PI3K-AKT-mTOR inhibitors for the systemic treatment of endometrial cancer

David N. Church; Romana Koppensteiner; Timothy A. Yap; Daniel Fink; Konstantin J. Dedes

doi:10.1586/eog.12.51

PI3K-AKT-mTOR inhibitors for the systemic treatment of endometrial cancer

David N. Church, Romana Koppensteiner, Timothy A. Yap, Daniel Fink, Konstantin J. Dedes

Research output: Contribution to journal › Review article › peer-review

1 Scopus citations

Abstract

Advanced and metastatic endometrial cancer (EC) is associated with a poor prognosis, despite the availability of systemic treatments including endocrine therapy and combination cytotoxic chemotherapy. Response rates of systemic treatments are associated with high toxicity, have poor response rates and responses are genenrally short-lived. Recent findings on the molecular aberrations of the subtypes of EC have enabled in vitro and in vivo studies to exploit targeted treatment for this disease. One of the most common molecular aberrations in EC is the PI3K-AKT-mTOR pathway being activated through different mechanisms in both type I and type II ECs. The aim of this review is to summarize the numerous preclinical and clinical studies, and discuss the future directions.

Original language	English (US)
Pages (from-to)	421-430
Number of pages	10
Journal	Expert Review of Obstetrics and Gynecology
Volume	7
Issue number	5
DOIs	https://doi.org/10.1586/eog.12.51
State	Published - Sep 1 2012

Keywords

AKT mouse models
mTOR inhibitors
PI3KCA
PTEN
targeted treatments
uterine cancers

ASJC Scopus subject areas

Obstetrics and Gynecology
Reproductive Medicine
Maternity and Midwifery
Pediatrics, Perinatology, and Child Health

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10.1586/eog.12.51

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title = "PI3K-AKT-mTOR inhibitors for the systemic treatment of endometrial cancer",

abstract = "Advanced and metastatic endometrial cancer (EC) is associated with a poor prognosis, despite the availability of systemic treatments including endocrine therapy and combination cytotoxic chemotherapy. Response rates of systemic treatments are associated with high toxicity, have poor response rates and responses are genenrally short-lived. Recent findings on the molecular aberrations of the subtypes of EC have enabled in vitro and in vivo studies to exploit targeted treatment for this disease. One of the most common molecular aberrations in EC is the PI3K-AKT-mTOR pathway being activated through different mechanisms in both type I and type II ECs. The aim of this review is to summarize the numerous preclinical and clinical studies, and discuss the future directions.",

keywords = "AKT mouse models, mTOR inhibitors, PI3KCA, PTEN, targeted treatments, uterine cancers",

author = "Church, {David N.} and Romana Koppensteiner and Yap, {Timothy A.} and Daniel Fink and Dedes, {Konstantin J.}",

note = "Funding Information: D Church is funded by a research grant from the Oxford Cancer Research Centre. R Koppensteiner and KJ Dedes are funded in part by a grant from the Julius M{\"u}ller Stiftung. TA Yap is recipient of the 2011 Scott Minerd Prostate Cancer Foundation Young Investigator Award. The authors have no other relevant affiliations or financial involvement with any organization or entity with a financial interest in or financial conflict with the subject matter or materials discussed in the manuscript apart from those disclosed.",

year = "2012",

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doi = "10.1586/eog.12.51",

language = "English (US)",

volume = "7",

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AU - Church, David N.

AU - Koppensteiner, Romana

AU - Yap, Timothy A.

AU - Fink, Daniel

AU - Dedes, Konstantin J.

N1 - Funding Information: D Church is funded by a research grant from the Oxford Cancer Research Centre. R Koppensteiner and KJ Dedes are funded in part by a grant from the Julius Müller Stiftung. TA Yap is recipient of the 2011 Scott Minerd Prostate Cancer Foundation Young Investigator Award. The authors have no other relevant affiliations or financial involvement with any organization or entity with a financial interest in or financial conflict with the subject matter or materials discussed in the manuscript apart from those disclosed.

PY - 2012/9/1

Y1 - 2012/9/1

N2 - Advanced and metastatic endometrial cancer (EC) is associated with a poor prognosis, despite the availability of systemic treatments including endocrine therapy and combination cytotoxic chemotherapy. Response rates of systemic treatments are associated with high toxicity, have poor response rates and responses are genenrally short-lived. Recent findings on the molecular aberrations of the subtypes of EC have enabled in vitro and in vivo studies to exploit targeted treatment for this disease. One of the most common molecular aberrations in EC is the PI3K-AKT-mTOR pathway being activated through different mechanisms in both type I and type II ECs. The aim of this review is to summarize the numerous preclinical and clinical studies, and discuss the future directions.

AB - Advanced and metastatic endometrial cancer (EC) is associated with a poor prognosis, despite the availability of systemic treatments including endocrine therapy and combination cytotoxic chemotherapy. Response rates of systemic treatments are associated with high toxicity, have poor response rates and responses are genenrally short-lived. Recent findings on the molecular aberrations of the subtypes of EC have enabled in vitro and in vivo studies to exploit targeted treatment for this disease. One of the most common molecular aberrations in EC is the PI3K-AKT-mTOR pathway being activated through different mechanisms in both type I and type II ECs. The aim of this review is to summarize the numerous preclinical and clinical studies, and discuss the future directions.

KW - AKT mouse models

KW - mTOR inhibitors

KW - PI3KCA

KW - PTEN

KW - targeted treatments

KW - uterine cancers

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PI3K-AKT-mTOR inhibitors for the systemic treatment of endometrial cancer

Abstract

Keywords

ASJC Scopus subject areas

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