The p53 gene normally springs into action in DNA-damaged cells. It can prompt those cells to die, stopping cancer before it starts.
The p53 gene can also stop DNA-damaged cells from dividing. That process, called senescence, prevents a cancer from growing.
But if the p53 gene isn't working right, DNA-damaged cells may keep on growing, paving the way for cancer to take root.
Manuel Serrano, PhD, works in Madrid at the Spanish National Cancer Research Center.
He reviewed three recent studies on the p53 gene. The studies were done by three teams of scientists who studied mice, not people.
In their labs, the scientists stimulated the p53 gene, turning the gene on. In two of the three studies, the mice's cancers faded when the p53 gene was turned on.
"The results were spectacular: in some cases, near-complete regression was achieved just two days after p53 activation. In other cases, regression took longer (about 10 days)," Serrano writes.
In the third study, p53 gene activation delayed -- but didn't completely repress -- the progression of an aggressive lymphoma in the mice, according to Serrano.
In the studies, activating the p53 gene didn't appear to harm the mice's healthy cells.
P53 Gene Target
"These three studies strongly support the search for targeted p53-activating drugs," Serrano writes in The New England Journal of Medicine.
However, the lab studies "should be interpreted with some caution," writes Serrano.
He notes that the mice started the study with a completely inactive p53 gene that the researchers turned on. Human cancers with an intact but flawed p53 gene may be more resistant to p53 gene treatments.
"This does not mean that such a therapy would be inefficient, but it would be unlikely to be as effective as the methods used by these investigators" in the lab tests on mice, writes Serrano in The New England Journal of Medicine.
The studies don't mean that other genes aren't also involved in cancer. A mix of genetic and environmental factors can affect cancer's development.