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Updated: Jun 23, 2026

A Simple Bioassay for the Evaluation of Vascular Endothelial Growth Factors
09:04

A Simple Bioassay for the Evaluation of Vascular Endothelial Growth Factors

Published on: March 15, 2016

Cellular source and amount of vascular endothelial growth factor and platelet-derived growth factor in tumors

Barbara Sennino1, Frank Kuhnert, Sebastien P Tabruyn

  • 1Cardiovascular Research Institute, Comprehensive Cancer Center, and Department of Anatomy, University of California, San Francisco, CA 94143-0452, USA. barbara.sennino@ucsf.edu

Cancer Research
|April 30, 2009
PubMed

Insights

Simultaneous inhibition of vascular endothelial growth factor (VEGF) and platelet-derived growth factor (PDGF) shows varied efficacy. Tumor type significantly impacts whether combined VEGF and PDGF inhibition is more effective than targeting either alone.

Area of Science:

  • Oncology
  • Cancer Biology
  • Angiogenesis Research

Background:

  • Vascular endothelial growth factor (VEGF) and platelet-derived growth factor (PDGF) signaling pathways are critical regulators of tumor angiogenesis.
  • Targeting VEGF and PDGF is a key strategy in anti-cancer therapies aimed at inhibiting tumor blood vessel formation.
  • The comparative efficacy of combined versus single inhibition of VEGF and PDGF remains incompletely understood.

Purpose of the Study:

  • To compare the effects of inhibiting VEGF alone, PDGF alone, and both VEGF and PDGF together on tumor vascularity and pericyte density.
  • To investigate the influence of distinct tumor microenvironments and growth factor expression patterns on the response to anti-angiogenic therapy.

Main Methods:

  • Utilized two contrasting tumor models: RIP-Tag2 and Lewis lung carcinoma (LLC).
  • Employed adenovirally generated soluble receptors and tyrosine kinase inhibitors (AG-013736, imatinib) to inhibit VEGF and/or PDGF.
  • Assessed tumor vascularity, pericyte density, and growth factor expression patterns (VEGF, PDGF) within the tumor models.

Main Results:

  • In RIP-Tag2 tumors, combined inhibition reduced vascularity and pericytes; however, single VEGF inhibition primarily affected vascularity, and single PDGF inhibition affected pericytes.
  • In LLC, single inhibition of VEGF or PDGF yielded similar reductions in vessels and pericytes as combined inhibition.
  • Differential expression of VEGF and PDGF in LLC (pericytes and endothelial cells, respectively) versus RIP-Tag2 tumors (more widespread) correlated with observed therapeutic responses.

Conclusions:

  • The effectiveness of combined VEGF and PDGF inhibition is dependent on the specific tumor model and its underlying growth factor expression profile.
  • Tumor pericytes play a crucial role in maintaining tumor vasculature, particularly in models where they are a primary source of VEGF.
  • These findings highlight the interdependence of tumor endothelial cells and pericytes and underscore the importance of tumor phenotype in guiding anti-angiogenic therapy strategies.

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