ArticleTranslational oncology2026
CD38 overexpression drives glioblastoma progression via L1CAM/ICAM1/JAK-STAT-Driven tumor microenvironment rewiring.
Article in Translational oncology, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. It is linked to trial NCT04922723 (A Study of Radiation/Temozolomide and Immunotherapy With Daratumumab to Improve Antitumor Efficacy in Glioblastoma), which is not on this 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.
A Study of Radiation/Temozolomide and Immunotherapy With Daratumumab to Improve Antitumor Efficacy in Glioblastoma (PRIDE).
Who cites it
1 citing paper in PubMed.
- Improving T-cell engager efficacy in glioblastoma with multi-antigen targeting and novel delivery approaches.Acta neuropathologica · 2026Review
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2 authors.
Funding
No grant is acknowledged in the PubMed record.
Abstract
backgroundGlioblastoma (GBM), a lethal primary brain malignancy, is characterized by dysregulated recruitment of tumor-associated macrophages and myeloid-derived suppressor cells, which promotes tumor growth, and enables immune evasion. Given CD38's role as a multifunctional glycoprotein in hematological malignancies where it regulates immune cell trafficking, we hypothesized that CD38 overexpression in GBM modulates the tumor immune microenvironment.
methodsWe utilized the CRISPRa system to enhance CD38 expression in mouse syngeneic GL-261 cells. A murine GBM model was generated by intracranial injection of CD38-overexpressing (CD38-OE) GL-261 cells or CD38 wild-type (WT) or (parental)GL-261 cells into C57BL/6 mice. We utilized serial brain MRIs for tumor progression and assessed overall survival using Kaplan-Meier analysis. We performed multiplex flow cytometry and cytokine assays on brain tumor tissue. Data were analyzed using one-way ANOVA and unpaired t-tests.
resultsMedian OS was significantly reduced in CD38-OE mice (26.5 days) versus CD38-WT (35.7 days; p < 0.0001; n = 11/group). Tumor size (in vivo) in CD38-OE vs CD38-WT at day 10 (8.44 mm³ vs. 2.16 mm³; p = 0.0004) and day 17 (34.75 mm³ vs. 8.51 mm³; p = 0.0048). Compared to CD38-WT, CD38-OE tumors showed increased infiltration of glioma-associated macrophages (GAMs) (8.43-fold increase; p < 0.0001), monocytic MDSCs (12.53-fold increase; p < 0.0002), polymorphonuclear MDSCs (15.66-fold increase; p < 0.0001), and T-regs (7.22-fold increase; p < 0.0001). Cytokine profiling indicated elevated CXCL10/IP-10, TIMP-1, and ICAM-1 in CD38-OE tumors.
conclusionsCD38 overexpression in GBM drives tumor progression by amplifying immunosuppressive TME remodeling, positioning CD38 as a compelling target for further clinical investigation, supported by preliminary efficacy of daratumumab (NCT04922723) in patients with GBM.
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