Regulation of proliferation, apoptosis and cell cycle in gastrointestinal disorders

Curr Opin Pharmacol. 2009 Dec;9(6):708-14. doi: 10.1016/j.coph.2009.06.024. Epub 2009 Jul 31.

Abstract

Carcinogenesis is a multifactorial process representing the accumulation of acquired and genetic defects, and it has become apparent that many gastrointestinal cancers originate from a state of chronic inflammation. Advances in the field of inflammation-induced carcinogenesis over the past several years have focused on the creation of agonists or antagonists of cytokines and pathways regulating proliferation and apoptosis, and include advances such as the discovery of pharmacological inhibitors of the histone deacetylase (HDAC) family of transcriptional co-repressors, which induce apoptosis of neoplastic cells; discovery of natural products, such as curcumin, which have been shown to regulate cytokine expression; and further investigation into the role of annexin A1, a downstream mediator of glucocorticoid action, in the regulation of inflammation, to name a few.

Publication types

  • Review

MeSH terms

  • Apoptosis / drug effects*
  • Apoptosis / physiology
  • Cell Cycle / drug effects*
  • Cell Cycle / physiology
  • Cell Proliferation / drug effects*
  • Colorectal Neoplasms / drug therapy*
  • Drug Delivery Systems
  • Humans
  • Inflammation / drug therapy
  • Inflammation Mediators / agonists
  • Inflammation Mediators / antagonists & inhibitors
  • Inflammatory Bowel Diseases / drug therapy*
  • Models, Immunological

Substances

  • Inflammation Mediators