Figure 7. β-catenin acts as a gatekeeper of Kras-induced reprogramming of acini into ductal PanINs.
Pattern of β-catenin signaling activity during acinar regeneration versus Kras-induced ADM/PanIN. β-catenin levels are kept below a critical threshold during the initiation of Kras-induced ductal reprogramming but increase as PanIN lesions form. Therefore, β-catenin antagonizes specification of a ductal state capable of forming PanINs, but likely contributes to PanIN progression and tumor growth.