ArticleOncology research2025
Assessing the impact of CD73 inhibition on overcoming anti-EGFR resistance in glioma cells.
Article in Oncology research, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 2 papers.
What it found
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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.
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.
Who cites it
2 citing papers in PubMed.
- Dual-mechanism anti-CD73 antibodies CR201 and CR202 targeting distinct domains for cancer immunotherapy.Frontiers in immunology · 2026Article
- PIK3R1 as a Gastric Cancer Biomarker Linked to CD73Oncology research · 2026Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
9 authors.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Objectives: Glioblastoma (GB) is a grade IV glial tumor characterized by high malignancy and dismal prognosis, primarily due to high recurrence rates and therapeutic resistance. The epidermal growth factor receptor (EGFR), a receptor tyrosine kinase (RTK), regulates signaling pathways, including cell growth, proliferation, survival, migration, and cell death. Many cancers utilize immune checkpoints (ICs) to attenuate immune responses. CD73 is an enzyme that functions as an IC by hydrolyzing AMP to adenosine, suppressing immune cells in the tumor microenvironment. However, the role of CD73 in resistance to EGFR inhibitors is poorly understood. This study aims to elucidate the resistance mechanisms induced by anti-EGFR treatment and to evaluate an anti-CD73 approach to overcome resistance mediated by anti-EGFR monotherapy. Methods: The U251 GB cell line was treated with AG1478, an EGFR inhibitor, and the resistance markers MRP-1, PD-L1, and CD73 were evaluated using flow cytometry. Additionally, we assessed the combination effects of AG1478 and APCP (an EGFR and a CD73 inhibitor, respectively) on cell cycle progression, proliferation, apoptosis, and migration Results: We observed high EGFR, PD-L1, and CD73 expression in human GB cells. The treatment with AG1478 increased the expression of resistance markers MRP-1, PD-L1, and CD73, whereas it decreased CTLA-4. The combination of AG1478 and APCP did not alter proliferation or apoptosis but interfered with cell cycling, arresting the cells in the G1 phase, decreasing cell motility and partially reversing MRP-1 overexpression. Conclusion: In summary, our findings indicate that CD73 inhibition has a modest effect in overcoming resistance to EGFR monotherapy
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Registered trials
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