What is it about?
Our study sheds light on a groundbreaking approach to enhance drug delivery and efficacy in solid tumors. By targeting specific regulators downstream of VEGF, we achieved more selective and effective outcomes, leading to improved vessel patency, better oxygenation, and enhanced drug response.
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Why is it important?
Most solid tumors display irregular and dysfunctional blood vessels, which are also unevenly distributed within the tumor. This leads to undersupply and more malignant, invasive tumor behavior. Importantly, drug transport into the tumor is also reduced, and the drug amounts that reach the tumor are heterogeneously distributed. Improving the tumor vasculature has the potential to increase response to all systemically applied drugs at our disposal but also to improve response to radiotherapy.
Perspectives
Reducing pro-angiogenic signaling via targeting the VEGF pathway has been proposed as a way to improve or normalize the tumor vasculature because the constant pro-angiogenic stimulus within the tumor is thought to cause the defective vessel phenotype. Unfortunately, blocking key angiogenic pathways like VEGF also reduces overall vessel density, further hampering supply and drug transport. We demonstrate that improving the tumor vasculature without reducing vessel density is possible by approaching downstream of the master regulators of angiogenesis by targeting more specific switches of vessel dysfunction, such as the transcription factor Snai1. This opens the perspective to strategically re-engineer the tumor vasculature to increase therapy response.
Erik Henke
Julius-Maximilians-Universitat Wurzburg
Read the Original
This page is a summary of: Normalization of Snai1-mediated vessel dysfunction increases drug response in cancer, Oncogene, August 2024, Springer Science + Business Media,
DOI: 10.1038/s41388-024-03113-1.
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