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Institute of Pharmacology

Molecular mediators of pain caused by bone cancer and tumor-nerve interactions

Pain is one of the most severe and debilitating symptoms associated with various forms of cancer. About 30% of cancer patients suffer from excruciating pain during early stages of the disease and the proportion increases to 70% as the disease progresses.

 

Cancer pain is a unique and complex form of pain and represents a largely unexplored area. Cancer pain is distinguished by the unique aspect of tumor-nerve interactions, in particular, by mediators that are released from tumor cells or cancerous tissue in large quantities. These substances include glutamate, endothelins and a variety of growth factors and cytokines, several of which are capable of either directly activating pain-transducing nerve terminals and/or sensitising them against non-painful stimuli. In several projects, we are currently addressing pathophysiological changes induced by these agents in nerve endings in cancer-affected tissue using a broad base of molecular, pharmacological, electrophysiological and behavioural techniques. We use mouse models of bone cancer, which demonstrate the hallmark distinguishing features of pain associated with cancer of bone and connective tissues in humans. Transgenic and viral-based approaches are used to induce molecular perturbations in nerve endings and/or tumors and changes in pain and pain sensitization are addressed using behavioural assays. This work is partly funded by the Association for International Cancer Research, U.K.

 

Group members involved: Matthias Schweizerhof, Gurpreet Kaur Satagopam, Martina Kurejova, Dunja Baumgärtner-Ahlert

 


Collaborations: Don Simone (University of Minnesota, USA)