ArticleJournal of neuro-oncology2025
IDO2-AhR axis as central regulator of the kynurenine pathway in glioblastoma.
Article in Journal of neuro-oncology, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 3 papers, 1 of them a synthesis that pooled 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.
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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.
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Who cites it
3 citing papers in PubMed, 1 synthesis or guideline pooled it.
- Metabolic modulation of glioblastoma by dietary intervention: a systematic review.Journal of neuro-oncology · 2026Pooled it
- Nexus of IDO1/Kynurenine Pathway to T-Cell Exhaustion: Hypoxia-Induced Tryptophan Metabolism in Glioblastoma.Metabolites · 2026Review
- Tryptophan metabolism in tumor immune escape: mechanisms, cellular crosstalk, and therapeutic opportunities.Frontiers in immunology · 2026Review
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Authors and funding
14 authors.
Funding
No grant is acknowledged in the PubMed record.
Abstract
purposeUpregulation of the Kynurenine Pathway (KP) in Glioblastoma (GBM) plays an important role in driving its treatment-resistant immunosuppressive microenvironment. Factors driving this exaggerated pathway remain poorly understood. Our aim was to explore the correlation between key KP markers; IDO1, IDO2, TDO2, its primary effector target aryl hydrocarbon receptor (AhR) and a comprehensive set of clinical- and tumour characteristics.
methodsTissue samples from 108 newly diagnosed GBM patients were analyzed for the expression of TDO2, IDO1, IDO2, and AhR using immunohistochemistry and QuPath software. Exploratory analyses were conducted to evaluate correlations between KP marker expression and clinical, radiological, and molecular data.
resultsIDO1 expression was primarily correlated with inflammatory blood markers, while TDO2 was correlated with patient age, gender, smoking habit and medication use. In contrast, AhR and IDO2 demonstrated hardly any correlations with clinical or tumour characteristics. Notably, IDO2 exhibited a strong association with AhR expression and tumour cell density, with no observed correlation between AhR and either IDO1 or TDO2.
conclusionsWe validated the inflammatory influences on IDO1 expression and found that TDO2 was mostly correlated with medication and patient characteristics. We could not confirm IDO1 and TDO2 as most prominent drivers of AhR activity in the KP. However, we found a strong correlation between IDO2-AhR which may be responsible for the sustained and enhanced immunosuppression within the tumour microenvironment. This could explain recent failures of IDO1 and TDO2 antagonists and might redirect future studies to intervene in the kynurenine-AhR-IDO2 axis.
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