Table 2.

Common molecular alterations in endometrial cancer.

Molecular (pathway) alteration	Frequency in EC	Description	Prognosis	Potential targeted therapies
POLE mutation	6–12%	DNA repair	Excellent	PD-1/PD-L1 immune checkpoint inhibitors*
MMRd	20–40%	DNA repair	Intermediate	PD-1/PD-L1 immune checkpoint inhibitors*
TP53 mutation	9–29%	Tumor suppressor	Poor	PARPi; platinum derivatives
L1CAM overexpression	16–28%	Cell adhesion/signaling protein	Poor	n/a*
ER/PR expression	72–95%	Hormone receptors	Good	Endocrine therapy (with PI3K/mTOR inhibitors)
Wnt-ß-catenin pathway	18–25%	Wnt signaling pathway	Intermediate	n/a
PI3K-AKT-mTOR pathway	> 80%	PI3K/AKT/mTOR signaling pathway	Good-intermediate	PI3K, AKT, mTOR inhibitors
HER2/Neu overexpression	14–47%	Epidermal growth factor receptor	Poor	Monoclonal antibodies, protein kinase inhibitors
ARID1A mutation	30–40%	Tumor suppressor	Good-intermediate	EZH2 inhibitors

EC, endometrial cancer; n/a, not available. For abbreviations see text

*The addition of PARP inhibitors (PARPi) has been explored for several molecular alterations, however evidence of efficacy is still limited