Cancer cachexia: How a tumor protein drives wasting in the body
Researchers at Helmholtz Munich, the Heidelberg Faculty of Medicine at Heidelberg University, the German Center for Diabetes Research (DZD) and the Technical University of Munich (TUM) have identified a previously unknown mechanism that can drive cancer cachexia—a wasting process in the body that primarily affects muscle and fat tissue.
Researchers at Helmholtz Munich, Heidelberg University, DZD, and TUM have discovered a mechanism that drives cancer cachexia, a wasting process primarily affecting muscle and fat tissue. A key factor in this process is a protein called ADAMTSL4, which is secreted by tumors. ADAMTSL4 activates the TGF-β signaling pathway in muscle and fat tissue, triggering a catabolic program that leads to muscle and fat breakdown.
This finding could lead to new therapies for cancer cachexia, as ADAMTSL4 could be targeted without causing widespread side effects like those caused by blocking TGF-β directly. However, the researchers emphasize that cancer cachexia is a complex process with various contributing factors, and personalized therapeutic strategies may be necessary in the future.
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