That tactic is called senescence. In senescence, cells don't divide, which means a cancer could not grow.
Triggering senescence in certain cells appears to hamper the growth of some tumors, according to lab tests done on mice.
The tests were done by researchers at the University of Texas M.D. Anderson Cancer Center in Houston, including Sandy Chang, MD, PhD, an assistant professor of molecular genetics.
Their study appears online in EMBO Reports, a publication of the European Molecular Biology Organization (EMBO).
Chang and colleagues focused on the p53 gene, a gene within cells that works to nip cancer in the bud.
The p53 gene springs into action within DNA-damaged cells. Such damage can happen as cells age but can also be triggered by cancer risk factors.
Normally, the p53 gene within a DNA-damaged cell orders the cell to die -- a sort of cell suicide -- or to become senescent.
But p53 gene mutations can make that process go awry, promoting cancer instead of suppressing it, Chang tells WebMD in an email interview.
In their study, Chang's team looked at mice with a p53 gene mutation that only allowed the p53 gene to order senescence, not apoptosis (or self-destruction).
That is, the mutated p53 gene could prevent DNA-damaged cells from dividing, but it couldn't make the cells die.
The researchers damaged the mice's DNA by shortening the telomeres (the tips of the chromosomes) in some intestinal cells.
In response to that DNA damage, the mice's mutated p53 gene swung into action. Since it couldn't order DNA-damaged cells to die, it ordered them to become senescent.
The senescence helped stop tumor development in the intestinal cells, the study shows.
Chang says senescence ordered by the p53 gene is "extremely important" in suppressing tumor formation and is as important as apoptosis.
But in some cancers, senescence might not be enough to halt cancer, the researchers found.
Perhaps apoptosis is more important than senescence in fully suppressing some types of cancer, the researchers conclude.