The team first screened a set of protein mimics originally designed to target Alzheimer's disease and type 2 diabetes. The results identify a mimicry of the protein that potentially isolates the mutated p53 material and prevents further protein accumulation. The researchers then showed that segregation of mutated p53 grains by protein mimicking restored the suppressive function of the p53 tumor, leading to the death of a wide range of cancer cells. Importantly, protein mimicry therapy effectively reduces tumors that contain mutated p53 while showing no significant toxins for healthy tissue, resulting in significantly longer survival. "As the prevalence of cancer increases worldwide, there is an urgent need for new cancer therapies to complement or replace existing therapies," said the study's lead author. Here we show the first successful use of a small molecule amyloid inhibitor as an anticancer agent. We believe that this will have a far-reaching impact, as it effectively bridges the gap between amyloid disease and cancer and is the basis for passing on information approaches in the design of new and robust cancer mutation therapies for the p53 mutation. Keywords: Cancer; Cells; Tissues, Tumors; Prevention, Prognosis; Diagnosis; Imaging; Screening; Treatment; Management