ReviewBiomedicines2026
From Cerebrovascular Injury to Brain Cancer: The Role of Blood-Brain Barrier Dysfunction.
Review in Biomedicines, 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
8 authors.
Funding
Abstract
Stroke and brain cancer are severe disorders of the central nervous system (CNS) associated with high morbidity and mortality. Although each condition has been extensively studied individually, growing evidence suggests that cerebrovascular injury may influence the development of brain malignancies. This narrative review synthesizes current experimental, clinical, and epidemiological data supporting a mechanistic link between stroke and brain cancer, with a particular focus on blood-brain barrier (BBB) dysfunction. We discuss how stroke-induced hypoxia, oxidative stress, and neuroinflammation disrupt BBB integrity, promote endothelial activation, and induce the expression of adhesion molecules that facilitate arrest, extravasation, and survival of circulating tumor cells within the CNS. Additionally, post-stroke regenerative signaling, angiogenesis, and immune modulation may contribute to the formation of a permissive microenvironment that supports tumor initiation and metastatic growth. Available epidemiological studies, clinical observations, and case reports are reviewed to evaluate the strength and limitations of the association between cerebrovascular events and subsequent brain cancer. Although the co-occurrence of stroke and brain cancer remains relatively uncommon, elucidating the shared molecular and cellular mechanisms underlying this relationship can improve risk stratification and allow the development of diagnostic and therapeutic strategies aimed at preserving BBB integrity and reducing long-term oncological complications after stroke.
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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.