Table 1.

A summary of inflammation and pancreatic cancer

Inflammatory factors	Role
NF-κB	Switches from tumor suppressor to tumor promoter during an early phase of tumorigenesis
IL-6	Promotes pancreatic intraepithelial neoplasia
TLRs	TLR4 promotes angiogenesis and TLR9-induced epithelial cell proliferation
TGF-β	Plays tumor promoter through genomic instability, neo-angiogenesis, immune evasion, cell motility, and metastasis
TNF-α	Activates transcription factor NF-κB
IL-1-α	Favors metastatic and invasive behavior of pancreatic cells by inducing k63-linked polyubiquitination of TRAF6 leading to activation of NF-κB
IL-4	Increases expression of antiapoptotic proteins and mediates the downregulation of cell adhesion molecules
IL-8	Mimics VEGF and promotes angiogenesis
IL-1-β	Stimulates autophagy and induces endoplasmic reticulum stress
COX-2	A key enzyme responding to various cytokines and growth factor
SPINK-1	Mutations lead to premature trypsinogen activation and resultant hereditary pancreatitis
ROS	Induces oxidative damage to DNA, lipids, and proteins
CP	KRAS mutations are found in patients with CP
Autophagy	Cleaning of damaged organelles to guarantee pancreatic cell survival
CXCL-12	Enhances growth and restricts immune surveillance through local autocrine and paracrine mechanisms

NF-κB: Nuclear factor-κB; IL-6: Interleukin-6; TLR: Toll-like receptor; TGF: Transforming growth factor; TRAF6: TNF-receptor-associated factor 6; TNF: Tumor necrosis factor; VEGF: Vascular endothelial growth factor; COX: Cyclooxygenase-2; SPINK-1: Serine protease inhibitor Kazal type-1; ROS: Reactive oxygen species; CP: Chronic pancreatitis