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Uing the growth of melanoma cell lines that were exposed to the Raf inhibitor vemurafenib Rosiglitazone [60]. Antibody array analysis of secreted factors, comparing media from stromal cell lines that were or were not shown to be capable of rescuing melanoma cells from vemurafenib treatment, revealed a potential role for hepatocyte growth factor (HGF), mediated through the MAPK and PI3K-AKT pathways, in resistance to vemurafenib. Head and neck squamous cell carcinoma cells and fibroblasts produce more prostaglandin PGE2 when co-cultured [61]. Moreover, co-culture of colon cancer cells with normal colon fibroblasts produced a desmoplastic set of proteins expressed solely in the co-culture but not in the individual cultures. Secreted proteins in this set included collagen type XII, a marker of the invasive front of colorectal tumors [62]. These and other studies that were based on the well-established finding that stromal cells modify the behavior of tumor cells and vice versa have elucidated signaling molecules, proteases and other proteins that are crucial to this interaction. The challenge is to identify the most critical factors that might be targeted by small molecule or antibody therapeutics.Elucidating the role of immune cells in the microenvironment through proteomics There is intense interest in elucidating critical interactions between tumor cells and immune cells in the microenvironment. Cells with immunosuppressive potential include macrophages, regulatory T (Treg) cells and myeloid derived suppressor cells (MDSCs). Infiltrating immune cells are capable of stimulating tumor growth through the expression of signaling molecules (such as interleukins or cytokines) and growth factors (such as epidermal growth factor (EGF), TGF and fibroblast growth factor (FGF)), as well as through the secretion of ECM-modifying proteases [63-66]. Both antibody arrays and MS have been utilized to profile immune cells and their derived cytokines (Table 1). Anantibody array was used to analyze the expression of cytokines in mesothelioma pleural effusions and in conditioned media from cell lines established from the same tumors. This study detected HGF, macrophage inflammatory protein (MIP)-1d, MIP-3a, neutrophil-activating peptide (NAP)-2, and pulmonary activation-regulated chemokine (PARC) exclusively in the pleural effusions, suggesting that these cytokines may be primarily expressed by stromal or inflammatory cells [67]. Immunohistochemistry revealed infiltration of macrophages, NK cells and T-lymphocytes in the mesothelioma tumors. Mesothelioma cell lines expressed many chemokines that seem to recruit immune cells, PubMed ID:https://www.ncbi.nlm.nih.gov/pubmed/16989806 such as interferon-inducible protein-10 (CXCL10), macrophage migration inhibitory factor (MIF), monocyte chemoattractant protein-1 (MCP-1, also known as CCL2), epithelial neutrophil-activating protein-78 (ENA-78), MIP1b, IL-8, growth regulatory protein (GRO) and RANTES [67]. An LC-MS/MS analysis of the cell supernatants from tumor-associated monocytes or macrophages isolated from the ascites of ovarian cancer patients identified 14-3-3 zeta, an adapter protein that potentially regulates a large number of molecules in signaling pathways [68]. Oxidative stress promotes the infiltration of inflammatory cells by providing favorable growth conditions, and these cells further contribute to the hypoxic environment by producing reactive oxygen species (ROS) [69]. A comparative proteome analysis of naive CD45RA+T cells and their memory/effector CD45RO+T cell.