Molecular targets for cancer therapy and prevention

Chest. 2004 May;125(5 Suppl):97S-101S. doi: 10.1378/chest.125.5_suppl.97s-a.

Abstract

Despite major improvements in patient management, the prognosis for patients with lung cancer remains dismal. As our knowledge of the molecular biology of cancers has increased, new targets for therapeutic interventions have been identified. In this article, we discuss some of the more recent developments in this field. They include revisiting some of the established concepts, such as retinoid metabolism and the inhibition of cyclooxygenase-2 metabolism. In addition, newer targets, such as transforming growth factor-beta signaling, Janus-activated kinase/signal transducers and activators of transcription pathway, and cell invasion are discussed. These studies demonstrate that multiple, often overlapping, mechanisms of disruption are present in lung cancer cells, presenting a plethora of molecular targets.

Publication types

  • Review

MeSH terms

  • Cyclooxygenase 2
  • Humans
  • Isoenzymes / antagonists & inhibitors
  • Lung Neoplasms / drug therapy*
  • Lung Neoplasms / metabolism
  • Lung Neoplasms / pathology
  • Lung Neoplasms / prevention & control*
  • Membrane Proteins
  • Molecular Biology
  • Neoplasm Invasiveness
  • Neoplasm Metastasis
  • Prostaglandin-Endoperoxide Synthases
  • Protein-Tyrosine Kinases / physiology
  • Signal Transduction
  • Transcription, Genetic
  • Transforming Growth Factor beta / physiology
  • Tretinoin / metabolism

Substances

  • Isoenzymes
  • Membrane Proteins
  • Transforming Growth Factor beta
  • Tretinoin
  • Cyclooxygenase 2
  • PTGS2 protein, human
  • Prostaglandin-Endoperoxide Synthases
  • Protein-Tyrosine Kinases