Inflammation represents the immune system response to external or internal aggressors such as injury or infection in certain tissues. The body’s response to cancer has many parallels with inflammation and repair; the inflammatory cells and cytokines present in tumours are more likely to contribute to tumour growth, progression, and immunosuppression, rather than in building an effective antitumour defence. Using new proteomic technology, we have investigated serum profile of pro- (IL-1β, IL-6, IL-8, IL-12, GM-CSF, and TNF-α) and anti-inflammatory cytokines (IL-4, IL-10), along with angiogenic factors (VEGF, bFGF) in order to assess tumoural aggressiveness. Our results indicate significant dysregulation in serum levels of cytokines and angiogenic factors, with over threefold upregulation of IL-6, IL-1β, TNF-α, and IL-10 and up to twofold upregulation of VEGF, FGF-2, IL-8, IL-2, and GM-CSF. These molecules are involved in tumour progression and aggressiveness, and are also involved in a generation of disease associated pain.

Telocytes (TCs) are interstitial cells that are present in numerous organs, including the heart interstitial space and cardiac stem cell niche. TCs are completely different from fibroblasts.TCs release extracellular vesicles that may interact with cardiac stem cells (CSCs)viaparacrine effects. Data on the secretory profile ofTCs and the bidirectional shuttle vesicular signalling mechanism betweenTCs andCSCs are scarce. We aimed to characterize and understand thein vitroeffect of theTCsecretome onCSCfate. Therefore, we studied the protein secretory profile using supernatants from mouse cultured cardiacTCs. We also performed a comparative secretome analysis using supernatants from rat cultured cardiacTCs, a pureCSCline andTCs‐CSCs in co‐culture using (i) high‐sensitivity on‐chip electrophoresis, (ii) surface‐enhanced laser desorption/ionization time‐of‐flight mass spectrometry and (iii) multiplex analysis by Luminex‐xMAP. We identified several highly expressed molecules in the mouse cardiacTCsecretory profile: interleukin (IL)‐6,VEGF, macrophage inflammatory protein 1α (MIP‐1α),MIP‐2 andMCP‐1, which are also present in the proteome of rat cardiacTCs. In addition, rat cardiacTCs secrete a slightly greater number of cytokines,IL‐2,IL‐10,IL‐13 and some chemokines like,GRO‐KC. We found thatVEGF,IL‐6 and some chemokines (all stimulated byIL‐6 signalling) are secreted by cardiacTCs and overexpressed in co‐cultures withCSCs. The expression levels ofMIP‐2 andMIP‐1α increased twofold and fourfold, respectively, whenTCs were co‐cultured withCSCs, while the expression ofIL‐2 did not significantly differ betweenTCs andCSCs in mono culture and significantly decreased (twofold) in the co‐culture system. These data suggest that theTCsecretome plays a modulatory role in stem cell proliferation and differentiation.

Objectives We measured the serum concentration of a panel of inflammatory cytokines and evaluated their association with circulating proangiogenic biomarkers and with outcome in patients with pancreatic ductal adenocarcinoma (PDAC). Methods We collected serum samples from 36 patients with PDAC, 9 patients with chronic pancreatitis, and 22 healthy volunteers as a control. Inflammatory cytokines and proangiogenic biomarkers were measured using the multianalyte xMAP array and carcinoembryonic antigen (CEA) and carbohydrate 19-9 by immunoassay. Results Patients with PDAC had higher circulating levels of interleukin 6 (IL-6) than those of patients with pancreatitis or healthy individuals and higher levels of IL-10 and tumor necrosis factor α (TNF-α) compared with those of healthy individuals. In patients with PDAC, circulating IL-6, TNF-α, IL-1β, and IL-10 correlated with serum concentrations of vascular endothelial growth factor and basic fibroblast growth factor; circulating IL-6, IL-1β, and TNF-α correlated with carbohydrate 19-9; and IL-8, IL-10, and TNF-α correlated with CEA levels. Circulating IL-8, TNF-α, and CEA; tumor stage; and lymph node metastases were associated with a poor outcome. Conclusions The results of this exploratory study indicate that inflammatory cytokines should be pursued as potential prognostic biomarkers as well as targets for therapy in larger studies in PDAC.

The clinical and fundamental research in prostate cancer - the most common urological cancer in men - is currently entering the proteomic and genomic era. The focus has switched from one single marker (PSA) to panels of biomarkers (including proteins involved in ribosomal function and heat shock proteins). Novel genetic markers (such as Transmembrane protease serine 2 (TMPRSS2)-ERG fusion gene mRNA) or prostate cancer gene 3 (PCA3) had already entered the clinical practice, raising the question whether subsequent protein changes impact the evolution of the disease and the response to treatment. Proteomic technologies such as MALDI-MS, SELDI-MS, i-TRAQ allow a qualitative/quantitative analysis of the proteome variations, in both serum and tumor tissue. A new trend in prostate cancer research is proteomic analysis of prostasomes (prostate-specific exosomes), for the discovery of new biomarkers. This paper provides an update of novel clinical tests used in research and clinical diagnostic, as well as of potential tissue or fluid biomarkers provided by extensive proteomic research data.