Tumor vasculature disruption

Tumor vasculature disruption refers to the process by which agents—commonly called vascular disrupting agents (VDAs)—selectively target and damage the established blood vessels within tumors. This leads to rapid cessation or severe reduction in blood flow, resulting in central necrosis due to hypoxia. VDAs often act by binding tubulin in endothelial cells lining tumor vasculature, causing cytoskeletal collapse, increased permeability, exposure of pro-thrombotic surfaces, and subsequent thrombosis. The process is distinct from antiangiogenic therapy as it targets existing rather than newly forming vessels. While effective at inducing central necrosis within tumors lacking mature pericyte coverage, this approach typically leaves a viable rim at the tumor edge that can support regrowth unless combined with other therapies such as chemotherapy. Imaging modalities like perfusion MRI are used for monitoring efficacy. Despite promising preclinical results and some clinical advances with drugs like CA4P or DMXAA/ASA404, challenges remain regarding complete eradication due to resistant peripheral vasculature.[1][3] **Note:** "Tumor vasculature disruption" describes a therapeutic strategy or biological process rather than a specific molecular target such as a receptor or enzyme; therefore it is not itself considered a canonical drug target but rather an effect induced by certain drugs.[3]

Other names

Vascular shutdownTumor vascular disruptionVascular disrupting agent (VDA) effect

Disruption of tubulin polymerization in endothelial cells leading to cytoskeletal collapse and loss of vessel integrity[1]; Increased vascular permeability and exposure of basement membrane components, promoting thrombosis and vessel occlusion[1]; Inhibition of PI3K/Akt signaling pathway following VE-cadherin junction disruption[1]