To address the role of Stat3 signaling in intestinal epithelial cells (IEC) during colorectal carcinogenesis, we exposed mice with an IEC-specific ablation of Stat3 to a model of colitis-associated carcinogenesis (CAC) and to a genetic model for sporadic intestinal carcinogenesis. In both models, Stat3 modulated tumor development. During CAC, we observed a dramatic reduction in tumor number and size, due to a cell-autonomous impaired induction in anti-apoptotic and pro-proliferative genes. During early tumor promotion of sporadic intestinal carcinogenesis, ablation of Stat3 signaling lead to a survival advantage by increasing IEC-apoptosis. Interestingly, this increase was not mediated by a cell-autonomous impaired induction of anti-apoptotic genes, but depended on differential activation of immune cells and secretion of Interferon-γ.      «

To address the role of Stat3 signaling in intestinal epithelial cells (IEC) during colorectal carcinogenesis, we exposed mice with an IEC-specific ablation of Stat3 to a model of colitis-associated carcinogenesis (CAC) and to a genetic model for sporadic intestinal carcinogenesis. In both models, Stat3 modulated tumor development. During CAC, we observed a dramatic reduction in tumor number and size, due to a cell-autonomous impaired induction in anti-apoptotic and pro-proliferative genes. Durin...     »