Marker signals esophageal cancer
By Nathan Seppa
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.
