No abstract

All individuals rely on a fundamental set of mental capacities and functions, or bandwidth, in their economic and non-economic lives. Yet, many factors associated with poverty, such as malnutrition, alcohol consumption, or sleep deprivation, may tax this capacity. Previous research has demonstrated that such taxes often significantly alter judgments, preferences, and decision-making. A more suggestive but growing body of evidence points toward potential effects on productivity and utility. Considering the lives of the poor through the lens of bandwidth may improve our understanding of potential causes and consequences of poverty.

Wnt ligand expression and activation of the Wnt/β-catenin pathway have been associated with pancreatic ductal adenocarcinoma, but whether Wnt activity is required for the development of pancreatic cancer has remained unclear. Here we report the results of three different approaches to inhibit the Wnt/β-catenin pathway in a established transgenic mouse model of pancreatic cancer. First, we found that β-catenin null cells were incapable of undergoing acinar to ductal metaplasia, a process associated with development of premalignant PanIN lesions. Second, we addressed the specific role of ligandmediated Wnt signaling through inducible expression of Dkk1, an endogenous secreted inhibitor of the canonical Wnt pathway. Lastly, we targeted the Wnt pathway with OMP-18R5, a therapeutic antibody that interacts with multiple Frizzled receptors. Together, these approaches demonstrated that ligandmediated activation of the Wnt/β-catenin pathway is required to initiate pancreatic cancer. Moreover, they establish that Wnt signaling is also critical for progression of pancreatic cancer, a finding with potential therapeutic implications.