Contact: Sarah White, Ph.D.
[email protected]
212-450-1543
Ludwig Institute for Cancer Research
Inflammation directly linked to colon cancer
Potential new drug targets revealed
(New
York, February 2, 2009) -- While chronic inflammation is widely
believed to be a predisposing factor for colon cancer, the exact
mechanisms linking these conditions have remained elusive. Scientists
at the Melbourne Branch of the international Ludwig Institute for
Cancer Research (LICR) and the Technical University Munich have jointly
discovered a new piece of this puzzle by demonstrating how the Stat3
protein links inflammation to tumor development, a discovery that may
well lead to the identification of new therapeutic targets for colon
cancer.
Aberrant activation of the intracellular signaling
protein, Stat3, has been associated with inflammation and several
cancers, including those of the gastrointestinal tract. The results
published on-line today in the journal
Cancer Cell provide the
first direct evidence confirming the role for Stat3 in
inflammation-associated tumorigenesis. Using an inflammation-associated
cancer model in genetically manipulated mice, the team identified a
relationship between epithelial cell Stat3 activity and colonic tumor
incidence, as well as tumor growth. They also determined that
stimulation of Stat3 by the cytokines IL-6 and IL-11, chemicals
produced by inflammatory and other tumor-associated cells, promotes
both cell survival and growth of tumor cells.
The
collaboration was sparked by discussions between Professors Matthias
Ernst (LICR) and Florian Greten (Technical University Munich) at a
scientific meeting, when they discovered they were both individually
pursuing the mechanism by which Stat3 links inflammation to
gastrointestinal cancers. Rather than compete, the two decided to join
forces to discover the Stat3 connection between inflammation and colon
cancer.
"Colon cancer is the second most frequent malignancy
in the developed world so it was no surprise to find another group
working on the Stat3 question and trying to find new ways to target
colon cancer," said LICR's Professor Ernst, the joint senior author of
the publication. "Together we've been able to learn how Stat3 bridges
chronic inflammation and tumor promotion by mediating cell survival
during an inflammatory event and enhancing tumor cell growth. Our new
findings are very much in line with our previous work on the role of
Stat3 in mediating inflammation- associated gastric cancer. We expect
this knowledge to strengthen efforts for the development of
therapeutics that target the link between inflammation and cancer to
ultimately benefit the treatment of cancer patients."
Incidentally,
the group of Professor Michael Karin from the University of California
at San Diego, has reached similar conclusions in paper published in the
same issue of
Cancer Cell.
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About LICR
The
Ludwig Institute for Cancer Research (LICR) is the largest
international non-profit institute dedicated to understanding and
controlling cancer. With operations at 73 sites in 17 countries, LICR's
research network quite literally spans the globe. LICR has developed an
impressive portfolio of reagents, knowledge, expertise, and
intellectual property, and has also assembled the personnel,
facilities, and practices necessary to patent, clinically evaluate,
license, and thus translate, the most promising aspects of its own
laboratory research into cancer therapies.
Contact Sarah L.
White, Ph.D. Director, Office of Communications 605 Third Avenue / 33rd
Floor New York, NY 10158 USA Tel: +1 917 379 0398 Fax: +1 212 450 1500
E-mail: [email protected] Website: http://www.licr.org