Esophageal adenocarcinoma: treatment modalities in the era of targeted therapy

Dig Dis Sci. 2010 Dec;55(12):3304-14. doi: 10.1007/s10620-010-1187-4. Epub 2010 Mar 19.

Abstract

Esophageal adenocarcinoma is an aggressive malignancy with a poor outcome, and its incidence continues to rise at an alarming rate. Current treatment strategies combining chemotherapy, radiation, and surgery are plagued with high rates of recurrence and metastasis. Multiple molecular pathways including the epidermal growth factor receptor, vascular endothelial growth factor, v-erb-b2 erythroblastic leukemia viral oncogene homolog (ERBB2), and Aurora kinase pathways are activated in many esophageal adenocarcinomas. In many cases, these pathways have critical roles in tumor progression. Research on the mechanisms by which these pathways contribute to disease progression has resulted in numerous biologic agents and small molecules with the potential to improve outcome. The promise of targeted therapy and personalized medicine in improving the clinical outcome is now closer than it has ever been.

Publication types

  • Research Support, N.I.H., Extramural
  • Review

MeSH terms

  • Adenocarcinoma / drug therapy*
  • Adenocarcinoma / mortality
  • Adenocarcinoma / physiopathology
  • Adenocarcinoma / therapy
  • Angiogenesis Inhibitors / pharmacology
  • Antineoplastic Agents / pharmacology
  • Aurora Kinases
  • Barrett Esophagus / pathology
  • Clinical Trials as Topic
  • Combined Modality Therapy
  • Disease Progression
  • ErbB Receptors / antagonists & inhibitors
  • ErbB Receptors / drug effects
  • ErbB Receptors / physiology
  • Esophageal Neoplasms / drug therapy*
  • Esophageal Neoplasms / mortality
  • Esophageal Neoplasms / physiopathology
  • Esophageal Neoplasms / therapy
  • Esophagectomy
  • Humans
  • Molecular Targeted Therapy* / methods
  • Molecular Targeted Therapy* / trends
  • Protein Serine-Threonine Kinases / antagonists & inhibitors
  • Protein Serine-Threonine Kinases / pharmacology
  • Treatment Outcome

Substances

  • Angiogenesis Inhibitors
  • Antineoplastic Agents
  • ErbB Receptors
  • Aurora Kinases
  • Protein Serine-Threonine Kinases