Our aims are to identify and understand mechanisms regulating breast cancer cell death and how inflammatory signaling can be induced and influence breast cancer progression. We specifically study Smac mimetics, small molecules mimicking the effect of the pro-apoptotic protein Smac. We investigate determinants of Smac-responsiveness and ways to circumvent resistance to Smac mimetics. One goal is to identify factors that can give information about the most optimal co-treatment to optimize Smac mimetic efficiency. We have discovered that Smac mimetics can induce long-term changes in the breast cancer cell phenotype which includes inflammatory signaling. The mechanisms of this effect are analyzed. We also focus on the molecular pattern of stromal components of tumors. We utilize public data and molecular data generated within the SCANB project. We have discovered that the molecular composition, more than the extent, of stroma and tumor immune/inflammatory response is of prognostic importance.
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