The study revealed that the loss of function in the mutated p53 protein is the critical factor in cancer growth, disproving the previously suggested gain-of-function role. Using CRISPR gene editing, the researchers removed various mutated forms of p53 and found no change in cancer cell behavior or response to chemotherapy.
Restoring p53's normal functions reduced cancer growth in pre-clinical models. This discovery could redirect the focus of cancer treatment research away from targeting gain-of-function traits to restoring the protein's normal tumor-suppressing functions, potentially saving millions in drug development costs.