Biomaterials-Mediated Tumor Infarction Therapy

Abstract

Agents for tumor vascular infarction are recently developed therapeutic agents for the vascular destruction of tumors. They can suppress the progression of the tumor by preventing the flow of nutrition and oxygen to its tissues. Agents of tumor vascular infarction can be divided into three categories according to the differences in their pathways of action: those that use the thrombin-activating pathway, fibrin-activating pathway, and platelet-activating pathway. However, poor targeting ability, low permeation, and potential side-effects restrict the development of the corresponding drugs. Biomaterials can subtly avoid these drawbacks to suppress the tumor. In this article, the authors summarize currently used biomaterials for tumor infarction therapy with the goal of identifying its mechanism, and discuss outstanding deficiencies in methods of this kind.

Nanomaterial-Based Antivascular Therapy in the Multimodal Treatment of Cancer

“…(3) Vascular blockade therapy aims to restrict blood flow in vessels by inducing the formation of blood clots or gel phase transitions within blood vessels, thereby blocking the supply of blood, nutrients, and oxygen to the tumor [11]. Three different blocking pathways can be activated: the thrombin activation pathway, the fibrin activation pathway, and the platelet activation pathway [12]. However, single-agent antivascular therapy does not have a prominent antitumor effect.…”

Manipulating Neovasculature-Targeting Capability of Biomimetic Nanodiscs for Synergistic Photoactivatable Tumor Infarction and Chemotherapy

“…Besides, considering the fact that thrombotic occlusion does not attack tumor cells or influence their signal pathways, it is less likely to induce treatment resistance. Thrombus-causing drugs, such as thrombin and combretastatin A4, were loaded in various nanocarriers to improve the tumor-targeted delivery efficiency. − A truncated form of tissue factor (tTF) connected to vessel endothelial cells-targeting ligand was reported to rapidly induce thrombosis in tumors and significantly reduced tumor growth in animal models. , Although increased drug accumulation in tumors can be achieved by targeting ligand or nanocarriers, procoagulatory drugs that remain in normal tissues could still block normal blood vessels and cause injury to the body. A phase I clinical trial with aminopeptidase N targeted tTF shows that, despite the effectiveness in inducing tumor infarction, occasional thromboembolic events were found and the progression of cancer was not affected by tumor infarction therapy alone .…”