ArticleJournal of translational medicine2026
Article in Journal of translational medicine, 2026. 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
10 authors.
Funding
Abstract
purposeGlioblastoma (GBM) invariably develops resistance to temozolomide (TMZ), necessitating novel therapeutic strategies. This study demonstrates that inhibiting exosome secretion with GW4869 remodels the glucose metabolic phenotype to suppress malignant behavior and reverse TMZ resistance in GBM.
methodsTMZ-resistant glioblastoma cells (U87TR) were established via concentration-gradient induction. Metabolic profiling was performed using LC-MS. GW4869’s effects were assessed via functional assays (invasion, migration, colony formation), exosome add-back experiments, and ¹⁸F-FDG PET/CT in xenografts. Glycolytic proteins (GLUT-1/HK2/PKM2) were analyzed by immunofluorescence/western blot.
resultsU87TR cells exhibited glycolytic hyperactivation. GW4869 (10 µM) suppressed invasion, migration and colony formation without cytotoxicity. It reversed TMZ resistance by downregulating GLUT-1/HK2/PKM2 and inhibiting glycolysis. Exosomes conferred resistance via metabolic remodeling—blocked by glycolytic inhibitor 2-DG. In vivo, GW4869 reduced tumor ¹⁸F-FDG uptake by 28.0% (P < 0.01), and this reduction strongly correlated with in vitro IC₅₀ reduction.
conclusionGW4869 overcomes TMZ resistance by inhibiting exosome-mediated glycolytic reprogramming. ¹⁸F-FDG PET provides a clinically applicable quantitative tool for monitoring resistance reversal.
Indexed as
Identifiers
What Socratic 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 Socratic graph.