The role of p53/p73 family members in the cytotoxic response

Every cell in the human body carries a built-in safety switch—the p53 family of proteins—that decides whether a damaged cell should repair itself or die. This lab is working out exactly how that decision gets made when cells are hit by drugs, chemicals, or free radicals. The problem is that toxic exposure, whether from the environment, the workplace, or cancer therapy, is a major driver of disease. While scientists know the p53 family controls the cellular stress response, the precise molecular steps that link a specific toxin to tumour progression remain unclear. This project fills that gap by combining genetically modified mouse models with high-throughput analysis to map how these transcription factors regulate injury response. If the research succeeds, it could lead to synthetic compounds that dial p53 family activity up or down on demand. That would matter most for cancer treatment—where boosting the death signal in tumour cells is the goal—and for protecting healthy tissue during chemotherapy. The work is fundamental science: it asks how a master regulatory network works, not how to build a drug tomorrow. But understanding that wiring diagram is the necessary first step before anyone can design a targeted therapy that flips the right switch.