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Anti-EGFL7 antibodies enhance stress-induced endothelial cell death and anti-VEGF efficacy

Leisa Johnson1, Mahrukh Huseni, Tanya Smyczek

  • 1Genentech Inc., South San Francisco, California 94080, USA. johnson.leisa@gene.com

The Journal of Clinical Investigation
|August 16, 2013
PubMed

Insights

This study identified the optimal dose for anti-EGFL7, an antiangiogenesis agent, by integrating preclinical and clinical data. This approach enhances anti-VEGF therapy efficacy in non-small cell lung cancer models and guides ongoing clinical trials.

Area of Science:

  • Oncology
  • Immunology
  • Biochemistry

Background:

  • Many cancer drugs are given at maximum tolerated doses, not necessarily optimal effective doses.
  • EGFL7 is an extracellular matrix protein in activated endothelium, crucial for endothelial cell (EC) function.
  • Anti-EGFL7 antibodies can disrupt EC adhesion and protect ECs from apoptosis.

Purpose of the Study:

  • To identify the optimal dose for the antiangiogenesis agent, anti-EGFL7.
  • To evaluate the synergistic effects of anti-EGFL7 with anti-VEGF therapy.
  • To establish a biomarker for anti-EGFL7 efficacy in preclinical and clinical settings.

Main Methods:

  • Integrated preclinical (murine tumor models) and clinical (Phase I trial) data.
  • Assessed anti-EGFL7 efficacy in a genetically engineered mouse model of non-small cell lung cancer (NSCLC).
  • Identified and evaluated circulating progenitor cells regulated by EGFL7 in mice and cancer patients.

Main Results:

  • Anti-EGFL7 antibodies inhibited EC adhesion and protected ECs from apoptosis, augmenting anti-VEGF therapy.
  • Anti-EGFL7 demonstrated a dose-dependent enhancement of progression-free and overall survival in NSCLC models.
  • A specific circulating progenitor cell type was identified as a biomarker for anti-EGFL7 response.

Conclusions:

  • A multifaceted approach integrating preclinical and clinical data successfully identified the optimal dose for anti-EGFL7.
  • The identified biomarker and efficacy data support the rational selection of anti-EGFL7 doses for Phase II trials.
  • This strategy optimizes anti-cancer drug dosing for improved therapeutic outcomes.

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