Russell O. Pieper

EPCO-39. CLARIFYING THE MOLECULAR CONSEQUENCES OF ONCOGENIC MUTATIONS THROUGH MULTISCALE AND MULTIOMIC ANALYSIS OF INDIVIDUAL TUMORS

Metabolic imaging detects elevated glucose flux through the pentose phosphate pathway associated with TERT expression in low-grade gliomas

PI3K/mTOR inhibition of IDH1 mutant glioma leads to reduced 2HG production that is associated with increased survival

Mutant and Wild-Type Isocitrate Dehydrogenase 1 Share Enhancing Mechanisms Involving Distinct Tyrosine Kinase Cascades in Cancer

Mutant IDH1 Cooperates with ATRX Loss to Drive the Alternative Lengthening of Telomere Phenotype in Glioma

Rapid Conversion of Mutant IDH1 from Driver to Passenger in a Model of Human Gliomagenesis

UBE2S, a novel substrate of Akt1, associates with Ku70 and regulates DNA repair and glioblastoma multiforme resistance to chemotherapy

Mutant IDH1 Expression Drives <i>TERT</i> Promoter Reactivation as Part of the Cellular Transformation Process

<i>IDH1</i> Mutation Induces Reprogramming of Pyruvate Metabolism

Metabolic Reprogramming in Mutant IDH1 Glioma Cells

Hyperpolarized [1-13C] Glutamate: A Metabolic Imaging Biomarker of IDH1 Mutational Status in Glioma

Mutant IDH1-Driven Cellular Transformation Increases RAD51-Mediated Homologous Recombination and Temozolomide Resistance

Glioma Cells with the IDH1 Mutation Modulate Metabolic Fractional Flux through Pyruvate Carboxylase

Changes in Pyruvate Metabolism Detected by Magnetic Resonance Imaging Are Linked to DNA Damage and Serve as a Sensor of Temozolomide Response in Glioblastoma Cells

Non-invasive in vivo assessment of IDH1 mutational status in glioma

Pyruvate Kinase M2 Expression, but Not Pyruvate Kinase Activity, Is Up-Regulated in a Grade-Specific Manner in Human Glioma

Sensitivity of Glioblastomas to Clinically Available MEK Inhibitors Is Defined by Neurofibromin 1 Deficiency