Mechanisms of Inhibition of the Epidermal Growth Factor Receptor: Implications for Novel Anti-Cancer Therapies

Abstract

The epidermal growth factor receptor (EGFR) is a member of the erbB family of receptor tyrosine kinases (RTKs). These receptors and their cognate ligands are frequently overexpressed in human tumors, including carcinoma of the breast. No secreted or extracellular ErbB receptor inhibitors have been reported in mammals. However, two natural inhibitors of the highly homologous Drosophila EGF receptor are found in Drosophila melanogaster. My research proposal focuses on obtaining a detailed mechanistic and structural understanding of how these natural inhibitors, Argos and Kekkon, function to antagonize EGFR activity. Our studies have uncovered a novel mechanism of EGF receptor inhibition. In our examination into the mechanism Argos mediated inhibition we unexpectedly discovered that Argos functions as a ligand sink rather than a competitive antagonist or inverse agonist of the receptor as previously thought. Our demonstration that ligand sequestration can efficiently regulate the EGFR axis may provide a basis for the development of future therapies that neutralize erbB receptor agonists when such overexpression contributes to oncologic processes.

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Document Details

Document Type
Technical Report
Publication Date
May 01, 2005
Accession Number
ADA437913

Entities

People

  • Daryl E. Klein

Organizations

  • University of Pennsylvania

Tags

DTIC Thesaurus Topics

  • Amino Acids
  • Biomedical Research
  • Carrier Proteins
  • Cell Physiological Processes
  • Cells
  • Chemical Synthesis
  • Chemistry
  • Demonstrations
  • Growth Factors
  • Inhibition
  • Inhibitors
  • Peptide Growth Factors
  • Polysaccharides
  • Proteins
  • Surface Plasmon Resonance
  • Surface Plasmons
  • Tyrosine

Fields of Study

  • Biology

Readers

  • Breast cancer cell signaling and growth regulation.