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Breast cancer is the most commonly occurring malignancy in women and is responsible for approximately 500 000 deaths yearly world wide (WHO).Carcinomas —the most frequent form of human cancer — result mainly from the accumulation of somatic mutations in epithelial cells.However, it has become clear that the genesis and thrive of carcinomas depend also on alterations in their microenvironment (stroma).In this presentation I will provide evidence that carcinoma-associated fibroblasts (CAFs) and their adjacent "normal" counterparts (TCFs) are myofibroblasts and show tumor-associated features.Indeed CAFs but not TCFs are defective in the p53/p21 response pathway to γ-rays.Interestingly, both TCFs and CAFs express high levels of the cancer marker survivin, and consequently exhibit high resistance to cisplatin and UV light.Moreover, most CAFs are positive for the proliferation marker Ki-67 and exhibit high proliferation rate as compared to TCFs.However, PCNA was highly expressed in both CAFs and TCFs.Using the 2 dimensional gel electrophoresis technique, we have also shown that CAF, TCF and normal breast fibroblast cells present different proteome profiles, with many proteins differentially expressed between these cells.