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Molecular pathway suspected in precancerous stomach lesions, Dana-Farber Cancer Institute
Researchers at Dana-Farber Cancer Institute have identified a chain of molecular signals that generate the specialized
lining of the stomach during fetal development - a discovery that could lead to better diagnosis, treatment and prevention of
stomach and esophageal cancer in adults.
Damage to the stomach lining, such as from acid reflux or helicobacter pylori (H. pylori) infections, might reactivate the
newly found signaling pathway - but in this situation it would work in the opposite direction. As a result, the lining
reverts to a more generic intestinal type of cells that form cancer-prone lesions.
Ramesh Shivdasani, MD, PhD, of Dana-Farber, senior author of a report in the April 4 issue of Developmental Cell, said the
finding "opens a window that could help us eventually interfere with these pathways when they become abnormal. It should give
us a list of potential therapeutic targets and could even help us to prevent the development of the precancerous lesions."
The lead author is Byeong-Moo Kim, PhD, also of Dana-Farber.
Patients with the increasingly common disorder known as Gastroesophageal Reflux Disease, or GERD, are at risk of developing
precancerous lesions in the upper end of the stomach or the adjoining lower end of the esophagus. These lesions require
intense frequent monitoring by endoscopy and sometimes prophylactic surgery to decrease the threat of this dangerous form of
cancer. Cancer of the "gastroesophageal junction" has increased dramatically in the past two decades, especially in patients
younger than 40 years.
Shivdasani's laboratory studies the "rules" according to which body tissues develop their distinctive form and function at
the beginning of life, because they may be reactivated, abnormally, when cancer arises later.
"Cancers of the stomach are almost always preceded by the conversion of the stomach type of lining to an intestinal type,"
says Shivdasani. In the developing fetus, the entire digestive tract is initially lined with intestinal-type cells. At a
certain point, the activation of a molecular signaling pathway causes this layer to become more specialized, or
differentiated, for the lining of the stomach and esophagus. Thereafter, the pathway falls silent, unless, many years later,
damage to the lining sets it in motion again.
In the mouse fetus, the differentiation of intestinal lining into stomach lining happens rapidly, during a window of only one
day, around the 12th and 13th days of gestation. (The corresponding period in the human fetus is during the 8th to 10th
weeks.)
"We found that the epithelium [lining layer] is malleable, and depends completely on this pathway to instruct it to become
stomach," says Shivdasani. "In the absence of this pathway, the epithelium would develop into the default intestinal state."
In experiments in mice, and with cultured mouse stomach and intestinal tissue, the scientists demonstrated that the signals
that drive the differentiation of stomach lining are sent by a layer of cells, known as mesenchyme, that lie directly beneath
the intestinal lining. The key player in the signaling pathway, they found, is a transcription factor - a protein that
governs the expression of genes under its control - called Barx1. The main action of Barx1 in stomach lining formation is to
block signaling through another pathway known as Wnt, the scientists found.
"Barx1 gives us a handle on what elements of the pathway might allow the stomach to differentiate abnormally into intestine
as a result of injury to the stomach lining, setting the stage for cancer," Shivdasani says.
"These research findings offer the hope of identifying a protein marker that can be used to screen for these diseases and
even to serve as a target for newly designed forms of therapy," said Robert Mayer, MD, director of Dana-Farber's Center for
Gastrointestinal Oncology, who was not involved in the study.
Other authors of the report were at the Institute for Craniofacial Biology at Kings College in London, who supplied
genetically engineered mice used in the experiments.
The work was supported by the Robert Black Charitable Foundation, the National Institutes of Health, and the Wellcome Trust
and UK Medical Research Council.
Dana-Farber Cancer Institute is a principal teaching affiliate of the Harvard Medical School and is among the leading cancer
research and care centers in the United States. It is a founding member of the Dana-Farber/Harvard Cancer Center (DF/HCC), a
designated comprehensive cancer center by the National Cancer Institute.
Contact: Bill Schaller or Richard Saltus
william_schaller@dfci.harvard.edu
617-632-5357
Dana-Farber Cancer Institute
http://www.dfci.harvard.edu
Molecular cale suspectate în precancerous stomac leziuni, Dana-Farber Cancer Institute - Molecular pathway suspected in precancerous stomach lesions, Dana-Farber Cancer Institute - articole medicale engleza - startsanatate