Barrett's lesions that are 'born to be bad' predict esophageal cancer risk

Analysis of esophageal cells can predict cancer risk in people with Barrett’s esophagus, researchers demonstrated. Also, this risk won’t change over time, so more care could focus on high-risk patients while freeing low-risk patients from unnecessary endoscopies, according the study published online August 19, 2016 in Nature Communications.

Although few patients with Barrett’s esophagus eventually develop esophageal cancer, the cancer is particularly aggressive for those unfortunate few. For this investigation, these researchers sought to develop a method to stratify those at high risk from those at low risk.

“We have shown that some Barrett’s esophagus lesions are ‘born to be bad’—and conversely that some are ‘born to be benign,’” explained Trevor Graham, PhD, Lecturer in Tumor Biology at Queen Mary University of London’s Barts Cancer Institute, in London, UK.

“Once these results are validated in other patients and over longer periods of time, we will be able to say with confidence which people with the benign form can be spared unnecessary endoscopy and worry,” Dr. Graham explained. “This will dramatically improve the quality of life for people with Barrett’s, and provide substantial cost saving to healthcare providers.”

Using multicolor fluorescence in situ hybridization (FISH), Dr. Graham and colleagues measured genetic diversity in individual esophageal cells from 320 patients with non-dysplastic Barrett’s esophagus. During a three-year follow-up of these patients, researchers watched the cells for clonal evolution to indicate neoplastic progression.

Progression was rare, they found. “We only observed one significant clonal expansion every 36.8 patient-years of follow-up, and in those cases, the clones grew at an average of 1.58 cm² per year,” the researchers noted.

From this, they concluded that measurement of the genetic diversity between Barrett’s cells in any given lesion is a good predictor of which patients are at high risk of developing cancer.

“Our findings are important because they imply that a person’s risk of developing esophageal cancer is fixed over time,” Dr. Graham said. “In other words, we can predict from the outset which Barrett’s patients fall into a high risk group of developing cancer—and that risk does not change thereafter.”

These results also show “that measures of clonal diversity are more prognostic than ‘traditional biomarkers’ that are based on the detection of particular individual genetic abnormalities,” the authors wrote in their article.

“Recognizing that only a subset of non-dysplastic Barrett’s are ‘born to be bad’ offers new hope for effective risk stratification of this challenging patient group,” the researchers concluded.