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Ludwig Links Inflammation To Colon Cancer; New Targets

March 12th 2009 21:58
Tuesday February 3, 2009

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* ASX UP, BIOTECH DOWN: PSIVIDA UP 30%, GENETIC TECHNO DOWN 19%

* LUDWIG LINKS INFLAMMATION TO COLON CANCER; NEW TARGETS

* CORRECTION: BIOTECH DAILY AND ASX MARKET CAPITALIZATIONS

* TGA APPROVES NANOSONICS’ TROPHON EPR; FEBRUARY SALES

* MONASH RESEARCH BREAKTHROUGH TO TREAT MALARIA

* NOMINATIONS FOR 2009 PRIME MINISTER'S SCIENCE PRIZES

* ETHICAL INVESTOR FORUM: BIOTECH A SUSTAINABLE INVESTMENT

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* PSIVIDA PROMOTES M-D DR PAUL ASHTON TO PRESIDENT, CEO


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LUDWIG INSTITUTE FOR CANCER RESEARCH

The Ludwig Institute for Cancer Research and the Technical University Munich say they have shown how the Stat3 protein links inflammation to tumor development.
A media release issued by the Ludwig Institute said the discovery “may lead to the identification of new therapeutic targets for colon cancer”.
The Ludwig Institute said chronic inflammation was “widely believed to be a predisposing factor for colon cancer [but] the exact mechanisms linking these conditions have remained elusive”.
The Institute said aberrant activation of the intracellular signaling protein, Stat3, was associated with inflammation and cancers, including those of the gastrointestinal tract.
The collaboration was sparked by discussions between Prof Matthias Ernst of the Melbourne branch of the Ludwig Institute and Prof Florian Greten of the Technical University Munich at a scientific meeting, when they discovered they were separately pursuing the mechanism by which Stat3 links inflammation to gastrointestinal cancers.
The two joined forces and the results of their collaboration entitled ‘gp130-Mediated Stat3 Activation in Enterocytes Regulates Cell Survival and Cell-Cycle Progression during Colitis-Associated Tumorigenesis’ were published on-line today in the journal Cancer Cell Really Long Link
The Ludwig Institute said the paper provided “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,” the Ludwig Institute said.
“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 Institute said.
“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,” Prof Ernst said.
“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,” Prof Ernst said.
“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 … benefit the treatment of cancer patients,” Prof Ernst said.
The Ludwig Institute said the University of California at San Diego’s Prof Michael Karin reached similar conclusions in a paper published in the same issue of Cancer Cell.

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