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Updated: Jun 27, 2026
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A Syngeneic Mouse Model of Metastatic Renal Cell Carcinoma for Quantitative and Longitudinal Assessment of Preclinical Therapies
Published on: April 12, 2017
[Angiogenesis: the renal cancer model]
1Service d'Urologie, Université Paris Descartes, France. arnaud.mejean@nck.aphp.fr
Summary
Von Hippel-Lindau (VHL) gene inactivation causes hypoxia-inducible factor (HIF) accumulation, promoting angiogenesis in metastatic renal carcinoma. Targeted therapies aim to inhibit this tumor blood vessel growth through complex mechanisms.
Area of Science:
- Oncology
- Molecular Biology
- Genetics
Context:
- VHL gene inactivation is a key event in most metastatic non-inherited renal carcinomas.
- This inactivation leads to the accumulation of hypoxia-inducible factor (HIF).
Purpose:
- To elucidate the molecular mechanisms linking VHL inactivation to tumor progression.
- To understand the role of HIF in activating pro-angiogenic genes.
Summary:
- VHL gene inactivation results in HIF accumulation, which activates genes like VEGF and PDGF.
- VEGF signaling promotes tumoral angiogenesis by acting on endothelial cell receptors.
- Targeted therapies are being developed to inhibit tumor angiogenesis, likely through multifaceted mechanisms.
Impact:
- Provides insights into the pathogenesis of metastatic renal carcinoma.
- Highlights potential therapeutic targets for anti-angiogenic strategies.
- Contributes to understanding the complex interplay between VHL, HIF, and tumor vascularization.
