Targeting mutant p53 in cancer: a long road to precision therapy.

摘要: The TP53 tumor suppressor is the most frequently mutated gene in human cancers. In recent years, a blooming of research efforts based on both cell lines and mouse models have highlighted how deeply mutant p53 proteins affect fundamental cellular pathways with cancer-promoting outcomes. Neomorphic activities spread over multiple levels, impinging chromatin structure, transcriptional regulation microRNA maturation, shaping proteome cell's metabolic pathways, also exerting cytoplasmic functions displaying cell-extrinsic effects. These tumorigenic are inextricably linked blend highly corrupted processes that characterize context. Recent studies indicate successful strategies to extract core aspects oncogenic potential identify unique dependencies entail superimposition large-scale analyses performed experimental systems, together mindful use animal models. This will hopefully soon lead long-awaited inclusion as an actionable target clinical antitumor therapies.