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Quest for origin of Ewing Sarcoma successful

The left image shows the anlage of a leg with EWS / FLI1 expression in which bone should already be formed. But the stem cells fail to produce precursor cells that support a healthy bone structure (arrows, compare to image right). Copyright: Unrestricted unmodified use with reference to the copyright holder Ludwig Boltzmann Gesellschaft

In order to develop better therapies against cancer, researchers are now faced with ever-increasing efforts. Since cancer is a complex disease affecting the entire organism, genetically modified mice play an important role in cancer research. Above all in rare cancers, clinically relevant animal models are essential to investigate the effect of new drugs. For this reason, researchers have tried for many years but failed to develop a suitable model for Ewing sarcoma.

Stress hormones accelerate obesity and diabetes upon aging

More than 600.000 people suffer from diabetes in Austria and every third person is not yet aware of that metabolic disease. Even a greater number of the population is seriously overweight, which underlies many age-related diseases including development of type II diabetes. Preventive medications and detailed understanding to avert these diseases are therefore an important health issue.

New paper out on EGFR-signaling protecting from liver injury

Emilio Casanova contributed to a recent manuscript demonstrating that STAT3 protects from cholestatic liver injury. Specific ablation of STAT3 in liver cells aggravated liver damage and fibrosis in a mouse model for cholestatic disease. Upregulation of bile acid biosynthesis genes and downregulation of epidermal growth factor receptor (EGFR) expression were observed, the functional consequences of these processes in cholestatic liver injury remained unclear.

New paper out on STAT5 promoting oxidative stress in chronic myeloid leukemia

Richard Moriggl contributed to a recent publication in oncotarget demonstrating that sustained activation of STAT5 induced by Bcr-Abl in chronic myeloid leukemia (CML) cells promotes production of reactive oxygen species (ROS) by repressing expression of two antioxidant enzymes, catalase and glutaredoxin-1(Glrx1). Downregulation of catalase and Glrx1 expression was also observed in primary cells from CML patients.