# From Cerebrovascular Injury to Brain Cancer: The Role of Blood–Brain Barrier Dysfunction

## TL;DR

This paper explores how cerebrovascular injury, like stroke, might increase the risk of brain cancer by disrupting the blood-brain barrier.

## Contribution

It highlights novel mechanistic links between stroke-induced BBB dysfunction and brain cancer development.

## Key findings

- Stroke-induced hypoxia and oxidative stress disrupt BBB integrity.
- Post-stroke immune and regenerative signals may promote tumor growth in the CNS.
- Epidemiological data suggest a potential link between cerebrovascular injury and brain cancer.

## 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.