ArticleCancer prevention research (Philadelphia, Pa.)2014
Complete protection against aflatoxin B(1)-induced liver cancer with a triterpenoid: DNA adduct dosimetry, molecular signature, and genotoxicity threshold.
Article in Cancer prevention research (Philadelphia, Pa.), 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 38 papers.
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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.
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Who cites it
38 citing papers in PubMed, 79 citations in OpenAlex.
- Intervention trial with calcium montmorillonite clay in a south Texas population exposed to aflatoxin.Food additives & contaminants. Part A, Chemistry, analysis, control, exposure & risk assessment · 2016Trial
- Clinical Trial of 2-Phenethyl Isothiocyanate as an Inhibitor of Metabolic Activation of a Tobacco-Specific Lung Carcinogen in Cigarette Smokers.Cancer prevention research (Philadelphia, Pa.) · 2016Trial
- Aflatoxin B1 and food safety: Mechanisms of action associated to Hepatocellular Carcinoma.Archives of microbiology · 2026Review
- Profound primary prevention of liver cancer following a natural experiment in China: A 50-year perspective and public health implications.International journal of cancer · 2025Article
- Health risks evaluation of mycotoxins in plant-based supplements marketed in Malaysia.Scientific reports · 2025Article
- Review
- Aflatoxin BOpen medicine (Warsaw, Poland) · 2024Review
- A Point Mutation at C151 ofMolecular pharmacology · 2023Article
- Reactive Oxygen Species and NRF2 Signaling, Friends or Foes in Cancer?Biomolecules · 2023Review
- Carcinogenesis: Failure of resolution of inflammation?Pharmacology & therapeutics · 2021Review
- Oxidative stress and redox signaling in CRPC progression: therapeutic potential of clinically-tested Nrf2-activators.Cancer drug resistance (Alhambra, Calif.) · 2021Review
- Review
- Resolution of eicosanoid/cytokine storm prevents carcinogen and inflammation-initiated hepatocellular cancer progression.Proceedings of the National Academy of Sciences of the United States of America · 2020Article
- Current Landscape of NRF2 Biomarkers in Clinical Trials.Antioxidants (Basel, Switzerland) · 2020Review
- NRF2 as a regulator of cell metabolism and inflammation in cancer.Carcinogenesis · 2020Review
- Nrf2 in liver toxicology.Archives of pharmacal research · 2020Review
- Risk assessment of aflatoxins in food.EFSA journal. European Food Safety Authority · 2020Article
- Aflatoxins: Producing-Molds, Structure, Health Issues and Incidence in Southeast Asian and Sub-Saharan African Countries.International journal of environmental research and public health · 2020Review
- Chronic and Acute Toxicities of Aflatoxins: Mechanisms of Action.International journal of environmental research and public health · 2020Review
- Serum miR-182 is a predictive biomarker for dichotomization of risk of hepatocellular carcinoma in rats.Molecular carcinogenesis · 2019Article
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9 authors at 4 institutions in 1 country.
Funding
Abstract
In experimental animals and humans, aflatoxin B1 (AFB1) is a potent hepatic toxin and carcinogen. The synthetic oleanane triterpenoid 1-[2-cyano-3-,12-dioxooleana-1,9(11)-dien-28-oyl]imidazole (CDDO-Im), a powerful activator of Keap1-Nrf2 signaling, protects against AFB1-induced toxicity and preneoplastic lesion formation (GST-P-positive foci). This study assessed and mechanistically characterized the chemoprotective efficacy of CDDO-Im against AFB1-induced hepatocellular carcinoma (HCC). A lifetime cancer bioassay was undertaken in F344 rats dosed with AFB1 (200 μg/kg rat/day) for four weeks and receiving either vehicle or CDDO-Im (three times weekly), one week before and throughout the exposure period. Weekly, 24-hour urine samples were collected for analysis of AFB1 metabolites. In a subset of rats, livers were analyzed for GST-P foci. The comparative response of a toxicogenomic RNA expression signature for AFB1 was examined. CDDO-Im completely protected (0/20) against AFB1-induced liver cancer compared with a 96% incidence (22/23) observed in the AFB1 group. With CDDO-Im treatment, integrated level of urinary AFB1-N(7)-guanine was significantly reduced (66%) and aflatoxin-N-acetylcysteine, a detoxication product, was consistently elevated (300%) after the first AFB1 dose. In AFB1-treated rats, the hepatic burden of GST-P-positive foci increased substantially (0%-13.8%) over the four weeks, but was largely absent with CDDO-Im intervention. The toxicogenomic RNA expression signature characteristic of AFB1 was absent in the AFB1 + CDDO-Im-treated rats. The remarkable efficacy of CDDO-Im as an anticarcinogen is established even in the face of a significant aflatoxin adduct burden. Consequently, the absence of cancer requires a concept of a threshold for DNA damage for cancer development.
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