PI3K has emerged as a potential therapeutic target for serious endometrial cancer but efficacy and duration of response is limited. Here, the authors develop a serous endometrial cancer murine model driven by PIK3CA mutation, TP53 loss and MYC overexpression, identifying FGFR pathway activation as a driver of PI3K-targeted therapeutic resistance and immune suppression.
- Xin Cheng
- Yadong Zhang
- Jean J. Zhao
