MYC and p53 alterations cooperate through VEGF signaling to repress cytotoxic T cell and immunotherapy responses in prostate cancer.
Katherine C MurphyKelly D DeMarcoLin ZhouYvette Lopez-DiazYu-Jui HoJunhui LiShi BaiKarl SiminJulie Lihua ZhuArthur M MercurioMarcus RuscettiPublished in: bioRxiv : the preprint server for biology (2024)
Though immune checkpoint blockade (ICB) therapies can achieve curative responses in many treatment-refractory cancers, they have limited efficacy in CRPC. Here we identify a genetic mechanism by which VEGF contributes to T cell suppression, and demonstrate that VEGFR2 blockade can potentiate the effects of PD-L1 ICB to immunologically treat CRPC.