The pro-cancer changes involved primarily upregulation of pathways involved in inflammation, e.g. IL-6, IL-8, IL-17, HMGB1, TREM-1 and tumor microenvironment signaling, while the anti-cancer effects were predominantly related to control of cell cycle through downregulation of cyclins, cyclin-dependent kinases, polo-like kinase and metaphase signaling pathway. The gene discussed is IL6; the disease is neoplasm.