Researchers have developed a new two-step treatment strategy that targets mutations in the TP53 gene, a defect present in more than half of all cancers. Unlike older approaches that often cause significant toxicity, this method is designed to specifically attack cancer cells while leaving healthy cells largely unharmed.
The treatment works in two stages. First, a drug causes DNA damage. Healthy cells can repair this damage using normal p53 function, but cancer cells with TP53 mutations cannot, so DNA damage builds up. In the second step, another drug blocks a survival checkpoint that these mutant cells depend on, leading to their selective death.
This strategy could be useful across multiple cancers, including lung, breast, colorectal, ovarian, and pancreatic cancers. It is currently being tested in an early clinical trial for colorectal and gastroesophageal cancers. According to senior author Andrei Bakin, the approach turns a weakness in cancer cells into an advantage for treatment, while aiming to reduce the side effects that have limited similar therapies in the past.