ArticleGastroenterology2009
In vitro recapitulating of TP53 mutagenesis in hepatocellular carcinoma associated with dietary aflatoxin B1 exposure.
Article in Gastroenterology, 2009. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 33 papers, 1 of them a synthesis that pooled it.
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33 citing papers in PubMed, 1 synthesis or guideline pooled it, 78 citations in OpenAlex.
- Population attributable risk of aflatoxin-related liver cancer: systematic review and meta-analysis.European journal of cancer (Oxford, England : 1990) · 2012Pooled it
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- Risk assessment of aflatoxins in food.EFSA journal. European Food Safety Authority · 2020Article
- Mechanisms underlying aflatoxin-associated mutagenesis - Implications in carcinogenesis.DNA repair · 2019Review
- It takes a team: a gain-of-function story of p53-R249S.Journal of molecular cell biology · 2019Review
- Hepatocellular carcinoma in non-cirrhotic liver: A comprehensive review.World journal of hepatology · 2019Review
- Pathways of Metabolite-Related Damage to a Synthetic p53 Gene Exon 7 Oligonucleotide Using Magnetic Enzyme Bioreactor Beads and LC-MS/MS Sequencing.Biochemistry · 2018Article
- The Lambda Select cII Mutation Detection System.Journal of visualized experiments : JoVE · 2018Article
- Mutation Analysis in Cultured Cells of Transgenic Rodents.International journal of molecular sciences · 2018Article
- Dual Role of Dietary Curcumin Through Attenuating AFBFrontiers in pharmacology · 2018Article
- Limited mutagenicity of electronic cigarettes in mouse or human cells in vitro.Lung cancer (Amsterdam, Netherlands) · 2017Article
- Expression of P62 in hepatocellular carcinoma involving hepatitis B virus infection and aflatoxin B1 exposure.Cancer medicine · 2017Article
- Mutational Signatures in Breast Cancer: The Problem at the DNA Level.Clinical cancer research : an official journal of the American Association for Cancer Research · 2017Article
- Forthcoming Challenges in Mycotoxins Toxicology Research for Safer Food-A Need for Multi-Omics Approach.Toxins · 2017Review
- Distinct response of the hepatic transcriptome to Aflatoxin B1 induced hepatocellular carcinogenesis and resistance in rats.Scientific reports · 2016Article
- Article
- Risk Factors for the Development of Hepatocellular Carcinoma in Thailand.Journal of clinical and translational hepatology · 2015Review
- C. elegans whole-genome sequencing reveals mutational signatures related to carcinogens and DNA repair deficiency.Genome research · 2014Article
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Authors and funding
4 authors at 2 institutions in 2 countries.
Funding
Abstract
BACKGROUND &
aimsDietary exposure to aflatoxin B(1) (AFB(1)), in addition to other known factors, increases risk for human hepatocellular carcinoma (HCC). HCCs from AFB(1)-exposed individuals frequently have distinct TP53 mutations, such as G to T transversions in the second guanine of codon 249 (AGG to AGT), and a characteristic mutational spectrum predominated by G:C to T:A mutations.
methodsTo recapitulate the distinctive features of TP53 mutations in AFB(1)-associated HCC, we investigated AFB(1)-induced DNA adduction in relation to mutagenesis in transgenic mouse fibroblasts exposed to AFB(1) in vitro.
resultsImmunodotblot determination of DNA adducts in the overall genome of AFB(1)-exposed cells revealed the dose-dependant formation of persistent imidazole ring-opened AFB(1)-DNA adducts. DNA footprinting analysis of the cII transgene in AFB(1)-exposed cells verified the dose-dependent and sequence-specific formation of DNA adducts. The preferential formation of AFB(1)-induced DNA adducts along the cII transgene was almost exclusively localized to guanine-containing sequences encompassing CpG dinucleotides. Mutation analysis of the cII transgene in AFB(1)-exposed cells revealed a dose-dependent induction of cII mutant frequency (P < .001) and a unique induced mutational spectrum characterized by predominant induction of G:C to T:A transversions that occurred within CpG sequence contexts. Notably, codons 42 and 45 of the cII transgene, which have identical sequence contexts to that of codon 249 of human TP53, constituted 2 frequently mutated sites in AFB(1)-exposed cells that contained the G to T transversion signature mutation at their third base positions.
conclusionsIn this model system, AFB(1)-induced DNA adduction and mutagenesis recapitulate the unique mutational features of TP53 in AFB(1)-associated human HCC.
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