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Updated: Jun 23, 2026
Preparation Of Neovascular Tissues from Human Glioma Tissues for Quantitative Proteomics Analysis of Tumor Angiogenesis
Published on: March 20, 2026
Targeting tumor angiogenesis
Puja Gaur1, Debashish Bose, Shaija Samuel
1Department of Surgical Oncology, The University of Texas M.D. Anderson Cancer Center, Houston, TX, USA.
Abstract:
Our understanding of the process of tumor angiogenesis has changed significantly since the late 1970s, when vascular endothelial growth factor (VEGF) was first identified as vascular permeability factor and later found to be the major mediator of physiologic and pathologic angiogenesis. Since then, several additional VEGF-related ligands, VEGF receptors (VEGFRs), and complementary/alternative pathways that regulate tumor angiogenesis have been identified. Over the last decade, several antiangiogenic agents have been developed with the aim to inhibit new blood vessel growth, and we have learned that VEGF inhibition does far more than simply block new blood vessel growth. Clinical studies have demonstrated an improvement of progression-free and overall survivals with anti-VEGF therapy (with or without chemotherapy) in patients with advanced-stage malignancies. Unfortunately, even when anti-VEGF therapy is effective, the benefit of therapy is short-lived, with the development of tumor growth. We now recognize the presence of numerous complementary and redundant pathways that regulate tumor vasculature. For example, VEGF/VEGFR and angiopoietin/Tie-2 axes are two redundant, complementary components regulating tumor angiogenesis and vascular maintenance. The current clinical challenge is to identify: (1) factors that predict efficacy, and (2) markers of tumor response to anti-VEGF therapy, which can be achieved only by developing a thorough understanding of the biology of the VEGF system and the role of complementary pathways that may mediate resistance to anti-VEGF therapy.
Insights
Vascular endothelial growth factor (VEGF) therapies improve cancer survival but are short-lived. Understanding complementary pathways is key to overcoming resistance and improving anti-VEGF treatment efficacy.
Area of Science:
- Oncology
- Molecular Biology
- Biochemistry
Background:
- Tumor angiogenesis, crucial for cancer growth, is primarily mediated by vascular endothelial growth factor (VEGF).
- Significant advancements in understanding VEGF and related pathways have occurred since the 1970s.
- Anti-VEGF therapies have shown clinical benefits in advanced malignancies, improving progression-free and overall survival.
Purpose of the Study:
- To review the evolving understanding of tumor angiogenesis and the role of VEGF.
- To discuss the clinical efficacy and limitations of anti-VEGF therapies.
- To highlight the importance of complementary pathways in mediating resistance to anti-VEGF therapy.
Main Methods:
- Literature review of studies on tumor angiogenesis, VEGF, and anti-angiogenic agents.
- Analysis of clinical trial data regarding anti-VEGF therapy outcomes.
- Exploration of molecular mechanisms underlying VEGF-mediated angiogenesis and resistance pathways.
Main Results:
- VEGF inhibition offers survival benefits but is often transient due to tumor adaptation.
- Redundant and complementary pathways, such as the angiopoietin/Tie-2 axis, contribute to tumor vascular maintenance and resistance.
- Current anti-VEGF therapies do not fully address the complexity of tumor angiogenesis regulation.
Conclusions:
- A deeper understanding of VEGF biology and complementary pathways is essential for improving anti-VEGF therapy.
- Identifying predictive biomarkers for treatment efficacy and resistance is a critical clinical challenge.
- Future strategies must target multiple pathways to overcome resistance and enhance long-term patient outcomes.
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