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Pavithra Viswanath, PhD
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Publications
Pavithra Viswanath, PhD's Publications
Combined inhibition of de novo glutathione and nucleotide biosynthesis is synthetically lethal in glioblastoma.
Lactylation fuels nucleotide biosynthesis and facilitates deuterium metabolic imaging of tumor proliferation in H3K27M-mutant gliomas.
The 1p/19q co-deletion induces targetable and imageable vulnerabilities in glucose metabolism in oligodendrogliomas.
Understanding and imaging PHGDH-driven intrinsic resistance to mutant IDH inhibition in gliomas.
GABA production induced by imipridones is a targetable and imageable metabolic alteration in diffuse midline gliomas.
Hyperpolarized δ-[1- 13C]gluconolactone imaging visualizes response to TERT or GABPB1 targeting therapy for glioblastoma.
Imaging telomerase reverse transcriptase expression in oligodendrogliomas using hyperpolarized δ-[1-13C]-gluconolactone.
Telomerase reverse transcriptase induces targetable alterations in glutathione and nucleotide biosynthesis in glioblastomas.
A 13C/31P surface coil to visualize metabolism and energetics in the rodent brain at 3 Tesla.
Deuterium magnetic resonance spectroscopy enables noninvasive metabolic imaging of tumor burden and response to therapy in low-grade gliomas.
Deuterium Metabolic Imaging Reports on TERT Expression and Early Response to Therapy in Cancer.
Imaging biomarkers of TERT or GABPB1 silencing in TERT-positive glioblastoma.
Acquisition and quantification pipeline for in vivo hyperpolarized 13 C MR spectroscopy.
Deuterium Metabolic Imaging-Rediscovery of a Spectroscopic Tool.
Early Noninvasive Metabolic Biomarkers of Mutant IDH Inhibition in Glioma.
Imaging 6-Phosphogluconolactonase Activity in Brain Tumors In Vivo Using Hyperpolarized δ-[1-13C]gluconolactone.
Metabolic imaging detects elevated glucose flux through the pentose phosphate pathway associated with TERT expression in low-grade gliomas.
Non-invasive assessment of telomere maintenance mechanisms in brain tumors.
Ferronostics: Measuring Tumoral Ferrous Iron with PET to Predict Sensitivity to Iron-Targeted Cancer Therapies.
Glutamate Is a Noninvasive Metabolic Biomarker of IDH1-Mutant Glioma Response to Temozolomide Treatment.
In vivo detection of γ-glutamyl-transferase up-regulation in glioma using hyperpolarized γ-glutamyl-[1-13C]glycine.
MR-detectable metabolic biomarkers of response to mutant IDH inhibition in low-grade glioma.
In vivo investigation of hyperpolarized [1,3-13C2]acetoacetate as a metabolic probe in normal brain and in glioma.
PI3K/mTOR inhibition of IDH1 mutant glioma leads to reduced 2HG production that is associated with increased survival.
2-Hydroxyglutarate-Mediated Autophagy of the Endoplasmic Reticulum Leads to an Unusual Downregulation of Phospholipid Biosynthesis in Mutant IDH1 Gliomas.
HDAC inhibition in glioblastoma monitored by hyperpolarized 13 C MRSI.
Mutant IDH1 gliomas downregulate phosphocholine and phosphoethanolamine synthesis in a 2-hydroxyglutarate-dependent manner.
Clonal expansion and epigenetic reprogramming following deletion or amplification of mutant IDH1.
Development of a rapid and reliable assay for in vitro determination of compound cidality against the asexual stages of Plasmodium falciparum.
Hyperpolarized (13)C MR imaging detects no lactate production in mutant IDH1 gliomas: Implications for diagnosis and response monitoring.
Molecular Imaging of Metabolic Reprograming in Mutant IDH Cells.
Mutant IDH1 Expression Drives TERT Promoter Reactivation as Part of the Cellular Transformation Process.
Mutant IDH1 expression is associated with down-regulation of monocarboxylate transporters.
Rapid Conversion of Mutant IDH1 from Driver to Passenger in a Model of Human Gliomagenesis.
IDH1 Mutation Induces Reprogramming of Pyruvate Metabolism.
Metabolic reprogramming in mutant IDH1 glioma cells.
Metabolic reprogramming of pyruvate dehydrogenase is essential for the proliferation of glioma cells expressing mutant IDH1.
Triaminopyrimidine is a fast-killing and long-acting antimalarial clinical candidate.
Aminoazabenzimidazoles, a novel class of orally active antimalarial agents.
Repositioning: the fast track to new anti-malarial medicines?