ArticleOncotarget2017
AFB1 hepatocarcinogenesis is via lipid peroxidation that inhibits DNA repair, sensitizes mutation susceptibility and induces aldehyde-DNA adducts at p53 mutational hotspot codon 249.
Article in Oncotarget, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 31 papers.
What it found
Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.
The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
The trial behind it
Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.
Who cites it
31 citing papers in PubMed, 65 citations in OpenAlex.
- Review
- Multiple Aflatoxins Drive Cumulative Dietary Exposure and Hepatocellular Carcinoma Risk: An Age-Stratified Study in Guangzhou, China.Foods (Basel, Switzerland) · 2026Article
- Targeting Mycotoxin Toxicity: From Molecular Mechanisms to Nutritional Interventions.Veterinary sciences · 2026Review
- Aflatoxin B1 Impairs TACE Efficacy Through Downregulated Carbonic Anhydrase 2: A Bioinformatics Analysis.International journal of genomics · 2026Article
- Cancer and Environmental Xenobiotics: Mechanisms, Controversies, and Innovations.Journal of xenobiotics · 2025Review
- Mechanistic interplay between aflatoxin B1 and tissue inhibitor of metalloproteinase-3 in hepatocellular carcinoma.World journal of hepatology · 2025Article
- The Role of Epigenetic Mechanisms in the Treatment of GI Cancers.Current cancer drug targets · 2025Review
- Nucleotide excision repair of aflatoxin-induced DNA damage within the 3D human genome organization.Nucleic acids research · 2024Article
- Polymorphisms of DNA Repair Genes in Thyroid Cancer.International journal of molecular sciences · 2024Review
- Fungal infections and the fungal microbiome in hepatobiliary disorders.Journal of hepatology · 2023Review
- Mycotoxin source and its exposure causing mycotoxicoses.Bioinformation · 2023Review
- Review
- Aflatoxin B1 targeted gene expression profiles in human placental primary trophoblast cells.Current research in toxicology · 2022Article
- A Narrative Review of the Role of Diet and Lifestyle Factors in the Development and Prevention of Endometrial Cancer.Cancers · 2021Review
- Genome Profiling for Aflatoxin BG3 (Bethesda, Md.) · 2020Article
- Ligation-Mediated Polymerase Chain Reaction Detection of 8-Oxo-7,8-Dihydro-2'-Deoxyguanosine and 5-Hydroxycytosine at the Codon 176 of the p53 Gene of Hepatitis C-Associated Hepatocellular Carcinoma Patients.International journal of molecular sciences · 2020Article
- Insights into Aflatoxin B1 Toxicity in Cattle: An In Vitro Whole-Transcriptomic Approach.Toxins · 2020Article
- Characteristics, Occurrence, Detection and Detoxification of Aflatoxins in Foods and Feeds.Foods (Basel, Switzerland) · 2020Review
- Risk assessment of aflatoxins in food.EFSA journal. European Food Safety Authority · 2020Article
- Sensitive CometChip assay for screening potentially carcinogenic DNA adducts by trapping DNA repair intermediates.Nucleic acids research · 2020Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
10 authors at 2 institutions in 1 country.
Funding
Abstract
Aflatoxin B1 (AFB1) contamination in the food chain is a major cause of hepatocellular carcinoma (HCC). More than 60% of AFB1 related HCC carry p53 codon 249 mutations but the causal mechanism remains unclear. We found that 1) AFB1 induces two types of DNA adducts in human hepatocytes, AFB1-8,9-epoxide-deoxyguanosine (AFB1-E-dG) induced by AFB1-E and cyclic α-methyl-γ-hydroxy-1,N2-propano-dG (meth-OH-PdG) induced by lipid peroxidation generated acetaldehyde (Acet) and crotonaldehyde (Cro); 2) the level of meth-OH-PdG is >30 fold higher than the level of AFB1-E-dG; 3) AFB1, Acet, and Cro, but not AFB1-E, preferentially induce DNA damage at codon 249; 4) methylation at -CpG- sites enhances meth-OH-PdG formation at codon 249; and 5) repair of meth-OH-PdG at codon 249 is poor. AFB1, Acet, and Cro can also inhibit DNA repair and enhance hepatocyte mutational sensitivity. We propose that AFB1-induced lipid peroxidation generated aldehydes contribute greatly to hepatocarcinogenesis and that sequence specificity of meth-OH-PdG formation and repair shape the codon 249 mutational hotspot.
Indexed as
Identifiers
What OpenQuestion holds
Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.