The putative mechanisms of the radiosensitization effect in CaP cells include induction of apoptosis; redistribution to a more radiosensitive cell cycle phase and abolishment of RTinduced cell cycle arrest; induction of more DNA damage and inhibition of repair of RT-induced DNA DSBs through diminishing NHEJ and HR pathways. Combination of LBH589 and RT may provide a new treatment strategy to improve anticancer efficacy while reducing the toxicity of extreme high dose RT. Colorectal cancer is, after lung cancer, the second most common cause of cancer-related death in Europe. More than one fifth of the patients with CRC present with metastases already at time of diagnosis of the primary cancer and the same proportion will develop metastases during the course of disease. The lungs are the second most common site of distant Torin 1 metastasis, making pulmonary metastases an essential contributor to the high mortality of CRC. Besides cancer cells themselves, a tumor comprises stromal cells. The interactions of stromal and cancer cells is thought to be a major determinant of the tumor behavior and response to therapy. Cellular components of the stroma are fibroblasts, endothelial cells, immune cells and pericytes. Cancer-associated fibroblasts, and especially activated fibroblasts, play a major role in the tumor-stroma network, similar to dermal fibroblasts in wound healing. This contributed to the description of tumors as ��wounds that do not heal�� by Dvorak et al. in the late 80��s. CAF contribute to various tumor-promoting characteristics like extra-cellular matrix turnover, tumor growth, angiogenesis and metastasis. Due to the expression of ��- smooth muscle actin, activated CAF are often described as myofibroblasts. They have also been shown to be positive for fibroblast-activation protein-��/seprase, palladin and vimentin. Recently, efforts have been made to characterize the ��signature�� of these fibroblasts by proteome and gene expression profiling. In the context of benign diseases, wound healing and keloid formation it is well known that activated fibroblasts express high levels of heat-shock protein 27, which is crucial for fibroblast adhesion, contractility and motility. The TGF-beta induced p38-MAPK PI-103 pathway is the key regulator in the induction of Hsp27 in smooth muscle cells and myofibroblasts. Once synthesized, two main functions of Hsp27 are critical in wound healing process: promoting myofibroblast motility and angiogenesis. Hsp27 is involved in the stabilization of actin filaments and of SNAIL, an inducer of epithelial-mesenchymal transition. Both mechanisms contribute to the induction of the myofibroblastic phenotype. Another function of Hsp27 executed in a paracrine manner is enhancing angiogenesis. It was demonstrated that extracellular Hsp27 leads to Nf��B activation and subsequent expression of the proangiogenic factors VEGF and interleukin-8 in endothelial cells. Together with others, our group could show that an overexpression of Hsp27 is strongly linked to several benign and malign pathologies of the lung associated with fibroblast activation, including emphysema/ chronic obstructive pulmonary disease, idiopathic pulmonary fibrosis and nonsmall cell lung cancer.