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Updated: May 7, 2026

A Syngeneic Mouse Model of Metastatic Renal Cell Carcinoma for Quantitative and Longitudinal Assessment of Preclinical Therapies
06:38

A Syngeneic Mouse Model of Metastatic Renal Cell Carcinoma for Quantitative and Longitudinal Assessment of Preclinical Therapies

Published on: April 12, 2017

Progress of molecular targeted therapies for advanced renal cell carcinoma

Alessandro Conti1, Matteo Santoni, Consuelo Amantini

  • 1Department of Clinical and Specialist Sciences, Urology, Polytechnic University of the Marche Region, AOU Ospedali Riuniti Umberto I-GM Lancisi and G Salesi, Ancona, Italy.

Biomed Research International
|October 5, 2013
PubMed

Insights

Vascular endothelial growth factor (VEGF) drives tumor growth in metastatic renal cell carcinoma (mRCC). New targeted therapies inhibiting VEGF signaling pathways offer promising treatment options for mRCC patients.

Area of Science:

  • Oncology
  • Molecular Biology
  • Pharmacology

Background:

  • Vascular endothelial growth factor (VEGF) is a key regulator of tumor angiogenesis, essential for the growth and metastasis of cancers.
  • In metastatic renal cell carcinoma (mRCC), VEGF expression is primarily controlled by hypoxia through the hypoxia-induced factor (HIF)/Von Hippel-Lindau (VHL) pathway.
  • Understanding VEGF's role has led to the development of targeted therapies for mRCC.

Purpose of the Study:

  • To illustrate the key steps in the tumor angiogenesis process relevant to mRCC.
  • To identify and define critical therapeutic targets within the VEGF pathway.
  • To review the efficacy and toxicity profiles of novel anti-VEGF agents for mRCC treatment.

Main Methods:

  • Review of scientific literature on tumor angiogenesis, VEGF signaling, and targeted therapies in mRCC.
  • Analysis of established and investigational agents targeting VEGF and its receptors.
  • Summarization of clinical data regarding the efficacy and safety of these agents.

Main Results:

  • Several targeted therapies, including tyrosine kinase inhibitors (e.g., sorafenib, sunitinib), have been approved for mRCC.
  • Numerous agents targeting various components of the VEGF pathway (e.g., tivozanib, cediranib, VEGF-Trap) are under evaluation.
  • These therapies target multiple signaling molecules including kinases, integrins, and mTOR pathway components.

Conclusions:

  • Targeting the VEGF pathway represents a significant advancement in mRCC treatment.
  • Ongoing research and clinical trials continue to expand the armamentarium of anti-angiogenic therapies for mRCC.
  • Careful consideration of efficacy and toxicity profiles is crucial for optimizing patient outcomes.

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