Overcoming endocrine resistance in breast cancer: role of the PI3K and the mTOR pathways

Expert Rev Anticancer Ther. 2013 Feb;13(2):143-7. doi: 10.1586/era.12.173.

Abstract

Overcoming endocrine resistance is a 21st century hurdle in the treatment of hormone receptor-positive breast cancers. Estrogen plays a role in the growth of 70% of breast cancers. There are many strategies evolved to overcome estrogen resistance. Established strategies include using drugs such as tamoxifen, a selective estrogen receptor modulator to selectively block estrogen receptors and aromatase inhibitors to decrease the synthesis of estrogen. However, endocrine resistance is commonly encountered in treating patients with standard single-therapy regimens. Recently, the role of the PI3K and the mTOR pathways has been targeted to overcome resistance. The mTOR pathway is a complex pathway regulating cell metabolism, growth and apoptosis. Novel agents such as mTOR inhibitors, PI3K inhibitors and Akt inhibitors are transitioning from bench-top research to clinical application with promising results. This article reviews the common mechanisms of endocrine resistance, and combination therapies that utilize the mTOR/PI3K pathways to overcome resistance.

Publication types

  • Review

MeSH terms

  • Antineoplastic Agents, Hormonal / pharmacology
  • Antineoplastic Agents, Hormonal / therapeutic use
  • Antineoplastic Combined Chemotherapy Protocols
  • Aromatase Inhibitors / pharmacology
  • Aromatase Inhibitors / therapeutic use
  • Breast Neoplasms / drug therapy*
  • Breast Neoplasms / metabolism*
  • Drug Resistance, Neoplasm / drug effects
  • Female
  • Humans
  • Phosphatidylinositol 3-Kinases / metabolism*
  • Selective Estrogen Receptor Modulators / pharmacology
  • Selective Estrogen Receptor Modulators / therapeutic use
  • Signal Transduction / drug effects
  • TOR Serine-Threonine Kinases / antagonists & inhibitors
  • TOR Serine-Threonine Kinases / metabolism*
  • Tamoxifen / pharmacology
  • Tamoxifen / therapeutic use

Substances

  • Antineoplastic Agents, Hormonal
  • Aromatase Inhibitors
  • Selective Estrogen Receptor Modulators
  • Tamoxifen
  • MTOR protein, human
  • TOR Serine-Threonine Kinases