ArticleProceedings of the National Academy of Sciences of the United States of America2002
The aflatoxin B(1) formamidopyrimidine adduct plays a major role in causing the types of mutations observed in human hepatocellular carcinoma.
Article in Proceedings of the National Academy of Sciences of the United States of America, 2002. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 85 papers.
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Who cites it
85 citing papers in PubMed, 207 citations in OpenAlex.
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- Dynamic Assemblies in Genome Maintenance.Advances in experimental medicine and biology · 2026Review
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- Cooperation Between Aflatoxin-Induced p53 Aberrations and Hepatitis B Virus in Hepatocellular Carcinoma.Journal of xenobiotics · 2025Review
- Aflatoxin BEnvironmental toxicology and pharmacology · 2025Article
- Structurally Similar Mycotoxins Aflatoxin BToxins · 2025Article
- Goniodomic Acid, a Transient Oxirane Intermediate in the Conversion of the Macrolide Algal Toxin Goniodomin A to Seco Acids.Chemical research in toxicology · 2025Article
- Nucleotide excision repair of aflatoxin-induced DNA damage within the 3D human genome organization.Nucleic acids research · 2024Article
- Functional characterization of single nucleotide polymorphic variants of DNA repair enzyme NEIL1 in South Asian populations.DNA repair · 2024Article
- Mass Spectrometry-Based Method to Measure Aflatoxin BChemical research in toxicology · 2024Article
- Frequencies and spectra of aflatoxin BNAR molecular medicine · 2024Article
- Tissue Organoid Cultures Metabolize Dietary Carcinogens Proficiently and Are Effective Models for DNA Adduct Formation.Chemical research in toxicology · 2024Article
- Comparative metabolism of aflatoxin BArchives of toxicology · 2023Article
- Diverse mycotoxin threats to safe food and feed cereals.Essays in biochemistry · 2023Review
- Functional analyses of single nucleotide polymorphic variants of the DNA glycosylase NEIL1 in sub-Saharan African populations.DNA repair · 2023Article
- Genotoxic effects of the major alkylation damage N7-methylguanine and methyl formamidopyrimidine.The Biochemical journal · 2023Article
- Synthesis and Characterization ofACS omega · 2023Article
25 more citing papers are in PubMed but not listed here.
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Authors and funding
6 authors at 3 institutions in 1 country.
Funding
Abstract
A G to T mutation has been observed at the third position of codon 249 of the p53 tumor-suppressor gene in over 50% of the hepatocellular carcinoma cases associated with high exposure to aflatoxin B(1) (AFB(1)). Hypotheses have been put forth that AFB(1), in concert with hepatitis B virus (HBV), may play a role in the formation of, and/or the selection for, this mutation. The primary DNA adduct of AFB(1) is 8,9-dihydro-8-(N(7)-guanyl)-9-hydroxyaflatoxin B(1) (AFB(1)-N7-Gua), which is converted naturally to two secondary lesions, an apurinic site and an AFB(1)-formamidopyrimidine (AFB(1)-FAPY) adduct. AFB(1)-FAPY is detected at near maximal levels in rat DNA days to weeks after AFB(1) exposure, underscoring its high persistence in vivo. The present study reveals two striking properties of this DNA adduct: (i) AFB(1)-FAPY was found to cause a G to T mutation frequency in Escherichia coli approximately 6 times higher than that of AFB(1)-N7-Gua, and (ii) one proposed rotamer of AFB(1)-FAPY is a block to replication, even when the efficient bypass polymerase MucAB is used by the cell. Taken together, these characteristics make the FAPY adduct the prime candidate for both the genotoxicity of aflatoxin, because mammalian cells also have similar bypass mechanisms for combating DNA damage, and the mutagenicity that ultimately may lead to liver cancer.
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