Therefore, the aim of the present study was to: i) evaluate the status of oxidative stress in HCC and the surrounding non-tumor liver tissues; ii) determine the occurrence of ɛ-dA in these tissues; iii) determine if the formation of ɛ-dA was associated with liver inflammatory activity and fibrosis development; iv) assess if a correlation exists between the formation of ɛ-dA and mutant p53 expression in HCC tissue to elucidate its potential as a contributor to human hepatocarcinogenesis. This evidence concerns the gene TP53 and neoplasm.