Beside the loss of epithelial markers the expression of mesenchymal markers like FSP-1 is also an important step in the process of EMT. FSP-1, also called S100A4, correlates with the metastatic potential in neoplasms and some authors demonstrated that a high level of FSP-1 is associated with poor prognosis in various cancer types. EMT is regulated by several transcription factors. One of the most important is SNAIL1, which acts also as E-cadherin repressor. It has been shown that high SNAIL1 expression is associated with poor prognosis in lung cancer. EMT can be induced by several growth factors and cytokines, most importantly by TGFbeta but also by EGF, FGF, HGF and others. Most of these factors are present in the tumor environment and produced by the tumor cells itself or by surrounding cellular components. The microenvironment of solid tumors is a complex mixture of cellular and non cellular factors, in which the tumor associated macrophages represents up to 50% of the tumor mass. TAMs are alternatively activated macrophages secreting a specific pattern of several tumor promoting cytokines and growth factors. One of these cytokines is the human specific CC-Chemokine Ligand 18 which is highly present in lung tissue and involved in several pathological processes of malignant diseases or fibrosis. We already demonstrated that CCL18 is highly elevated in sera of patients with non small cell lung cancer and correlates with tumor stage and overall survival in the subgroup of adenocarcinoma. Lung cancer is one of the malignancies with the highest incidence in the Western world and despite all advances in diagnosis and therapy one of the leading causes of cancer related death. Nearly 85% of these patients suffer from non-small cell lung cancer, which is subdivided into squamous carcinoma, adenocarcinoma, large cell carcinomas and other rare subtypes. Adenocarinoma represents the highest proportions of NSCLC and since the 1970s its proportion is increasing. At time of diagnosis the majority of patients with NSCLC suffer already from advanced or metastatic disease, which is associated with poor prognosis. The mechanism of metastasis in lung cancer is not fully understood, but epithelial to mesenchymal transition seems to be one key event in the process of metastasis. Some authors already demonstrated that various mediators released in the microenvironment of solid tumors are able to induce EMT and therefore promote rs1042522 amino acid change demonstrated disease progression. CCL18 is a chemokine produced and released by tumorassociated macrophages in the microenvironment of cancer cells and pulmonary fibrosis. We could demonstrate that CCL18 is highly elevated in patients with NSCLC and correlates with T-stage and mean survival time in the adenocarcinoma subgroup. This leads to the question if CCL18 is directly involved in pathogenic processes in cancer diseases. Since CCL18 was found to induce collagen in lung fibroblasts and to act in a similar way as TGFbeta, we hypothesized that CCL18 may promote the process of metastasis via EMT. A549 cells are a well characterized human cell line isolated from an adenocarcinoma of the lung, which has already been used in several studies investigating the induction of EMT by TGF-b. In agreement with others, we demonstrate that A549 cells treated with even low dose of TGF-b underwent morphological changes from cuboid epithelial cells to spindle shaped fibroblastlike cells and acquired a mesenchymal phenotype after 24 hours of treatment.