Triple negative breast cancers (TNBCs), which are negative for both hormone and HER2 receptors, represent approximately 10-20% of the breast cancer cases and are characterized by a poor prognosis with limited therapeutic options. TNBC is a heteterogenous disease that can be subdivided based on molecular characteristics  into multiple subtypes, including the basal-like and claudin-low subtypes. ZEB1, a potent EMT-transcription factor is often upregulated in TNBC. We identified ZEB1 as an important factor in the etiology of TNBC. The aim of this project is  to identify pathways that collaborate with ZEB1 in the malignant transformation of basal like BC. We will determine how EMT contributes in the crosstalk between immune and cancer cells and adress if this is important for the malignant behavior of cancer cells or immunosuppression of basal-like and claudin-low BC. On the basis of our findings we will test if differentiation strategies can be the basis of future TNBC therapy.