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.

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