Evidence map›Paper›PMID 41863390›Full record

ArticleNeuro-oncology2026

1p/19q codeletion induces targetable and imageable vulnerabilities in glucose metabolism in oligodendrogliomas.

Suresh Udutha, Georgios Batsios, Céline Taglang, Anne Marie Gillespie, Pavithra Viswanath

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Article in Neuro-oncology, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 1 paper.

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1citing papers in PubMed
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1 · What the graph read from it

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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.

2 · The registry

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3 · Its place in the literature

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1 citing paper in PubMed.

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4 · The record

Corrections and comments

5 · Who and what money

Authors and funding

5 authors.

Suresh UduthaDepartment of Radiology and Biomedical Imaging, University of California San Francisco, San Francisco, CA, USA.ORCID 0000-0003-3542-8245
Georgios BatsiosDepartment of Radiology and Biomedical Imaging, University of California San Francisco, San Francisco, CA, USA.ORCID 0000-0002-2340-1486
Céline TaglangDepartment of Radiology and Biomedical Imaging, University of California San Francisco, San Francisco, CA, USA.ORCID 0000-0002-3927-6675
Anne Marie GillespieDepartment of Radiology and Biomedical Imaging, University of California San Francisco, San Francisco, CA, USA.ORCID 0000-0003-4279-3961
Pavithra ViswanathDepartment of Radiology and Biomedical Imaging, University of California San Francisco, San Francisco, CA, USA.ORCID 0000-0003-2980-3109

Funding

Targeting metabolic vulnerabilities induced by the 1p19q codeletion in oligodendrogliomasR21CA277325 · NCI · UNIVERSITY OF CALIFORNIA, SAN FRANCISCO · PI VISWANATH, PAVITHRA · 2023 to 2024
$404k
Gianna Rae Meadows Fund for the Oligodendroglioma CureNCI NIH HHS R21 CA277325NIH HHS R21CA277325
6 · The paper itself

Abstract

backgroundThe 1p/19q codeletion is a hallmark of oligodendrogliomas. The goal of this study was to exploit the metabolic vulnerabilities induced by the 1p/19q codeletion for the treatment and imaging of oligodendrogliomas.

methodsWe used stable isotope tracing, mass spectrometry, and genetic and pharmacological approaches to interrogate [U-13C]-glucose metabolism in patient-derived oligodendroglioma models (SF10417, BT88, BT54, TS603, NCH612). We examined whether tracing [6,6'-2H]-glucose metabolism using deuterium metabolic imaging (DMI) provided an early readout of treatment response.

resultsThe glycolytic enzyme enolase 1 (ENO1; chromosome 1p36.23) was downregulated in patient-derived oligodendroglioma cells and patient tissue due to the 1p/19q codeletion and histone hypermethylation. Conversely, inactivation of the CIC transcriptional repressor, driven by activated mitogen-activated protein kinase (MAPK) signaling, upregulated the ENO2 isoform specifically in oligodendrogliomas. Genetic ablation of ENO2 or pharmacological inhibition using POMHEX inhibited proliferation with nanomolar potency but was not cytotoxic to oligodendroglioma cells. Mechanistically, ENO2 loss abrogated [U-13C]-glucose metabolism to lactate but shunted glucose toward biosynthesis of serine and purine nucleotides, an effect that was driven by the rate-limiting enzyme for serine synthesis, phosphoglycerate dehydrogenase (PHGDH). Importantly, combining the PHGDH inhibitor D8 with POMHEX resulted in synthetic lethality in vitro and induced tumor regression in vivo. Furthermore, DMI of lactate production from [6,6'-2H]-glucose provided an early readout of response to combination therapy that preceded MRI-detectable alterations and reflected extended survival.

conclusionsWe have identified ENO2 and PHGDH as metabolic vulnerabilities induced by the 1p/19q codeletion in oligodendrogliomas and [6,6'-2H]-glucose as a noninvasive tracer of early response to therapy.

Indexed as

Brain NeoplasmsChromosome DeletionChromosomes, Human, Pair 1Chromosomes, Human, Pair 19GlucoseOligodendrogliomaAnimalsDNA-Binding ProteinsHumansMicePhosphopyruvate HydrataseRepressor ProteinsTumor Suppressor ProteinsCIC protein, humanDNA-Binding ProteinsENO1 protein, humanGlucosePhosphopyruvate HydrataseRepressor ProteinsTumor Suppressor Proteinsdeuterium metabolic imagingENO2oligodendrogliomaPHGDHserine biosynthesis

Identifiers

PMID41863390
PMCPMC13179595

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Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.