The p53 transcription factor is the most frequently mutated tumor suppressor gene in human cancer. In approximately 50% of human cancers p53 is mutated and in many of the remaining cases, the function of the retained wild type p53 protein is compromised. p53 knockout mice develop tumors with short latency and 100% penetrance. These observations demonstrate the critical role of p53 in tumor prevention.
The Hippo tumor suppressor pathway is emerging as an important regulator of cancer-related processes. At the core of the Hippo pathway are two kinases, LATS1 and LATS2, which negatively regulate the pathway effectors, YAP and TAZ. YAP and TAZ are transcriptional co-activators that have been shown to promote or inhibit oncogenic transformation, in different contexts.
The exciting recent breakthroughs in cancer immunotherapy have stimulated great interest in cancer immunology. Therefore, in view of the major roles of p53 mutations and Hippo deregulation in cancer, we wish to elucidate the impact of these pathways on the crosstalk between tumors and the immune system.
