PI3K alterations are well-established drivers of breast cancer. However, PI3K-targeted therapy often results in treatment resistance and recurrence. By modeling PI3K tumorigenesis and inactivation in mice, this report shows that resistance may arise from alternative activation of the PI3K signaling pathway or by acquired alterations in other oncogenic drivers. As these mechanisms are also present in human tumors, they could be useful indicators to monitor and improve treatment responses.
- Pixu Liu
- Hailing Cheng
- Jean J Zhao
