Cells possess a variety of ways of dealing with mutations that can cause them to grow uncontrollably and eventually form a tumor. The tumor suppressor gene p53 plays a critical role in these cancer prevention processes, largely by triggering a form a cell death known as apoptosis.
Many research groups are working to develop strategies for boosting p53 levels in precancerous and malignant cells. However, since approximately half of all cancers have mutations that prevent p53 from triggering apoptosis, these approaches are limited in their effectiveness in treating cancer.
To overcome the mechanisms that cancer cells develop to circumvent p53's efforts to kill those cells, a team of investigators at the Beatson Institute for Cancer Research in Glasgow, Scotland, have turned to a related gene, known as p73, that also trigger apoptosis by a more circuitous but equally effective biochemical process. In a study published in the Journal of Clinical Investigation, this team, led by Kevin Ryan, Ph.D., found that a protein designed to turn on p73, delivered to tumors using a nanoparticle, kills both primary tumor cells and those that have spread from the original tumor.
Activating p73 to trigger apoptosis is a particularly promising approach to treating cancer because this gene is rarely mutated in human cancer cells. In this study, the researchers showed that turning on p73 starts the apoptosis process even when p53 is missing or damaged. To turn on p73, the investigators used a small fragment of the normal p53 protein, which they named "37AA." Although this protein triggered apoptosis in a wide variety of cancer cells, it had no effect on healthy cells.