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Tumor vasculature occlusion via oxidative stress

Molecular classification
Other (process, not a molecule), VEGF signaling, HIF-1α activation, NADPH oxidase family
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Overview

Tumor vasculature occlusion via oxidative stress" refers to a therapeutic approach in which the abnormal blood vessels supplying tumors are targeted and blocked by increasing oxidative stress, usually through the production of reactive oxygen species (ROS). This process exploits the susceptibility of tumor vasculature to ROS-mediated damage, leading to occlusion (blockade) of blood supply, tumor ischemia, and subsequent cell death. The strategy involves modulation of angiogenic pathways (such as VEGF/VEGFR and HIF-1α), induction of direct endothelial cell injury, and may be potentiated by drugs or nanoparticles that generate or amplify oxidative stress within the tumor microenvironment. This mechanism is not a singular molecular target but rather an approach that utilizes molecular and cellular vulnerabilities within the tumor's vascular network, ultimately aiming to control tumor growth, metastasis, and therapy resistance.

Other names
Tumor vascular occlusion via ROSVascular shutdown by oxidative stressOxidative stress-induced vessel blockade
02

Mechanism of action

Promotion of reactive oxygen species (ROS) in tumor vasculature; Induction of endothelial damage and vessel thrombosis/occlusion; Inhibition or normalization of abnormal angiogenesis via VEGF pathway blockade or ROS-induced endothelial cell death; Modulation of key signaling pathways (VEGF/VEGFR, HIF-1α, NF-κB, MAPKs)

03

Biological functions

Angiogenesis regulation (disruption)Induction of cell death (necrosis, apoptosis via ischemia)Immune response modulation (altered by tumor vasculature changes)Signal transduction (via ROS intermediates)
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Disease associations

Cancer (primary context and disease association)Therapy resistance (from aberrant vasculature)Metastasis (role in minimizing metastatic spread by vessel blockade)
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Safety considerations

Off-tumor toxicity (damage to normal vasculature or tissue)Inflammation and immune dysregulationHypoxia and tissue necrosis leading to therapy-related adverse events (e.g., organ ischemia)Heterogeneous tumor responses due to spatial variation in oxidative stress
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Interacting drugs

Chloroquine (CQ; vessel normalization and modulation)

3 more in the full profile.

07

Biomarkers

Oxidative stress markers (e.g., ROS/RNS levels, glutathione depletion, lipid peroxidation derivatives)VEGF and HIF-1α expressionVessel endothelial markers (CD31, VE-cadherin; for assessing vessel integrity/disruption)

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