ErbB-targeted therapeutic approaches in human cancer

Exp Cell Res. 2003 Mar 10;284(1):122-30. doi: 10.1016/s0014-4827(02)00104-0.

Abstract

The overexpression and aberrant function of the epidermal growth factor receptor (EGFR, erbB1, HER1) and its ligands and coreceptors in a wide spectrum of epithelial cancers have provided a rationale for targeting this signaling network with novel treatment approaches. Several antireceptor therapeutic strategies have been pursued, but two stand ahead in their clinical development. One approach has been the generation of small molecules that compete with adenosine triphosphate (ATP) for binding to the receptor's kinase pocket, thus blocking receptor activation and the transduction of postreceptor signals. The second approach utilizes humanized monoclonal antibodies generated against the receptor's ligand-binding extracellular domain. These antibodies block binding of receptor-activating ligands and, in some cases, can induce receptor endocytosis and downregulation. Clinical studies already suggest that both of these approaches, either alone or in combination with standard anticancer therapies, are well tolerated and can induce clinical responses and tumor stabilization in a variety of common carcinomas.

Publication types

  • Research Support, U.S. Gov't, P.H.S.
  • Review

MeSH terms

  • Adenosine Triphosphate / metabolism
  • Antibodies, Monoclonal / therapeutic use*
  • Antineoplastic Agents / therapeutic use*
  • Cell Transformation, Neoplastic
  • Clinical Trials as Topic
  • Down-Regulation
  • Endocytosis
  • Enzyme Inhibitors / therapeutic use*
  • ErbB Receptors / antagonists & inhibitors*
  • ErbB Receptors / physiology
  • Gene Expression Regulation, Neoplastic
  • Humans
  • Immunotherapy
  • Neoplasms / drug therapy*
  • Neoplasms / immunology
  • Neoplasms / pathology
  • Protein-Tyrosine Kinases / antagonists & inhibitors*
  • Signal Transduction / physiology

Substances

  • Antibodies, Monoclonal
  • Antineoplastic Agents
  • Enzyme Inhibitors
  • Adenosine Triphosphate
  • ErbB Receptors
  • Protein-Tyrosine Kinases