Evidence map›Paper›PMID 40319462›Full record

ArticleNeuro-oncology2025

Multiomic profiling of glioblastoma metabolic lesions reveals complex intratumoral genomic evolution and dipeptidase-1-driven vascular proliferation.

Atul Anand, Jeanette Krogh Petersen, Lars van Brakel Andersen, Mark Burton, Clara Rosa Levina Oudenaarden, Martin Jakob Larsen, Philip Ahle Erichsen, Christian Bonde Pedersen, Frantz Rom Poulsen, Peter Grupe and 3 more

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Article in Neuro-oncology, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. An erratum has been issued. Cited by 2 papers.

0numbers the graph read from it
0cells of the map it votes in
2citing papers in PubMed
–field-weighted citation impact
1 · What the graph read from it

What it found

Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.

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

The trial behind it

Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.

Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.

3 · Its place in the literature

Who cites it

2 citing papers in PubMed.

  1. Article
  2. Review
4 · The record

Corrections and comments

5 · Who and what money

Authors and funding

13 authors.

Atul AnandDepartment of Pathology, The Bartholin Institute, Rigshospitalet, Copenhagen University Hospital, Copenhagen, Denmark.ORCID 0000-0001-7474-5433
Jeanette Krogh PetersenDepartment of Pathology, Odense University Hospital, Odense, Denmark.
Lars van Brakel AndersenClinical Genome Center, Department of Clinical Research, University of Southern Denmark, Odense, Denmark.
Mark BurtonClinical Genome Center, Department of Clinical Research, University of Southern Denmark, Odense, Denmark.
Clara Rosa Levina OudenaardenDepartment of Pathology, The Bartholin Institute, Rigshospitalet, Copenhagen University Hospital, Copenhagen, Denmark.ORCID 0000-0002-5466-0755
Martin Jakob LarsenClinical Genome Center, Department of Clinical Research, University of Southern Denmark, Odense, Denmark.
Philip Ahle ErichsenDepartment of Pathology, The Bartholin Institute, Rigshospitalet, Copenhagen University Hospital, Copenhagen, Denmark.
Christian Bonde PedersenBRIDGE, Brain Research - Inter Disciplinary Guided Excellence, Odense University Hospital and University of Southern Denmark, Odense, Denmark.
Frantz Rom PoulsenBRIDGE, Brain Research - Inter Disciplinary Guided Excellence, Odense University Hospital and University of Southern Denmark, Odense, Denmark.
Peter GrupeDepartment of Nuclear Medicine, Odense University Hospital, Odense, Denmark.
Torben A KruseClinical Genome Center, Department of Clinical Research, University of Southern Denmark, Odense, Denmark.
Mads ThomassenClinical Genome Center, Department of Clinical Research, University of Southern Denmark, Odense, Denmark.
Bjarne Winther KristensenDepartment of Pathology, The Bartholin Institute, Rigshospitalet, Copenhagen University Hospital, Copenhagen, Denmark.ORCID 0000-0002-6352-0826

Funding

Danish Cancer SocietyNovo Nordisk Foundation NNF19OC0058427Regions of Southern Denmark Research Funds
6 · The paper itself

Abstract

backgroundGlioblastoma undergoes a complex and dynamic evolution involving genetic and epigenetic changes. Understanding the mechanisms underlying this evolution is vital for the development of efficient therapeutic strategies. Although treatment resistance is associated with intratumoral heterogeneity in glioblastoma, it remains uncertain whether hypometabolic and hypermetabolic lesions observed through clinical positron emission tomography (PET) imaging are influenced by spatial intratumoral genomic evolution.

methodsIn this study, we precisely isolated autologous hypometabolic and hypermetabolic lesions from glioblastoma using advanced neurosurgical and brain tumor imaging technologies, followed by comprehensive whole-genome, exome, transcriptome, and imaging analyses.

resultsOur findings unveil that hypermetabolic lesions, originating from hypometabolic lesions, exhibit strategic focal amplifications and deletions, and heightened APOBEC3 activity. Furthermore, we identify dipeptidase 1 as a novel vascular endothelial tip marker for hypermetabolic lesions in glioblastoma, facilitating angiogenesis and tumor metabolism by regulating transporter activities.

conclusionsHypermetabolic lesions are associated with a higher frequency of genomic abnormalities and dipeptidase 1 emerges as a novel diagnostic and prognostic vascular marker for hypermetabolic lesions. This study underscores a spatial genomic evolution with diagnostic implications and elucidates challenges and opportunities crucial for the development of novel therapeutic strategies.

Indexed as

Biomarkers, TumorBrain NeoplasmsDipeptidasesGlioblastomaNeovascularization, PathologicCell ProliferationFemaleGenomicsHumansMalePositron-Emission TomographyPrognosisBiomarkers, TumorDipeptidasesdipeptidase 1hypermetabolismmutational burdentumor evolutionvascular tip

Identifiers

PMID40319462
PMCPMC12833548

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Registered trials

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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.