LAUSR

Senescence induction in cancer works as a potent weapon to eradicate tumorigenesis. Therapies that enhance senescence not only promote a stable cell growth arrest but also work as a strong stimulus for the activation of the tumor immune response. However, cancer cells bypass senescence by either acquiring new genetic alterations or by disrupting the tumor immune response. Here, I will discuss the identification of oncogenic pathways that bypass Pten-loss-induced cellular senescence, thereby promoting prostate cancer progression and metastasis. Next, I will present evidence demonstrating that both tumor-infiltrating myeloid-derived suppressor cells (MDSCs) and tumor-associated macrophages (TAMs) control senescence induction in chemotherapy-treated prostate cancers and that immunotherapies that interfere with either MDSCs9 recruitment or the polarization of TAMs promote senescence in advanced PTEN-deficient prostate cancer. Citation Format: Andrea Alimonti. Dual targeting of senescence and tumor immunity for cancer therapy [abstract]. In: Proceedings of the American Association for Cancer Research Annual Meeting 2018; 2018 Apr 14-18; Chicago, IL. Philadelphia (PA): AACR; Cancer Res 2018;78(13 Suppl):Abstract nr SY26-03.