Chronic inflammation induced by biological, chemical, and physical factors has 
been found to be associated with the increased risk of cancer in various organs. 
We revealed that infectious agents including liver fluke, Helicobacter pylori, 
and human papilloma virus and noninfectious agents such as asbestos fiber 
induced iNOS-dependent formation of 8-nitroguanine and 8-oxo-7, 
8-dihydro-2'-deoxyguanosine (8-oxodG) in cancer tissues and precancerous 
regions. Our results with the colocalization of phosphorylated ATM and γ-H2AX 
with 8-oxodG and 8-nitroguanine in inflammation-related cancer tissues suggest 
that DNA base damage leads to double-stranded breaks. It is interesting from the 
aspect of genetic instability. We also demonstrated IL-6-modulated iNOS 
expression via STAT3 and EGFR in Epstein-Barr-virus-associated nasopharyngeal 
carcinoma and found promoter hypermethylation in several tumor suppressor genes. 
Such epigenetic alteration may occur by controlling the DNA methylation through 
IL-6-mediated JAK/STAT3 pathways. Collectively, 8-nitroguanine would be a useful 
biomarker for predicting the risk of inflammation-related cancers.