The crosstalk between acinar cells with Kras mutations and M1-polarized macrophages leads to initiation of pancreatic precancerous lesions

Recent studies on the processes that lead to the development of pancreatic cancer indicate that inflammatory macrophages have key functions in the initiation of pre-neoplastic lesions. Specifically, acquisition of an activating Kras mutation in pancreatic acinar cells leads to upregulation of intercellular adhesion molecule-1 (ICAM-1), which serves as a chemoattractant for M1-polarized macrophages. M1 macrophages then contribute to acinar cell metaplasia and development of precancerous lesions through inflammatory cytokines and secreted proteases.