Inflammation and cancer

Table 1 Overexpression of inflammatory factors in gastrointestinal carcinogenesis

Factors	Gastrointestinal cancers
NF-κB	Differential expression and constitutive activation was correlated with severity of oral lesions in the course of oral cancer development[112]
	Elevated activated nuclear factor-κB-regulated cytokines were found in oral lichen planus patients and in the saliva of patients with oral squamous cell carcinoma[113,114]
	Associated with hepatocarcinogenesis induced by viral hepatitis B or viral hepatitis C infection[115,116]
COX-2	Associated with pathogenesis in mucositis[117]
	Associated in Barrett's metaplasia with a change in the local inflammatory reaction[118]
	Important overexpression in the pathogenesis of cholangiocarcinomas[119]
	Contribute to suppression of local immune responses and enhancement of metastatic potential in human hepatocellular carcinoma[120]
	Predictive marker in the early stages of hepatocarcinogenesis[121]
	Related to the histological grade of intraductal papillary-mucinous tumor of the pancreas[122]
	Gene expression was elevated in human colorectal cancer compared to normal mucosa[123]
	Associated with prognosis and intestinal pathways in gastric carcinogenesis[124,125]
STAT-3	Associated with the tumorigenesis of colorectal carcinoma[126]
	Associated with cell survival in gastric cancer[127]
	Associated with the development and proliferation of colorectal cancer[128]
IL-6	Associated with the development of apoptosis resistance Barrett's esophagus[129]
	Associated with the growth and proliferation in human colorectal cancer[130,131]
NOS	Correlated with Barrett's-associated neoplastic progression[132]
5-LOX	Associated with the development of pancreatic cancer[133]

NF-κB: Nuclear factor-κB; COX-2: Cyclooxygenase-2; STAT-3: Signal transducer and activator transcription 3; IL-6: Interleukin-6; NOS: Nitric oxide lipoxygenase; 5-LOX: 5-lipoxygenase.