Abstract
Uterine serous carcinomas show more frequent mutations of TP53, FBXW7, PIK3CA, and PP2R1A. Furthermore, cyclin-dependent kinase, human epidermal growth factor receptor 2, phosphatidylinositol 3-kinase/protein kinase B, and mammalian target of rapamycin signaling pathways are involved in uterine serous carcinoma progression. However, most patients with uterine serous carcinoma develop chemoresistance to paclitaxel and carboplatin. Moreover, uterine serous carcinoma shows immunosuppressive microenvironment with lower frequency of microsatellite instability. However, some clinical trials of human epidermal growth factor receptor 2/neu and WEE1 targeted therapies showed good effects in prolonging the survival in patients with uterine serous carcinoma. More effective targeted therapies and immunotherapies need to be developed in recurrent uterine serous carcinomas.
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