Endometrial Cancer

The incidence of endometrial cancer, the most common gynecologic malignancy, has continued to increase over the past decade. Given the myriad of molecular alterations in endometrial cancer, there is a realopportunity for targeted therapies to become mainstay treatment for patients with advanced or recurrent stage disease. This chapter discusses pathways and molecular targets that are the most developed for targeted therapy in endometrial cancer, including the PI3K/AKT and Ras/Raf/MEK pathways, RTKs, EGFR and HER2, and VEGFR. A schematic of these relevant pathways and targets in endometrial cancer is also illustrated. Additionally, the benefit of exploiting PARP inhibitors and the use of metformin in endometrial cancer is discussed along with brief discussion on targeting challenging yet prevalent molecular alterations of p53 and E-cadherin. E-cadherin is a cell-cell adhesion protein and its downregulation in tumors is associated with epithelial-to-mesenchymal transition (EMT) and tumor cell migration and invasion.