Breaking up is hard to do: PI3K isoforms on the rebound

Cancer Cell. 2015 Jan 12;27(1):5-7. doi: 10.1016/j.ccell.2014.12.003.

Abstract

In this issue of Cancer Cell, Schwartz and colleagues and Costa and colleagues demonstrate that inhibition of PI3Kα or PI3Kβ in cancer cells with hyperactivated PI3Kα or PI3Kβ, respectively, activates the other isoform, leading to a "rebound" of the PI3K activity through different compensation mechanisms.

Publication types

  • Comment

MeSH terms

  • Aniline Compounds / pharmacology*
  • Animals
  • Antineoplastic Combined Chemotherapy Protocols / pharmacology*
  • Breast Neoplasms / drug therapy*
  • Chromones / pharmacology*
  • Class I Phosphatidylinositol 3-Kinases / metabolism*
  • Female
  • Humans
  • Neoplasms / drug therapy*
  • PTEN Phosphohydrolase / genetics*
  • Phosphoinositide-3 Kinase Inhibitors*
  • Protein Kinase Inhibitors / pharmacology*
  • Pyrimidinones / pharmacology*
  • Thiazoles / pharmacology*
  • ortho-Aminobenzoates / pharmacology*

Substances

  • 2-(1-(7-methyl-2-morpholin-4-yl-4-oxo-4H-pyrido(1,2-a)pyrimidin-9-yl)ethylamino)benzoic acid
  • AZD8186
  • Aniline Compounds
  • Chromones
  • Phosphoinositide-3 Kinase Inhibitors
  • Protein Kinase Inhibitors
  • Pyrimidinones
  • Thiazoles
  • ortho-Aminobenzoates
  • Alpelisib
  • Class I Phosphatidylinositol 3-Kinases
  • PTEN Phosphohydrolase