PMID- 23218708
OWN - NLM
STAT- MEDLINE
DCOM- 20130510
LR  - 20220321
IS  - 1532-1967 (Electronic)
IS  - 0305-7372 (Print)
IS  - 0305-7372 (Linking)
VI  - 39
IP  - 4
DP  - 2013 Jun
TI  - Defining biomarkers to predict sensitivity to PI3K/Akt/mTOR pathway inhibitors in 
      breast cancer.
PG  - 313-20
LID - S0305-7372(12)00234-4 [pii]
LID - 10.1016/j.ctrv.2012.11.002 [doi]
AB  - BACKGROUND: Identification and validation of biomarkers is increasingly important 
      for the integration of novel targeted agents in the treatment of cancer. The 
      phosphatidylinositol 3-kinase (PI3K)/Akt/mammalian target of rapamycin (mTOR) 
      pathway represents a promising therapeutic target in breast carcinoma, and 
      inhibitors targeting different nodes of the PI3K/Akt/mTOR axis are in 
      development. Identification of biomarkers to help select patients who are most 
      likely to benefit from these treatments is an essential unmet need. DESIGN: 
      MEDLINE and international conference abstracts were searched for evidence of 
      markers of sensitivity to PI3K/Akt/mTOR pathway inhibitors in breast cancer 
      patients and preclinical models. RESULTS: Preclinical evidence suggests that 
      PI3K/Akt/mTOR pathway aberrations, notably in PIK3CA, may identify a 
      subpopulation of patients with breast cancer who preferentially respond to 
      PI3K/Akt/mTOR inhibitors. However, additional markers are needed to identify all 
      patients with de novo sensitivity to PI3K/Akt/mTOR pathway inhibition. Early 
      clinical studies to validate these biomarkers have as yet been inconclusive. 
      CONCLUSIONS: Prospective, adequately designed and powered clinical trials are 
      needed to test candidate biomarkers of sensitivity to PI3K/Akt/mTOR pathway 
      inhibitors in patients with breast cancer, and to determine whether certain 
      PI3K/Akt/mTOR pathway inhibitors are more appropriate in different subtypes 
      depending on the pattern of molecular alteration.
CI  - Copyright (c) 2012 Elsevier Ltd. All rights reserved.
FAU - Gonzalez-Angulo, A M
AU  - Gonzalez-Angulo AM
AD  - Department of Breast Medical Oncology, The University of Texas, M.D. Anderson 
      Cancer Center, Houston, TX, USA. agonzalez@mdanderson.org
FAU - Blumenschein, G R Jr
AU  - Blumenschein GR Jr
LA  - eng
GR  - K23 CA121994/CA/NCI NIH HHS/United States
GR  - P30 CA016672/CA/NCI NIH HHS/United States
PT  - Journal Article
PT  - Research Support, Non-U.S. Gov't
DEP - 20121206
PL  - Netherlands
TA  - Cancer Treat Rev
JT  - Cancer treatment reviews
JID - 7502030
RN  - 0 (Biomarkers, Tumor)
RN  - 0 (Phosphoinositide-3 Kinase Inhibitors)
RN  - 0 (Protein Kinase Inhibitors)
RN  - EC 2.7.1.1 (MTOR protein, human)
RN  - EC 2.7.11.1 (Oncogene Protein v-akt)
RN  - EC 2.7.11.1 (TOR Serine-Threonine Kinases)
SB  - IM
MH  - Antineoplastic Combined Chemotherapy Protocols/*therapeutic use
MH  - Biomarkers, Tumor/*metabolism
MH  - Breast Neoplasms/*drug therapy/*enzymology
MH  - Clinical Trials as Topic
MH  - Female
MH  - Humans
MH  - Molecular Targeted Therapy/methods
MH  - Oncogene Protein v-akt/*antagonists & inhibitors/metabolism
MH  - Phosphatidylinositol 3-Kinases/metabolism
MH  - *Phosphoinositide-3 Kinase Inhibitors
MH  - Protein Kinase Inhibitors/administration & dosage/*therapeutic use
MH  - Signal Transduction/drug effects
MH  - TOR Serine-Threonine Kinases/*antagonists & inhibitors/metabolism
PMC - PMC3604032
MID - NIHMS423317
EDAT- 2012/12/12 06:00
MHDA- 2013/05/11 06:00
PMCR- 2014/06/01
CRDT- 2012/12/11 06:00
PHST- 2012/04/24 00:00 [received]
PHST- 2012/11/05 00:00 [revised]
PHST- 2012/11/06 00:00 [accepted]
PHST- 2012/12/11 06:00 [entrez]
PHST- 2012/12/12 06:00 [pubmed]
PHST- 2013/05/11 06:00 [medline]
PHST- 2014/06/01 00:00 [pmc-release]
AID - S0305-7372(12)00234-4 [pii]
AID - 10.1016/j.ctrv.2012.11.002 [doi]
PST - ppublish
SO  - Cancer Treat Rev. 2013 Jun;39(4):313-20. doi: 10.1016/j.ctrv.2012.11.002. Epub 
      2012 Dec 6.