**2. Hepatocarcinogenesis**

Hepatocarcinogenesis is the development of liver cancer due to the exposure of carcinogen (a chemical that produces cancer). Many hepatocarcinogens such as aflatoxins, acetylaminofluorene, diethylnitrosamine have been successfully used to develop hepatocarcinogenesis in animals. Experimentally, hepatocarcinogenesis is developed using different carcinogens and also in different animal species. Several genetic and epigenetic changes such as chromosomal deletions, rearrangements, aneuploidy, gene amplification, and mutations, formation of DNA adducts, DNA strand-break, modulation of DNA methylation, and modulation of cell signaling pathways, due to direct or indirect effect of carcinogen exposure lead to neoplastic transformation of hepatocytes in experimental animals. Hepatocarcinogenesis is a multistage complex process, which is preceded by early appearance of morphologically and genetically altered hepatic focal lesions, also known as preneoplastic lesions. Initially monoclonal populations of hepatocytes evolve primarily due to carcinogenic insult. These aberrant monoclonal populations of regenerative hepatocytes (focal lesions) develop hyperplastic nodules to dysplastic nodules, leading to hepatocellular carcinoma.
