Tumor-associated vasculature and hepatic tumor microvasculature

Tumor-associated vasculature and hepatic tumor microvasculature refer to the complex network of blood vessels that develop within and around solid tumors, particularly in the liver, to support their rapid growth and metabolic demands (Thorpe, 2004, Clin Cancer Res; Dunphy et al., 2017, AJR). Unlike normal vessels, this neovasculature is characterized by structural abnormalities, such as high permeability, tortuosity, and a lack of organized pericyte coverage, which are driven by pro-angiogenic factors like VEGF (Siemann, 2011, Cancer Treat Rev; Folkman, 1971, NEJM). In the context of hepatic tumors, the microvasculature is often predominantly supplied by the hepatic artery rather than the portal vein, a feature exploited by locoregional therapies like transarterial chemoembolization (TACE) and radioembolization (Dunphy et al., 2017, AJR; Ribatti, 2016, Cancer Lett). Therapeutic strategies targeting this system include anti-angiogenic agents that inhibit new vessel formation, vascular disrupting agents that collapse existing vessels, and vascular normalization strategies to improve drug delivery (Thorpe, 2004, Clin Cancer Res). These vessels also serve as a critical interface for immune cell infiltration and are a major focus of combination therapies involving immunotherapy (Siemann, 2011, Cancer Treat Rev). Monitoring the response of the tumor microvasculature is essential for assessing the efficacy of angiotropic treatments (Dunphy et al., 2017, AJR). Drugs targeting this system often interact with molecular markers like VEGFR, integrins, or phosphatidylserine, or act physically through embolization (Thorpe, 2004, Clin Cancer Res; Folkman, 1971, NEJM).

Other names

Tumor neovasculatureTumor blood vesselsAngiogenic microvasculatureHepatic tumor vesselsTumor-associated endothelium

Inhibition of pro-angiogenic signaling (e.g., VEGF/VEGFR blockade), disruption of established tumor vessels (e.g., tubulin depolymerization), or physical occlusion and embolization of the microvascular network.