ArticleScience advances2025
Ara-C suppresses H3 K27-altered spinal cord diffuse midline glioma growth and enhances immune checkpoint blockade sensitivity.
Article in Science advances, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 3 papers.
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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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Who cites it
3 citing papers in PubMed.
- Targeting WTAP/ROR1/WNT5A-Mediated Crosstalk Between Glioma Stem Cells and Macrophages to Normalize Tumor Vasculature and Enhance Chemotherapy.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2026Article
- Article
- Hypoxia-Induced Osteopontin-Positive Glioma-Associated Macrophages Facilitate Glioma Mesenchymal Transition via NF-κB Pathway Activation.Cancer communications (London, England) · 2026Article
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Authors and funding
13 authors.
Funding
No grant is acknowledged in the PubMed record.
Abstract
H3 K27-altered spinal cord diffuse midline glioma (H3-SCDMG) poses therapeutic challenges. Analysis of 73 clinical samples revealed heightened proliferation in H3-SCDMG versus wild-type tumors, suggesting therapeutic vulnerabilities. Drug screening identified cytarabine (Ara-C) as highly effective in inhibiting proliferation in H3 K27M cell models, recently established patient-derived cells, and patient-derived xenograft models. Mechanistically, Ara-C can suppress tumor growth through DNA damage, cell-cycle arrest, and apoptosis. An investigator-initiated clinical trial involving four patients showed benefits in three cases. In addition, a subset of cells exhibited senescence and senescence-associated secretory phenotype post-Ara-C treatment, accompanied by several immune checkpoint ligands' up-regulation and more immune cell infiltration. Combining Ara-C with dual Programmed cell death protein 1 (PD-1) and TIGIT blockade emerged as a promising strategy to disrupt immune evasion by senescent cells, enhancing antitumor responses. These findings highlight Ara-C's potential as a monotherapy and in synergy with immunotherapy for H3-SCDMG, offering potential strategies for clinical management.
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