Peter Canoll

This paper develops a tumor-targeting engineered bacterium that improves therapeutic efficacy and safety in cancer treatment.

The paper uses single-nuclei RNA sequencing to analyze intracranial thrombi, identifying distinct cell populations and transcriptional changes, and inferring ligand-receptor interactions relevant to stroke.

This study examines the spatiotemporal myeloid response to chemotherapy in glioblastoma using multiple models, showing chemotherapy-induced genotoxic stress and inflammatory remodeling in myeloid cells.

This study identifies the MAPK/ERK pathway as a key regulator of glioma susceptibility to immune checkpoint blockade, showing it modulates interferon responses, T cell recruitment, and tumor-microglia interactions.

This study identifies ATAT1 as a therapeutic target in glioblastoma by showing its role in promoting tumor invasion, proliferation, and resistance, with potential for combination therapies.

This study identifies disrupted O-GalNAc glycosylation as a mechanism and biomarker for SLC35A2-associated epilepsy using mouse models and human tissue analysis.

This study shows that IDH1-mutant glioma cells are more sensitive to cysteine-methionine deprivation and ferroptosis inducers, and that IDH inhibitors enhance this sensitivity.

This paper presents a high-bandwidth, wireless brain-computer interface device capable of chronic recordings in animals, demonstrating reliable performance over weeks.

This study identifies genetic regulators of microglial inflammation in Alzheimer's disease using CRISPRi screens and scRNA-seq, revealing key genes that modulate inflammatory states and disease-relevant clusters.

This paper evaluates convection-enhanced delivery of dexamethasone in glioma models, showing reduced systemic toxicity and suppressed myeloid inflammation.

The paper introduces a proteomic tool to identify protein markers for human microglial states and validates their utility in purification and differentiation.

The paper uses single-cell data to identify factors regulating an Alzheimer's disease-related microglial signature and proposes a new analytic framework for microglial classification.

This paper identifies a natural antisense transcript that regulates Glut1 expression and demonstrates its therapeutic potential in Glut1 deficiency syndrome.

This study investigates how mTOR inhibition reverses glioma-induced changes in excitatory neurons, showing effects on mRNA, dendritic spines, and neuronal activity.

This paper introduces DEFND-seq, a method for jointly profiling DNA and RNA from individual nuclei, enabling analysis of gene expression with copy number and SNV associations.

This study identifies STAT3 as a key driver of resistance to spindle inhibitors in glioblastoma, showing that therapy-induced senescence contributes to drug resistance by promoting quiescence and secreting factors that induce quiescence in proliferating cells.

The paper introduces a novel AS analysis method, Semi-Q, to identify GBM-specific splicing events and shows that dysregulated splicing of cell migration-related genes contributes to tumor growth and invasiveness.

This study shows that PDGF-BB overexpression in p53 null OPCs increases H3K27me3 and promotes proliferation by altering transcription.

The paper identifies Topoisomerase I inhibitors as immunomodulators for Alzheimer's disease by characterizing their effects on human microglial subtypes in vitro and in a zebrafish model.

The paper introduces consensus scHPF, a method to identify robust gene signatures from scRNA-seq data, and applies it to discover cell type-specific drug responses in glioma.

The paper validates an RNA-based platform for predicting drug sensitivity in treatment-resistant cancers using patient-derived xenograft models and multi-protein therapies.

This study identifies nuclear architecture disruption as a mechanism underlying SARS-CoV-2 induced anosmia by analyzing human and hamster olfactory tissues.

This study shows that low oxygen levels promote proliferation of mouse oligodendrocyte progenitors, unlike rat OPCs, and identifies factors affecting their differentiation.

SCOPE-seq2 integrates single-cell imaging and RNA-seq with improved throughput and accuracy for analyzing human glioblastoma cells.

This study tracks glioma progression in mice, showing decreased neuronal synchrony, disrupted neurovascular coupling, and seizure-related hypoxia in infiltrated cortex.

The paper identifies four molecularly distinct glioblastoma subtypes using single-cell protein-activity analysis and shows drug sensitivity is state-dependent.

This paper introduces scHPF, a Bayesian method for discovering gene signatures from scRNA-seq without prior normalization, and finds spatially biased expression patterns in glioma regions linked to poor survival.

The paper introduces the ENDURES consortium to study extreme survivors of glioblastoma by integrating clinical data and creating patient-specific tumor models.