Holistic paradigm in carcinogenesis: Genetics, epigenetics, immunity, inflammation and oral infections

Table 2 Summary of inflammation and cancer relationship

Basic observations	Interpretation
Chronic inflammation increases cancer risk	Causality is not proven[47]
	Inflammation from psoriasis actually reduces cancer risk
AIs decrease cancer	AIs are proven to decrease cancer risk as shown in Coley’s toxin[93]
	AIs may mobilize strong immune responses and create cancer resisting environment[94,95]
Metabolic inflammation may be an important risk factor	Causality is quite possible, via IGF, VEGF
Various type of immune, inflammatory cells are present in cancer loci	They can be innocent bystanders
Immune cells affect malignant cells through cytokines, chemokines, growth factors, prostaglandins, and reactive oxygen and nitrogen species	This fact proves that there is an interaction between immune cells and cancer cells but causal relationship is yet to be established
Inflammation is present from tumor initiation to metastasis	It does not mean inflammation causes cancer. Inflammation may be a part of disease processes in cancer
NF-κB signaling pathway can be two-way street: NF-κB from immune system can suppress cancer progress; also NF-κB from cancer cells to resist immune action	NF-κB is universal biologic transcription factor and difficult to prove its involvement as a causal factor in carcinogenesis
Certain immune/inflammatory actions are dispensable in some stages and indispensable in others

AIs: Acute infections; IGF: Insulin-like growth factor; VEGF: Vascular endothelial growth factor.