ArticleJournal of neuro-oncology2026
Annexin A2 associated with bevacizumab resistance and infiltrative escape in glioblastoma.
Article in Journal of neuro-oncology, 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
12 authors.
Funding
No grant is acknowledged in the PubMed record.
Abstract
backgroundThe clinical benefit of bevacizumab (Bev) in glioblastoma (GBM) is typically transient, as tumors develop adaptive resistance characterized by an infiltrative shift from angiogenesis dependent growth. This study investigated Annexin A2 (ANXA2), a regulator of both angiogenesis and invasion, as a potential biomarker of Bev resistance.
methodsWe analyzed 66 tissue-specimens from 33 GBM patients using quantitative real-time PCR and immunohistochemistry/immunofluorescence. The cohort included 15 Bev-naïve cases and 18 neoadjuvant Bev (neoBev) cases. 33 refractory specimens-including unique paired samples from the same patients at different treatment phases (initial resection vs. refractory stage) were evaluated to correlate ANXA2 expression levels with progression-free survival (PFS), overall survival (OS), and MRI recurrence patterns.
resultsMultivariate analysis identified high ANXA2 expression as a significant independent poor prognostic factor for both PFS and OS. In the neoBev group, patients with low ANXA2 mRNA expression levels demonstrated significantly superior survival outcome compared to those with high expression. While ANXA2 mRNA levels tended to increase at the refractory stage, a significant negative correlation was observed between the number of Bev cycles and ANXA2 expression levels. Histopathological analyses revealed intense ANXA2 expression in the tumor vasculature and stroma at the GBM leading edge, co-localization with the hypoxia marker hypoxia-inducible factor-1α.
conclusionsANXA2 may serve as a predictive biomarker of the adaptive transition from an angiogenic to infiltrative phenotype with Bev therapy. These findings suggest that ANXA2 serves as a predictive biomarker for Bev clinical benefit and may represent a candidate therapeutic target requiring further validation in GBM.
Indexed as
Identifiers
What 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.