mTOR signaling in glioblastoma: lessons learned from bench to bedside

Neuro Oncol. 2010 Aug;12(8):882-9. doi: 10.1093/neuonc/noq052. Epub 2010 May 14.

Abstract

Phosphatidyl-inositol-3 kinases (PI3Ks) constitute a family of intracellular lipid kinases that are frequently hyperactivated in glioblastoma. The PI3K complex links growth factor signaling with cellular proliferation, differentiation, metabolism, and survival. Mammalian target of rapamycin (mTOR) acts both as a downstream effector and upstream regulator of PI3K, thus highlighting its importance in glioblastoma. This review highlights laboratory and clinical evidence of mTOR's role in glioblastoma. Mechanisms of escape from mTOR inhibition are also discussed, as well as future clinical strategies of mTOR inhibition.

Publication types

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

MeSH terms

  • Animals
  • Brain Neoplasms / metabolism*
  • Glioblastoma / metabolism*
  • Humans
  • Intracellular Signaling Peptides and Proteins / metabolism*
  • Protein-Serine-Threonine Kinases / metabolism*
  • Signal Transduction / physiology*
  • TOR Serine-Threonine Kinases

Substances

  • Intracellular Signaling Peptides and Proteins
  • MTOR protein, human
  • TOR Serine-Threonine Kinases
  • Protein-Serine-Threonine Kinases