But in patients who ultimately progressed to esophageal cancer, Reid and his colleagues saw a sudden change about four years prior to cancer diagnosis. These cells seemed to tip suddenly toward a cancerous path, undergoing large, catastrophic mutations such as deletions of long stretches of chromosomes or doubling of entire genomes. This was contrary to what Reid expected to find. "We thought we'd find a fast rate of mutation [in progressors] and a slow rate [in non-progressors]," he said, noting that the striking findings are in keeping with recent observations by other researchers. Other studies examining ovarian, prostate, breast, and colon cancer have observed a pattern of drastic mutations and genome doubling.
Because the findings seem to be generalizable to other types of cancers, Reid is optimistic that they are a first step toward better screening and prevention strategies. The four-year window in which BE cells take a turn for the malignant should reassure patients, Reid said. It gives physicians plenty of time to identify cancerous cells, and findings like Reid's and others' are giving researchers a better picture of how to detect premalignant cells as they begin to progress toward cancer.
It may be that researchers will identify even earlier, smaller mutations that presage these cells' malignant future, extending the window of opportunity by several years. Additionally, research into less invasive screening tests may well make invasive screening methods like endoscopies a thing of the past.
Ideally, Reid noted, researchers will discover ways to stop precancerous cells before the tipping point. Such interventions may be as simple as popping a few aspirin, as research by Reid and his colleagues has already demonstrated that high-risk BE patients who use aspirin and non-steroidal anti-inflammatories cut their esophageal cancer risk by about half. "If something like that cou
|Contact: Deborah Bach|
Fred Hutchinson Cancer Research Center