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Modeling Spontaneous Metastatic Renal Cell Carcinoma (mRCC) in Mice Following Nephrectomy
11:27

Modeling Spontaneous Metastatic Renal Cell Carcinoma (mRCC) in Mice Following Nephrectomy

Published on: April 29, 2014

Anti-angiogenic targets in the treatment of advanced renal cell carcinoma

Daniel Y C Heng1, Ronald M Bukowski

  • 1Experimental Therapeutics, Cleveland Clinic Taussig Cancer Institute, Cleveland, OH 44106, USA.

Current Cancer Drug Targets
|December 17, 2008
PubMed

Insights

Targeting vascular endothelial growth factor (VEGF) and platelet-derived growth factor (PDGF) pathways has improved metastatic renal cell cancer (RCC) treatment. These targeted therapies offer superior progression-free survival compared to older treatments.

Area of Science:

  • Oncology
  • Pharmacology
  • Molecular Biology

Background:

  • Metastatic renal cell cancer (RCC) often involves von Hippel-Lindau gene mutations, leading to HIF-1 alpha accumulation.
  • This accumulation upregulates growth factors like VEGF and PDGF, promoting tumor angiogenesis and endothelial stabilization.

Purpose of the Study:

  • To review the pharmacologic and molecular activity of drugs targeting VEGF and PDGF pathways in metastatic RCC.
  • To correlate the clinical efficacy of these agents with their molecular actions.

Main Methods:

  • Review of existing literature on targeted therapies for metastatic RCC.
  • Analysis of drugs targeting VEGF and PDGF receptor tyrosine kinases (sunitinib, sorafenib) and VEGF (bevacizumab).
  • Examination of agents targeting the downstream mTOR pathway (temsirolimus, everolimus).

Main Results:

  • Sunitinib, sorafenib, and bevacizumab demonstrated superior progression-free survival in metastatic RCC patients versus interferon or placebo.
  • Newer anti-VEGF agents (axitinib, pazopanib, cediranib) are under investigation for future treatment options.

Conclusions:

  • Targeted therapies inhibiting VEGF and PDGF pathways represent a significant advancement in metastatic RCC treatment.
  • Understanding the molecular mechanisms of these drugs is crucial for optimizing clinical efficacy and developing novel therapeutic strategies.

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