Abstract
Pancreatic cancer (PC) remains a highly lethal malignancy worldwide. Increasing evidence indicates that inflammation is a critical factor in the pathogenesis of pancreatic ductal adenocarcinoma (PDAC). Inflammatory cell infiltration within the PDAC tumor microenvironment promotes tumor growth and metastasis, while both local and systemic chronic inflammation is associated with an elevated risk of developing the disease. Given that the same immune cell populations are involved in mediating both inflammatory and immune responses, there exists a close interrelationship between inflammation and immunity in the context of PDAC. Various studies have reported the relationship between inflammation and PC. This review article provided a comprehensive summary of the roles of erythrocyte sedimentation rate, plasma viscosity, procalcitonin, calprotectin, haptoglobin, serum amyloid A, ferritin, and fibrinogen in the pathophysiological mechanisms underlying PC.