Breast tumor cells with P13K mutation or HER2 amplification are selectively addicted to Akt signaling Academic Article uri icon

Overview

MeSH Major

  • Breast Neoplasms
  • Gene Amplification
  • Phosphatidylinositol 3-Kinases
  • Proto-Oncogene Proteins c-akt
  • Receptor, ErbB-2

abstract

  • These data demonstrate that breast cancers with PI3K mutation or HER2 amplification are selectively dependent on Akt signaling, and that effective inhibition of Akt in tumors is feasible and effective in vivo. These findings suggest that direct inhibition of Akt may represent a therapeutic strategy for breast and other cancers that are addicted to the pathway including tumors with resistant to Herceptin.

publication date

  • August 26, 2008

Research

keywords

  • Academic Article

Identity

Language

  • eng

PubMed Central ID

  • PMC2516933

Digital Object Identifier (DOI)

  • 10.1371/journal.pone.0003065

PubMed ID

  • 18725974

Additional Document Info

start page

  • e3065

volume

  • 3

number

  • 8