New preclinical cancer biology work in the British Journal of Cancer connects TP53 mutations in urothelial carcinoma to CD8+ T cell exhaustion and therapy resistance. The study describes how mutated TP53 reshapes the tumor immune microenvironment (TIME), biasing T cells toward an exhausted state. Separate research highlights PRMT6’s role in promoting angiogenesis in colorectal cancer, pointing to tumor vascularization as another pathway that may be therapeutically targetable. Together, the findings expand a growing set of mechanisms linking intrinsic tumor genetics, immune dysfunction, and microenvironmental support factors that drive treatment failure.