But what if DNA damage offers the occasional benefit? Or, to return to the analogy of the writer and the editor, what if the apparent mistake makes the story a little better? Maybe some of a writer's mistakes actually move the plot forward. Similarly, some DNA damage has been recognized as possibly useful to our cells.

Dr. Judy Campisi of the Berkeley National Laboratory at the University of California at Berkeley has written in the journal In Vivo about the possible benefits of DNA damage. Some recent research has suggested that genetic damage may trigger a process called cellular senescence (i.e., cellular old age). Senescent cells stop growing and dividing. And some don't die on schedule (Certain cells have a specific and finite life span.). Cellular senescence was previously thought to occur only after cells had completed a certain number of cell divisions. The fact that DNA damage may also trigger cellular senescence is intriguing.

Dr. Campisi notes that exposure to cancer causing agents is one of the major causes of DNA damage that seems to trigger cellular senescence. If a DNA-damaged cell becomes senescent rather than cancerous, then that particular DNA damage may actually protect the body by preventing a potential cancer. (This protective mechanism, of course, is not complete; most mammals, including humans, will develop cancer if they live long enough.) But is there something in this "unnatural" senescence that could provide a clue to stopping cancers before they start?

One drawback of the cellular senescence caused by DNA damage is that it may also be a trigger for age-related declines in our tissues and organs. Some researchers theorize that DNA-damaged senescent cells build up in our bodies and pave the way for aging to take place. Understanding the whole mechanism of DNA damage and repair, therefore, may not only suggest ways to fight cancers, but may help researchers understand, and ultimately slow, the process of human aging.