It was possible, the scientists knew, that skin was peculiar. Maybe inside the body, away from the onslaught of ultraviolet rays, were healthy cells that didn’t carry these key mutations.

To find out, the researchers decided to study cells of the esophagus. The team gathered tissue samples from nine healthy organ donors who had died, then they sliced the tissue into dozens of tiny squares and examined the same 74 cancer-related genes.

Dr. Martincorena and his colleagues found that new mutations arose more slowly in the esophagus than in skin. But once those mutations emerged, they caused the esophageal cells to multiply faster than normal esophageal cells. Over time, these rogue cells spread out across the esophagus, forming colonies of mutant cells, known as clones. Although these clones aren’t cancer, they do exhibit one of cancer’s hallmarks: rapid growth.

“These mutant clones colonize more than half of your esophagus by middle age,” said Dr. Martincorena. “It was eye-opening for me.” Dr. Martincorena and his colleagues reported their findings on Thursday in the journal Science.

By examining the mutations, the researchers were able to rule out external causes for them, like tobacco smoke or alcohol. Instead, the mutations seem to have arisen through ordinary aging. As the cells divided over and over again, their DNA sometimes was damaged. In other words, the rise of these mutations may just be an intrinsic part of getting older.

“It seems that no matter how well one takes care of oneself by eating well, getting exercise and limiting certain vices, there’s likely only so much one can do against the need of the body to replace its cells,” said Scott Kennedy, a cancer biologist at the University of Washington who was not involved in the study.

The study also raised questions about efforts to detect cancer at its earliest stages, when cancer cells are still rare, Dr. Kennedy said: “Just because someone has mutations associated with cancer doesn’t mean actually they have a malignancy.”