Abstract
The phosphoinositide 3 kinase (PI3K)/Akt pathway is frequently aberrantly activated in breast cancer and, basing on preclinical data, leads to cell growth and tumor proliferation. PI3K pathway activation has been suggested as a potential driver of resistance to endocrine and anti-HER2 therapies. Large genomic studies have observed that the PIK3CA gene is mutated in up to 40 % of breast cancers, mainly estrogen receptor- and HER2-positive. Some strategies targeting the PI3K/Akt/mTOR axis, in particular co-targeting the estrogen receptor and mTOR in endocrine resistant estrogen receptor-positive breast cancer, have proven successfully this hypothesis. Pan-class I PI3K inhibitors and more selective p110α inhibitors are currently under investigation in different clinical settings. In this review, clinical data on the prognostic and predictive role of PIK3CA mutations in different breast cancer subtypes are covered, and a picture on the current clinical research on PI3K inhibitors is provided.
| Original language | English |
|---|---|
| Pages (from-to) | 161-169 |
| Number of pages | 9 |
| Journal | Current Breast Cancer Reports |
| Volume | 7 |
| Issue number | 3 |
| DOIs | |
| Publication status | Published - Sep 24 2015 |
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Keywords
- Breast cancer
- PI3K
- PIK3CA
- Predictive factor
ASJC Scopus subject areas
- Oncology
Cite this
PIK3CA : a Target or a Marker in Breast Cancers. / Dieci, Maria Vittoria; Guarneri, Valentina.
In: Current Breast Cancer Reports, Vol. 7, No. 3, 24.09.2015, p. 161-169.Research output: Contribution to journal › Article
}
TY - JOUR
T1 - PIK3CA
T2 - a Target or a Marker in Breast Cancers
AU - Dieci, Maria Vittoria
AU - Guarneri, Valentina
PY - 2015/9/24
Y1 - 2015/9/24
N2 - The phosphoinositide 3 kinase (PI3K)/Akt pathway is frequently aberrantly activated in breast cancer and, basing on preclinical data, leads to cell growth and tumor proliferation. PI3K pathway activation has been suggested as a potential driver of resistance to endocrine and anti-HER2 therapies. Large genomic studies have observed that the PIK3CA gene is mutated in up to 40 % of breast cancers, mainly estrogen receptor- and HER2-positive. Some strategies targeting the PI3K/Akt/mTOR axis, in particular co-targeting the estrogen receptor and mTOR in endocrine resistant estrogen receptor-positive breast cancer, have proven successfully this hypothesis. Pan-class I PI3K inhibitors and more selective p110α inhibitors are currently under investigation in different clinical settings. In this review, clinical data on the prognostic and predictive role of PIK3CA mutations in different breast cancer subtypes are covered, and a picture on the current clinical research on PI3K inhibitors is provided.
AB - The phosphoinositide 3 kinase (PI3K)/Akt pathway is frequently aberrantly activated in breast cancer and, basing on preclinical data, leads to cell growth and tumor proliferation. PI3K pathway activation has been suggested as a potential driver of resistance to endocrine and anti-HER2 therapies. Large genomic studies have observed that the PIK3CA gene is mutated in up to 40 % of breast cancers, mainly estrogen receptor- and HER2-positive. Some strategies targeting the PI3K/Akt/mTOR axis, in particular co-targeting the estrogen receptor and mTOR in endocrine resistant estrogen receptor-positive breast cancer, have proven successfully this hypothesis. Pan-class I PI3K inhibitors and more selective p110α inhibitors are currently under investigation in different clinical settings. In this review, clinical data on the prognostic and predictive role of PIK3CA mutations in different breast cancer subtypes are covered, and a picture on the current clinical research on PI3K inhibitors is provided.
KW - Breast cancer
KW - PI3K
KW - PIK3CA
KW - Predictive factor
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U2 - 10.1007/s12609-015-0184-1
DO - 10.1007/s12609-015-0184-1
M3 - Article
AN - SCOPUS:84940182413
VL - 7
SP - 161
EP - 169
JO - Current Breast Cancer Reports
JF - Current Breast Cancer Reports
SN - 1943-4588
IS - 3
ER -