Akt-regulated pathways in prostate cancer

Oncogene. 2005 Nov 14;24(50):7465-74. doi: 10.1038/sj.onc.1209096.

Abstract

Prostate cancer remains a major cause of cancer-related mortality. Genetic clues to the molecular pathways driving the most aggressive forms of prostate cancer have been limited. Genetic inactivation of PTEN through either gene deletion or point mutation is reasonably common in metastatic prostate cancer and the resulting activation of phosphoinostide 3-kinase, AKT and mTOR provides a major therapeutic opportunity in this disease as mTOR inhibitors, HSP90 inhibitors and PI3K inhibitors begin to enter clinical development.

Publication types

  • Review

MeSH terms

  • Humans
  • Male
  • PTEN Phosphohydrolase / genetics*
  • PTEN Phosphohydrolase / physiology
  • Phosphatidylinositol 3-Kinases / genetics
  • Phosphatidylinositol 3-Kinases / metabolism
  • Prostatic Neoplasms / genetics*
  • Prostatic Neoplasms / physiopathology*
  • Protein Kinases / genetics
  • Protein Kinases / physiology
  • Proto-Oncogene Proteins c-akt / genetics*
  • Proto-Oncogene Proteins c-akt / physiology
  • Signal Transduction
  • TOR Serine-Threonine Kinases

Substances

  • Protein Kinases
  • Phosphatidylinositol 3-Kinases
  • MTOR protein, human
  • TOR Serine-Threonine Kinases
  • Proto-Oncogene Proteins c-akt
  • PTEN Phosphohydrolase
  • PTEN protein, human