Diet derived polycyclic aromatic hydrocarbons and its pathogenic roles in colorectal carcinogenesis. (December 2021)

• Record Type: Journal Article
• Authors: Cheng, Tracie; Lam, Alfred K.; Gopalan, Vinod
• Is Part Of: Critical reviews in oncology/hematology. Volume 168(2021)
• Publication Date: 2021-12
• Subjects: Polycyclic aromatic hydrocarbon -- Meat -- Colon -- Rectal -- Bowel -- Cancer -- Carcinoma -- Diet; Oncology -- Periodicals; Hematology -- Periodicals; 616.994
• DOI: 10.1016/j.critrevonc.2021.103522
• Languages: English
• ISSNs: 1040-8428

Abstract

Graphical abstract: Graphical abstract for the review article Diet derived polycyclic aromatic hydrocarbons and its pathogenic roles in colorectal carcinogenesis, highlighting associations that exist between genetic variants in genes associated with polycyclic aromatic hydrocarbon metabolism and DNA repair, and epidemiological studies linking these molecules to colorectal cancer. Highlights: Polycyclic aromatic hydrocarbons (PAH) are associated with colorectal cancer (CRC) in the population. Polymorphisms in PAH metabolic enzymes are associated with CRC. PAH metabolites create DNA adducts. Variants of nucleotide excision repair are linked to CRC. Abstract: Polycyclic aromatic hydrocarbon (PAHs) are molecules that contaminate meat products during the high-temperature cooking of meat. This study reviewed the pathogenic roles of meat derived polycyclic aromatic hydrocarbons in the carcinogenesis of colorectal cancer (CRC). Ingested PAHs undergo xenobiotic metabolism resulting in the activation of genotoxic metabolites that can induce DNA damage in the colorectum. Genetic polymorphisms in PAH xenobiotic enzymes are linked to the risk of CRC and suggest a role for PAH-meat ingestion in carcinogenesis of colorectal malignancies. Furthermore, PAH specific DNA adducts have been identified in colorectal cancer tissue and linked to high meat intake. DNA adduct resolution is mediated by the nucleotide excision repair, and polymorphisms within genes of this repair pathway and high meat intake are associated with increased CRC risk. In the literature, there is evidence from metabolic enzyme gene variants, DNA repair genes, PAH metabolites, and epidemiological studies suggesting PAH involvement in CRC.