Journal of Mammary Gland Biology and Neoplasia

, Volume 17, Issue 3–4, pp 205–216

Targeting the PI3K/Akt/mTOR Pathway for Breast Cancer Therapy

Article

DOI: 10.1007/s10911-012-9264-2

Cite this article as:
Cidado, J. & Park, B.H. J Mammary Gland Biol Neoplasia (2012) 17: 205. doi:10.1007/s10911-012-9264-2

Abstract

Recent advances in genetics and genomics have revealed new pathways that are aberrantly activated in many breast cancers. Chief among these genetic changes are somatic mutations and/or gains and losses of key genes within the phosphoinositide 3-kinase (PI3K) pathway. Since breast cancer cell growth and progression is often dependent upon activation of the PI3K pathway, there has been intense research interest in finding therapeutic agents that can selectively inhibit one or more constituents of this signaling cascade. Here we review key molecules involved with aberrant PI3K pathway activation in breast cancers and current efforts to target these components for therapeutic gain.

Keywords

PI3 Kinase PIK3CA Breast cancer Targeted therapy 

Abbreviation

4E-BP1

eIF4E-binding protein

Akt/PKB

protein kinase B

AMPK

AMP-activated protein kinase

CNS

central nervous system

DNA-PK

DNA-dependent protein kinase

EGFR

epidermal growth factor receptor

ER

estrogen receptor alpha

FDG

fluorodeoxyglucose

FGF

fibroblast growth factor

FISH

fluorescence in situ hybridization

FKBP12

FK506-binding protein

GPCR

G-protein-coupled receptors

HER2

human epidermal growth factor receptor 2

IGF-1R

insulin-like growth factor-1 receptor

ILK

integrin-linked kinase

IRS-1

insulin receptor substrate 1

miRNAs

microRNAs

mTOR

mammalian target of rapamycin

PARP

poly(ADP-ribose) polymerase

PDK-1

3’-phosphoinositide-dependent kinase 1

PET

positron emission tomography

PH

plextrin homology

PI3K

phosphoinositide 3-kinase

PI(3,4,5)P3

phosphatidylinositol-3,4,5-trisphosphate

PR

progesterone receptor

Pten

phosphatase and tensin homologue deleted on chromosome 10

pTyr

phosphotyrosine

RBD

Ras Binding Domain

Redd1

regulated in development and DNA damage response 1

Rheb

Ras homolog enriched in brain

RTK

receptor tyrosine kinase

SERD

selective estrogen receptor down-regulator

SERM

selective estrogen receptor modulator

SH2

Src homology 2

Tsc

tuberous sclerosis complex

Copyright information

© Springer Science+Business Media, LLC 2012

Authors and Affiliations

  1. 1.The Sidney Kimmel Comprehensive Cancer Center at Johns HopkinsBaltimoreUSA

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