Molecular mechanisms of alcohol-mediated carcinogenesis

By H. Seitz, F. Stickel. Nature Reviews. Cancer, 2007

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Alcohol consumption and site-specific cancer risk: a comprehensive dose–response meta-analysis (2014, background): “Polymorphisms of the genes that encode enzymes for ethanol metabolism affect the ethanol/acetaldehyde oxidising capacity, and are responsible for the limited action of the enzyme that converts acetaldehyde to acetate that is not toxic to the body (Pöschl and Seitz, 2004; Seitz and Stickel, 2007; Yu ”
Review of hepatocellular carcinoma: Epidemiology, etiology, and carcinogenesis (2017, background): “[71] Additional mechanisms proposed include iron overload, decreased vitamin A (retinoid acid) levels and downregulation of S‐adenosyl methionine.[69] A comparison of whole exome sequencing of HCC tumors from European and Asian cohorts demonstrated differences based on risk factors.”
American Cancer Society guidelines on nutrition and physical activity for cancer prevention (2002, background): “One possible mechanism involves an important product of alcohol metabolism, acetaldehyde, which can directly affect normal cells by damaging DNA.186 For breast cancer, alcohol consumption may lead to increases in blood levels of estrogens or other hormones.187 Reducing alcohol consumption is one of ”
Oral squamous cell carcinomas: state of the field and emerging directions (2023, background): “223 Global hypomethylation may facilitate tumorigenesis by diminishing the methylation of CpG dinucleotides across the entire genome.”