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Chronic inflammation and liver tissue damage brought on by alcohol drinking are assumed to be the source of the increased liver cell proliferation in chronic alcoholism. In an effort to repair the injured tissue, growth factors and cytokines like Transforming Growth Factor-alpha (TGF-alpha) and Interleukin-6 (IL-6) can be released as a result of this damage. Furthermore, long-term alcohol abuse can decrease the liver's capacity to process some chemicals and hormones, causing additional damage and inflammation that can encourage cell growth.
Due to the accumulation of genetic abnormalities and epigenetic modifications that interfere with normal cell cycle regulation and growth control, liver cancer results in an uncontrolled proliferation of liver cells. Mutations in tumor suppressor genes like p53 and p16, as well as oncogenes like c-Myc and Ras, can impair the normal control of the cell cycle, causing uncontrolled cell growth and division. Furthermore, epigenetic modifications like DNA methylation and histone modification can modify how genes are expressed, upregulating the genes that support cell growth and division.