ArticleAdvanced science (Weinheim, Baden-Wurttemberg, Germany)2026
Targeting WTAP/ROR1/WNT5A-Mediated Crosstalk Between Glioma Stem Cells and Macrophages to Normalize Tumor Vasculature and Enhance Chemotherapy.
Article in Advanced science (Weinheim, Baden-Wurttemberg, Germany), 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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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.
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Who cites it
1 citing paper in PubMed.
- Copper transporters promote the malignant progression of glioblastoma by regulating the immunosuppressive tumour microenvironment via the SLC31A1-WNT5A axis.Journal of translational medicine · 2026Article
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Authors and funding
16 authors.
Funding
Abstract
Glioma stem cells (GSCs) can trans-differentiate into glioma-derived endothelial cells (GDECs), contributing to glioblastoma progression and therapy resistance. The molecular basis underpinning GSC-GDEC differentiation remain incompletely elucidated. Here, ROR1 is identified as a key regulator of GSC-to-GDEC differentiation under hypoxia. ROR1 expression is elevated in GDECs across patient-derived cells, xenografts, and tumor samples, confirmed by single-cell multiomics, Western blotting, and multiplex staining. Mechanistically, WNT5A, secreted by tumor-associated macrophages (TAMs) under hypoxia, activates ROR1-mediated Wingless-type MMTV integration site family (WNT) signaling in GSCs, promoting GDEC formation. Interestingly, hypoxia-induced WTAP not only enhances ROR1 stability through m
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