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IL-1β on mouse skin [2,3]; The study of tumor promotion by both okadaic acid and TPA revealed that TNF-α is an essential tumor promoter in TNF-α-deficient mouse skin initiated with DMBA [3]; Inhibitors of PP1 and PP2A induced tumor promotion on mouse skin, in rat glandular stomach and rat liver initiated with carcinogens [4]; TNF-α, IL-1α and IL-1β induced clonal growth of v-Ha-ras-transfected BALB/3T3 cells (Bhas 42) [3]; Treatment with tumor promoters commonly released TNF-α from target organs [5]. In light of our evidence showing that TNF-α, IL-1α and IL-1β act as endogenous tumor promoters and/or cancer mediators [6,7], we specifically found a TNF-α–inducing protein (Tipα) gene in H. pylori genome [8,9]. Tipα dimer bind to nucleolin on cell surface of human gastric cancer cells as a receptor [10], and are secreted in large quantities from H. pylori of gastric cancer patients [11]. The Epithelial-Mesenchymal Transition (EMT) was induced in human gastric cancer cells by Tipα [12]. The Tipα and nucleolin complex shows a strong link between tumor promotion and clinical cancer development. Since TNF-α and IL-1 are tumor-promoting cytokines, we discussed the role of inflammasome signaling for tumor promotion using apoptosisassociated speck-like protein containing a caspase recruitment domain (ASC)-KO and caspase (CASP)-1-KO mice reported by Campanelli’s group [13].

Progressive Insight into Tumor Promotion with Proinflammatory Cytokines