancer cell lines
  • Prospective derivation of a living organoid biobank of colorectal cancer patients.
  • Functional impact of genomic complexity on the transcriptome of Multiple Myeloma.
  • A CRISPR Dropout Screen Identifies Genetic Vulnerabilities and Therapeutic Targets in Acute Myeloid Leukemia
  • Integrative analysis of pharmacogenomics in major cancer cell line databases using CellMinerCDB
  • Unsupervised correction of gene-independent cell responses to CRISPR-Cas9 targeting.
  • The germline genetic component of drug sensitivity in cancer cell lines
  • Loss of functional BAP1 augments sensitivity to TRAIL in cancer cells.
  • Transcription factor activities enhance markers of drug sensitivity in cancer.
  • Pathway-based dissection of the genomic heterogeneity of cancer hallmarks’ acquisition with SLAPenrich
  • GDSCTools for Mining Pharmacogenomic Interactions in Cancer.
  • CELLector: Genomics-Guided Selection of Cancer In Vitro Models.
  • Drug repurposing: progress, challenges and recommendations.
  • Identification of Intrinsic Drug Resistance and Its Biomarkers in High-Throughput Pharmacogenomic and CRISPR Screens
  • Analysis of CRISPR‐Cas9 screens identifies genetic dependencies in melanoma
  • Agreement between two large pan-cancer CRISPR-Cas9 gene dependency data sets
  • Drug mechanism-of-action discovery through the integration of pharmacological and CRISPR screens.
  • Structural rearrangements generate cell-specific, gene-independent CRISPR-Cas9 loss of fitness effects.
  • Cancer research needs a better map.
  • CellMinerCDB for Integrative Cross-Database Genomics and Pharmacogenomics Analyses of Cancer Cell Lines.
  • CELLector: Genomics Guided Selection of Cancer in vitro Models
  • Logic models to predict continuous outputs based on binary inputs with an application to personalized cancer therapy.
  • Characterizing Mutational Signatures in Human Cancer Cell Lines Reveals Episodic APOBEC Mutagenesis.
  • JACKS: joint analysis of CRISPR/Cas9 knockout screens.
  • Minimal genome-wide human CRISPR-Cas9 library.
  • Prioritization of cancer therapeutic targets using CRISPR-Cas9 screens.
  • Project Score database: a resource for investigating cancer cell dependencies and prioritizing therapeutic targets.
  • Computational estimation of quality and clinical relevance of cancer cell lines
  • Reduced gene templates for supervised analysis of scale-limited CRISPR-Cas9 fitness screens
  • Combinatorial CRISPR screen identifies fitness effects of gene paralogues
  • Integrated cross-study datasets of genetic dependencies in cancer.
  • CoRe: a robustly benchmarked R package for identifying core-fitness genes in genome-wide pooled CRISPR-Cas9 screens
  • Redefining false discoveries in cancer data analyses
  • BRAF inhibitor resistance mediated by the AKT pathway in an oncogenic BRAF mouse melanoma model.
  • Identification of drug-specific pathways based on gene expression data: application to drug induced lung injury.
  • A Semi-Supervised Approach for Refining Transcriptional Signatures of Drug Response and Repositioning Predictions.
  • Blood transcriptomics of drug-naive sporadic Parkinson's disease patients.
  • Pharmacogenomic agreement between two cancer cell line data sets.
  • Transcriptional response networks for elucidating mechanisms of action of multitargeted agents.
  • Hemopoietic-specific Sf3b1-K700E knock-in mice display the splicing defect seen in human MDS but develop anemia without ring sideroblasts
  • Efficient randomization of biological networks while preserving functional characterization of individual nodes
  • Stem cell-like transcriptional reprogramming mediates metastatic resistance to mTOR inhibition.
  • Genome-wide chemical mutagenesis screens allow unbiased saturation of the cancer genome and identification of drug resistance mutations.
  • Functional linkage of gene fusions to cancer cell fitness assessed by pharmacological and CRISPR-Cas9 screening.
  • Systematic identification of genomic markers of drug sensitivity in cancer cells
  • A screen for combination therapies in BRAF/NRAS wild type melanoma identifies nilotinib plus MEK inhibitor as a synergistic combination
  • Artificial neural network analysis of circulating tumor cells in metastatic breast cancer patients
  • A Yeast Synthetic Network for In Vivo Assessment of Reverse-Engineering and Modeling Approaches
  • Interactive data analysis and clustering of genomic data
  • Identifying network of drug mode of action by gene expression profiling
  • Transcriptional gene network inference from a massive dataset elucidates transcriptome organization and gene function
  • NIRest: A tool for gene network and mode of action inference
  • Gene ontology fuzzy-enrichment analysis to investigate drug mode-of-action
  • Transcriptional data: A new gateway to drug repositioning?
  • DvD: An R/Cytoscape pipeline for drug repurposing using public repositories of gene expression data
  • Cancer develops, progresses and responds to therapies through restricted perturbation of the protein-protein interaction network.
  • Heterogeneity of genomic evolution and mutational profiles in multiple myeloma.
  • Network based elucidation of drug response: from modulators to targets.
  • Fast randomization of large genomic datasets while preserving alteration counts.
  • Machine learning prediction of cancer cell sensitivity to drugs based on genomic and chemical properties.
  • Phosphoproteomics data classify hematological cancer cell lines according to tumor type and sensitivity to kinase inhibitors.
  • Identification of small molecules enhancing autophagic function from drug network analysis.
  • Discovery of drug mode of action and drug repositioning from transcriptional responses.
  • An interactive web application for processing, correcting, and visualizing genome-wide pooled CRISPR-Cas9 screens
  • A heuristic algorithm solving the mutual-exclusivity-sorting problem
  • Benchmark Software and Data for Evaluating CRISPR-Cas9 Experimental Pipelines Through the Assessment of a Calibration Screen
  • RAGE engagement by SARS-CoV-2 enables monocyte infection and underlies COVID-19 severity.
  • Highlights from the 1st European cancer dependency map symposium and workshop.
  • A comprehensive clinically informed map of dependencies in cancer cells and framework for target prioritization

Francesco Iorio's public data