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?2a, b; P?Sitaxentan was significantly increased in the dLN of mice in the treatment group compared with controls (by three-fold and two-fold, respectively). This phenomenon was only observed in the dLN, but not the ndLN, nor in the spleens in either treatment group, suggestive of a localized T-cell response to the S.?aureus ALK inhibitor BPM (Fig.?3a,b). To determine the direct effect of the S.?aureus BPM on tumour cell killing, cell viability was measured against increasing doses of treatment in human mesothelial and mesothelioma cells and mouse mesothelioma cells in vitro. S.?aureus BPM induced a decrease in cell viability for all human mesothelioma cell lines but not benign mesothelial cells (Fig.?4a). Of the four mouse mesothelioma cell lines tested, AB1-HA and AB22 (BALB/c derived) viability significantly decreased at the highest dose of treatment (Fig.?4b; P?Anti-cancer Compound Library molecular weight cells appeared to be mediated through the apoptotic pathway as shown by cells stained with Annexin V (BD Biosciences) and 7AAD (BD Biosciences). A significant increase in apoptosis was observed in all human mesothelioma cell lines at higher doses (CRL-2081: 1.88?��?0.20-fold, JU77: 1.31?��?0.09-fold and LO68: 1.81?��?0.18-fold over controls). However, benign human mesothelial cells appeared to be resistant to the apoptotic effects of treatment (Fig.?4c). In mouse cells, two of the four mesothelioma lines were susceptible to treatment-induced apoptosis (Fig.?4d; AB1-HA, 1.44?��?0.05-fold and AB22, 1.34?��?0.03-fold increase over controls). There was no significant difference in the release of cytokines known to induce mesothelioma growth following treatment with the bacterial compound (namely IL-8, MCP-1 or VEGF; Fig. 5a�Cc) in the three human mesothelioma cell lines tested compared with controls. No significant differences in cytokine levels were seen in any of the mouse mesothelioma cell lines following treatment (Fig.?5d�Cf).