Open AccessJournal Article
Aflatoxins as a cause of hepatocellular carcinoma.
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TLDR
Much remains to be learnt about the precise pathogenetic mechanisms responsible for aflatoxin B1-induced hepatocellular carcinoma as well as the interaction between the toxin and hepatitis B virus in causing the tumor.Abstract:
Aflatoxins, metabolites of the fungi Aspergillus flavus and Aspergillus parasiticus, are frequent contaminants of a number of staple foods, particularly maize and ground nuts, in subsistence farming communities in tropical and sub-tropical climates in sub-Saharan Africa, Eastern Asia and parts of South America. Contamination of foods occurs during growth and as a result of storage in deficient or inappropriate facilities. These toxins pose serious public health hazards, including the causation of hepatocellular carcinoma by aflatoxin B1. Exposure begins in utero and is life-long. The innocuous parent molecule of the fungus is converted by members of the cytochrome p450 family into mutagenic and carcinogenic intermediates. Aflatoxin-B1 is converted into aflatoxin B1-8,9 exo-epoxide, which is in turn converted into 8,9-dihydroxy-8-(N7) guanyl-9-hydroxy aflatoxin B1 adduct. This adduct is metabolized into aflatoxin B1 formaminopyrimidine adduct. These adducts are mutagenic and carcinogenic. In addition, an arginine to serine mutation at codon 249 of the p53 tumor suppressor gene is produced, abrogating the function of the tumor suppressor gene, and contributing to hepatocarcinogenesis. Aflatoxin B1 acts synergistically with hepatitis B virus in causing hepatocellular carcinoma. A number of interactions between the two carcinogens may be responsible for this action, including integration of hepatitis B virus x gene and its consequences, as well as interference with nucleotide excision repair, activation of p21waf1/cip1, generation of DNA mutations, and altered methylation of genes. But much remains to be learnt about the precise pathogenetic mechanisms responsible for aflatoxin B1-induced hepatocellular carcinoma as well as the interaction between the toxin and hepatitis B virus in causing the tumor.read more
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References
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Journal ArticleDOI
Hepatitis B virus x protein in the pathogenesis of hepatitis B virus-induced hepatocellular carcinoma.
TL;DR: Current experimental observations suggest that HBx protein may increase the expression of TERT and telomerase activity, prolonging the life‐span of hepatocytes and contributing to malignant transformation, and it may enhance the protein's ability to transform oncogenes, resulting in uncontrolled cell growth.
Journal ArticleDOI
Population attributable risk of aflatoxin-related liver cancer: systematic review and meta-analysis.
TL;DR: In high exposure areas, aflatoxin multiplicatively interacts with HBV to induce HCC; reducing aflat toxin exposure to non-detectable levels could reduce HCC cases in high-risk areas by about 23%.
Journal ArticleDOI
Synergistic interaction between aflatoxin B1 and hepatitis B virus in hepatocarcinogenesis.
TL;DR: C cohort studies of patients with HCC in China and Taiwan have provided compelling evidence for a multiplicative or sub‐multiplicative interaction between HBV and AFB1 in the genesis of human HCC.
Journal ArticleDOI
Aflatoxin exposure and risk of hepatocellular carcinoma in Taiwan
Li-Yu Wang,Maureen Hatch,Chien-Jen Chen,Bruce Levin,San Lin You,Sheng-Nan Lu,Mei-Huei Wu,Wei-Pin Wu,Lian-Wen Wang,Qiao Wang,Guan-Tarn Huang,Pei-Ming Yang,Hsuan-Shu Lee,Regina M. Santella +13 more
TL;DR: It is suggested that environmental aflatoxin exposure may enhance the hepatic carcinogenic potential of hepatitis B virus and a large‐scale study will be needed to evaluate the effect of a flatoxin exposure on HBsAg non‐carriers.
Journal ArticleDOI
Primary prevention of hepatocellular carcinoma in developing countries.
TL;DR: HBV vaccination has to be the priority in the reducing the incidence of HCC and measures to reduce food spoilage by fungi and the associated dietary exposure to aflatoxins is also a desirable public health goal.
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