ArticleAmerican journal of translational research2026
Progranulin promotes glioma progression through the M2-TGF-β axis: targeted therapy with SORT1-loaded HAMA hydrogel microspheres.
Article in American journal of translational research, 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
3 authors.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Glioblastoma (GBM) is the most aggressive primary brain tumor, and is characterized by rapid growth, therapeutic resistance, and a highly immunosuppressive tumor microenvironment (TME). Progranulin (GRN/PGRN), a secreted glycoprotein, promotes malignancy in various cancers, yet its role in GBM remains poorly defined. Bioinformatics analysis of GEO (Gene Expression Omnibus) and TCGA (The Cancer Genome Atlas) datasets revealed that GRN expression is significantly upregulated in GBM and is associated with shorter overall survival and progression-free survival. High GRN levels correlated strongly with increased M2 macrophage infiltration (marked by CD163 expression) and elevated immune and stromal scores, suggesting that GRN contributes to an immunosuppressive TME. In vitro, silencing GRN in GBM cells markedly inhibited cell proliferation, migration, invasion, and colony formation. Coculture assays demonstrated that GRN knockdown reduced GBM-induced M2 macrophage polarization (CD206
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.