Conventional chemotherapy with DNA-damaging agents has helped countless cancer patients become cancer survivors. This successful outcome is sometimes accompanied by long-term side effects, however. In young female patients, for example, the alkylating agent cyclophosphamide can compromise fertility. This occurs because the drug causes inappropriate activation of ovarian follicular development, thereby exposing oocytes to its DNA-damaging effects. Studying a mouse model, Goldman et al. showed that ovarian function and fertility are preserved when cyclophosphamide is coadministered with drugs called mTORC1/2 inhibitors, which suppress a signaling pathway required for follicular activation. mTORC1/2 inhibitors are already clinically approved for other purposes, including treatment of certain forms of breast cancer, and may merit exploration as a fertility-preserving strategy in female cancer patients.
