Since the early 1980s, cancer researchers have known that a protein called p53 plays a critical role in protecting cells from becoming cancerous. The protein is defective in about half of all human cancers; when it functions correctly, it appears to suppress tumor formation by preventing cells with cancer-promoting mutations from reproducing.
Knowing p53’s critical role in controlling cancer, researchers have been trying to develop drugs that restore the protein’s function, in hopes of re-establishing the ability to suppress tumor growth. One such drug is now in clinical trials.
In a new study that highlights a possible limitation of such drugs, MIT cancer biologists show that restoring p53’s function in mice with lung cancer has no effect early in tumor development, but restoring the function later on could prevent more advanced tumors from spreading throughout the body.
A representation of a complex between DNA and the protein p53.
Image: Thomas Splettstoesser