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Cao Cancer Evo-Dev

Acute Chronic infection
inflammation
Obesity
Diabetes
Hypertension
IL-6， TNFa UV injury
STAT3 Air pollution
M2 macrophage Over consumption of red meat
Lack of physical excise
Regular excise
Mediterranean diet
Type I IFNs Prompt vaccination
STAT1 Alternate work with recreation
M1 macrophage Good interpersonal relationship

Chronic
inflammation

Figure 1: Factors affecting chronic inflammations and their associations with acute inflammations. IFN: interferon; STAT: signal
transducers and activators of transcription; IL: interleukin; TNF: tumor necrosis factor; UV: ultraviolet

termed as resolving inflammation, is an initial stage B (CHB) . However, the risk of developing HCC is
[3]
of inflammation mediated through activation of innate significantly higher in the oral nucleos(t)ide analogues-
immunity; it lasts for short period. Chronic inflammation, complete responder group compared with the inactive
also termed as non-resolving inflammation, is the CHB group, regardless of the presence of baseline liver
second stage of inflammation that persists for a long cirrhosis , indicating that continuous active inflammation
[4]
period of time. Chronic inflammation may develop from in liver facilitates the development of HCC. Although
acute inflammation if the stimuli are not eradicated or surgical technologies for the treatment of liver cancer
inflammation appears with a chronic process, reflecting have been improved, postoperative prognosis remains to
the weak but active nature of host immunity. Although be precisely evaluated [5-7] . Active inflammation on chronic
the two kinds of inflammation are closely linked to form inflammation background, as reflected by an Ishak
a correlative antagonistic unity, inherent mechanisms hepatic inflammation score (> 6), a higher neutrophil-to-
regarding proinflammatory molecules, types of infiltrating lymphocyte ratio (> 5), and a higher C-reactive protein in
macrophages, and inflammatory pathways are distinct, as sera (> 0.3 mg/dL), etc., also indicate a poor postoperative
shown in Figure 1 . Acute inflammation is often regarded prognosis such as postoperative recurrence and shorter
[1]
as therapeutic inflammation to ward off infections recurrence-free survival in HBV-related HCC (HBV-
and/or to repair the tissue damage; whereas chronic HCC) patients [8,9] . Nuclear factor-κB (NF-κB) and signal
inflammation is now considered as pathogenic, being transducers and activators of transcription 3 (STAT3)
closely linked with most chronic illnesses, such as cancer, are two most important transcription factors involved
cardiovascular diseases, diabetes, obesity, pulmonary in inflammatory pathways that play predominant
diseases, neurologic disorders, and even depression . roles in carcinogenesis, especially in HBV-induced
[2]
Non-resolving inflammation is the prerequisite for the hepatocarcinogenesis [10,11] . Thus, inflammatory
development of most cancers. For examples, chronic microenvironment including proinflammatory molecules,
hepatitis B or C, chronic bronchitis, chronic colitis including tumor-associated fibroblasts, and tumor-associated
ulcerative colitis, chronic cervicitis, chronicatrophic immune cellswith altered expression of the inflammatory
gastritis, and chronic esophagitis (gastroesophageal pathways facilitates the evolution and development of
reflux disease - caused Barrett’s esophagus) often cancers.
precedes liver cancer, lung cancer, colorectal cancer,
cervical cancer, gastric cancer, and esophageal cancer, Maintenance of chronic HBV infection
respectively. Non-resolving inflammation is clearly evident andhepatic inflammation
in the development of hepatitis B virus (HBV)-induced Chronic transformation of HBV infection relies on three
hepatocellular carcinoma (HCC). It is generally believed aspects: infection occasion, the characteristics of
that oral-administered antiviral therapy decreases the HBV genotypes, and genetic predisposition of the key
risk of developing HCC in patients with chronic hepatitis immune molecules. HBV infection in early childhood
242 Hepatoma Research ¦ Volume 3 ¦ October 27, 2017