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A common denominator of inflammations and fatty liver
Date:5/27/2008

Many cancer patients lose a lot of weight during their disease: Fat and muscle mass are reduced, free fatty acids accumulate in the liver, and this eventually leads to fatty liver in affected patients. What is called tumor cachexia appears to be caused by signals emitted by the tumor itself. Despite vigorous searching, scientists have not yet been able to identify these degradation signals of tumors. Therefore, a research team at the German Cancer Research Center (Deutsches Krebsforschungszentrum, DKFZ) in Heidelberg, Germany, decided to take the opposite approach: Instead of searching for hunger signals in the tumor, they investigated the other end of the signaling chain: liver cells of mice affected by cancer. In the process, they discovered a molecular marker which controls both metabolic processes and inflammatory responses.

In advanced stages of cancer, particularly in pancreatic and lung cancers, patients frequently suffer from a wasting syndrome known as cancer cachexia. Affected patients grow very thin and weak, often there is a danger of organ failure. Body fat, in particular, is reduced and its accumulatation in the liver leads to fatty liver. This process seems to be caused by signals from the tumor itself, which radically direct metabolic processes in the body towards degradation and cause a state of chronic inflammation in the body. Despite intensive efforts to identify these signals, they remain unknown.

Stephan Herzig, head of the Emmy Noether and Marie Curie Junior Research Group Molecular Metabolic Control at DKFZ, and his co-workers have focused on the other end of the signaling chain: They studied liver cells of tumor-bearing mice showing signs of severe cancer cachexia. In particular, they searched for a molecule called RIP140, previously identified by Herzig as a regulator suppressing fat breakdown in the livers of healthy mice. Indeed, the investigators found a high activity of RIP140 in the cancerous mice and, accordi
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Contact: Dr. Stefanie Seltmann
s.seltmann@dkfz.de
Helmholtz Association of German Research Centres
Source:Eurekalert

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