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VA RESEARCH REVEALS PERSISTENT ACID REFLUX CAN
TURN INTO CANCER -- "The research supports why
it is
important to prevent reflux, because the more
reflux
you have and the longer you have it, the more
it
might predispose you to getting [cancer]."
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Story here...
http://www.utsouthwestern.
edu/utsw/cda/dept353744/files/399253.html
Story below:
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Investigators uncover intriguing clues to why
persistent acid reflux sometimes turns into cancer
DALLAS — New research from scientists at UT Southwestern Medical Center
and the Dallas Veterans Affairs Medical Center underscores the
importance of preventing recurring acid reflux while also uncovering
tantalizing clues on how typical acid reflux can turn potentially
cancerous.
In research published in July and August, scientists discovered that
people with acid reflux disease, particularly those with a complication
of acid reflux called Barrett’s esophagus, have altered cells in their
esophagus containing shortened telomeres, the ending sequences in DNA
strands. Combined with related research to be published this month, the
findings indicate that the shortened sequences might allow other cells
more prone to cancer to take over.
“The research supports why it is important to prevent reflux, because
the more reflux you have and the longer you have it, the more it might
predispose you to getting Barrett’s esophagus. So you want to suppress
that reflux,” said Dr. Rhonda Souza, associate professor of internal
medicine at UT Southwestern and lead author of the paper which appears
in the July issue of the American Journal of Physiology –
Gastrointestinal and Liver Physiology.
Heartburn occurs when acid splashes back up from the stomach into the
esophagus, the long feeding tube that connects the stomach and throat,
causing a burning sensation.
Over time, the persistent acid bath can cause normal skin-like cells in
the esophagus to change into tougher, more acid-resistant cells of the
type found in the stomach and intestine, a condition called Barrett’s
esophagus, explained Dr. Stuart Spechler, professor of internal medicine
and senior author of the paper. “Unfortunately, those acid-resistant
cells are also more prone to cancer,” Dr. Spechler said.
Adenocarcinoma of the esophagus, the cancer that is especially
associated with Barrett’s esophagus, is currently the most rapidly
rising cancer in the U.S., with a sixfold increase in cases during the
past 30 years, according to the National Cancer Institute.
Understanding how and why the cells change in some cases and not others
has been a major challenge for investigators.
Researchers compared telomere length and telomerase activity in biopsy
specimens from 38 patients with GERD and 16 control patients. This new
line of research suggests that the continuous acid bath affecting
esophageal cells causes them to divide more frequently in order to
regenerate the damaged lining. However, each time the cells divide, the
telomeres at the end of DNA become shorter. When they become too short,
the aging cell can no longer divide, Dr. Souza said.
Scientists suspect that when cells can no longer divide, other cells
might infiltrate the area to make up for the loss. And those cells may
be more likely to generate the acid-resistance that makes them more
likely to turn cancerous.
“If the telomeres get short enough, maybe the cells can’t regenerate any
more and maybe that’s why you start to see this change,” said Dr.
Spechler. “Perhaps the esophagus can’t regenerate the normal skin-like
squamous cells, and instead, it has to recruit cells from somewhere else
and that’s why you start getting these changes to intestinal-like
cells.”
Other studies by this group of UT Southwestern digestive disease
specialists suggest the alternate cells that eventually take over might
be bone-marrow cells.
“There could be cells circulating from the bone marrow that wouldn’t
ordinarily end up in the esophagus. But if you shorten the telomeres
enough and the esophagus can’t regenerate anymore, perhaps these
bone-marrow cells might have to replace that tissue, and bone-marrow
cells can turn into intestinal tissue,” Dr. Spechler said. “This hasn’t
been proven, but we have some data that supports that.”
In research available online prior to printing this month in Diseases of
the Esophagus, Drs. Souza, Spechler and colleagues demonstrate that
bone-marrow cells come into play to regenerate the esophageal lining in
rats that have heavy reflux.
“So the first paper shows that the telomeres are short, suggesting that
the normal squamous cells might not be able to divide anymore, so they
die out,” Dr. Spechler said. “The second paper suggests that the
bone-marrow cells may then come and take their place, giving rise to the
intestinal cells instead of the normal, skin-like cells.”
Further research will be needed to confirm that hypothesis, Dr. Souza
said.
“It’s an interesting series of experiments,” she said. “None of them
absolutely prove that this is what’s going on, but it’s an interesting
concept, and it certainly supports the theory that your normal cells
poop out and eventually they can’t replace the damaged ones, and maybe
that’s why you get Barrett’s esophagus.”
If confirmed, the research might also help scientists find a way to
prevent the bone-marrow cells from invading or to identify markers that
would allow an earlier diagnosis for Barrett’s esophagus, which doesn’t
usually have symptoms.
Other UT Southwestern researchers involved in the studies are Dr. Jerry
Shay, vice chairman of cell biology, and Dr. Geri Brown, associate
professor of internal medicine. In addition, researchers from the
University of Florida, Texas Tech University Health Science Center in El
Paso and the Mayo Clinic also participated.
The research was funded by the Department of Veteran’s Affairs, National
Institutes of Health, the Harris Methodist Health Foundation, the Dr.
Clark R. Gregg Fund and AstraZeneca.
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Larry Scott --
