ArticleJournal of neuro-oncology2025
Glioma cells achieve malignant progression by fusion with macrophages to gain high SLC7A5 expression.
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. Not yet cited in PubMed.
What it found
Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.
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
0 citing papers in PubMed.
No citing paper in PubMed yet.
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
3 authors.
Funding
Abstract
purposeThis study aimed to investigate the characteristics and functional role of macrophage(MΦ)-glioma hybrid cells formed through cell fusion, and to explore the underlying mechanisms and potential therapeutic targets in glioma progression.
methodsThe presence of MΦ-glioma double-positive cells was confirmed using single-cell sequencing data and human glioma specimens. An in vitro fusion model was established, and hybrid cells were analyzed for flow cytometry. Functional assays assessed proliferation and invasion capabilities. Mechanistic studies focused on the role of SLC7A5, a MΦ-derived gene, and drug sensitivity was tested using the SLC7A5 inhibitor JPH203.
resultsMΦ-glioma hybrid cells were identified both in vivo and in vitro. These hybrids exhibited increased chromosomal content and demonstrated significantly enhanced proliferation and invasion. Mechanistically, SLC7A5 was identified as a key driver of this malignant phenotype. Furthermore, hybrid cells showed greater sensitivity to the SLC7A5 inhibitor JPH203 compared to parental cells.
conclusionFusion with MΦs confers enhanced malignancy to glioma cells, characterized by increased proliferation and invasion, which is promoted by the MΦ-derived gene SLC7A5. Targeting SLC7A5 represents a promising novel therapeutic strategy for glioma.
Indexed as
Identifiers
41402663What OpenQuestion holds
Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.