Marker signals esophageal cancer.

A genetic abnormality in people with cancer of the esophagus might guide physicians in diagnosing and treating such patients and could become an indicator of cancer recurrences, report researchers at the University of Maryland School of Medicine in Baltimore.

The scientists found that in tumor tissue from 48 of 52 people with adenocarcinoma of the esophagus, a gene that encodes a tumor-suppressing protein called APC had been shut down. In contrast, the gene remained active in all the samples of esophageal tissue taken from 20 volunteers without cancer, the researchers report in the Nov. 15 JOURNAL OF THE NATIONAL CANCER INSTITUTE.

The gene encoding APC is inactivated, or silenced, in esophageal-tumor cells when the gene's promoter--nearby DNA that normally switches the gene on--becomes disabled. The culprit is hypermethylation, a chemical process in which extra methyl molecules latch onto the DNA, says study coauthor Stephen J. Meltzer, a gastroenterologist at Maryland.

A valuable application of the new findings may be a blood test for the active APC gene, Meltzer says. Further tests showed that three-fourths of patients with recurrent bouts of esophageal adenocarcinoma showed the hypermethylation in esophageal cells shed into the blood, as did one-fourth of patients fighting an initial occurrence of this cancer. None of 54 volunteers without esophageal cancer showed the hypermethylation in blood tests.

These findings, if confirmed, could help physicians determine the extent of such cancer. For example, a blood test showing that the APC gene is silenced might indicate the cancer is advanced and suggest aggressive treatment, or it might prove useful as a screen for cancer recurrence, Meltzer says.