ArticleCarcinogenesis2022
Detection of DNA adducts derived from the tobacco carcinogens, benzo[a]pyrene and dibenzo[def,p]chrysene in human oral buccal cells.
Article in Carcinogenesis, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 12 papers.
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Who cites it
12 citing papers in PubMed, 18 citations in OpenAlex.
- Inhibition of benzo[a]pyrene-induced DNA adduct in buccal cells of smokers by black raspberry lozenges.Carcinogenesis · 2025Trial
- The Effects of Black Raspberry as a Whole Food-Based Approach on Biomarkers of Oxidative Stress in Buccal Cells and Urine of Smokers.Cancer prevention research (Philadelphia, Pa.) · 2024Trial
- Article
- The multistep progression of areca nut-induced oral cancer: a mechanistic roadmap from pathogenesis to precision therapy.Life medicine · 2026Review
- The mediating effect of triglycerides and related indices on the association between polycyclic aromatic hydrocarbons and oral health in adults aged ≥ 45 years from the national health and nutrition examination survey 2003-2016.Lipids in health and disease · 2026Article
- The effects of Co-exposure of tobacco smoke with Dibenzo[a,l]pyrene diol epoxide on molecular targets and immune cells in the mouse oral cavity.Chemico-biological interactions · 2025Article
- Black Raspberry Modulates Cecal and Oral Microbiomes at the Early Stage of a Dibenzo[def,p]chrysene-Induced Murine Oral Cancer Model.Cancer prevention research (Philadelphia, Pa.) · 2025Article
- Metabolic reprogramming in saliva of mice treated with the environmental and tobacco carcinogen dibenzo[def, p]chrysene.Scientific reports · 2024Article
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- Article
- Saliva as a diagnostic tool to measure polycyclic aromatic hydrocarbon exposure in dental patients exposed to intimate partner violence (IPV).Biomedical journal · 2023Article
- Black Raspberry Extract Enhances Glutathione Conjugation of the Fjord-Region Diol Epoxide Derived from the Tobacco Carcinogen Dibenzo[Chemical research in toxicology · 2022Article
Corrections and comments
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Authors and funding
11 authors at 2 institutions in 1 country.
Funding
Abstract
Polycyclic aromatic hydrocarbons (PAHs) are recognized as potential etiological agents in the development of oral cancer in smokers. In particular, benzo[a]pyrene (B[a]P) and dibenzo[def,p]chrysene (DB[a,l]P) are detected in cigarette smoke and the environment and can induce DNA damage, mutagenesis and carcinogenesis in the oral cavity of rodents. Consequently, DNA adducts are regarded as the most direct markers of genotoxicity and can be used as biomarkers of cancer risk. Thus, this study used LC-MS/MS analysis with isotope labeled internal standard to detect and quantify DNA adducts derived from B[a]P and DB[a,l]P in buccal cells of cigarette smokers and non-smokers. Participants in this study include 21 smokers and 16 non-smokers. Our data are the first to report that levels (mean ± SD) of BPDE-N2-dG were significantly (P < 0.001) higher in smokers (20.18 ± 8.40 adducts/108 dG) than in non-smokers (0.84 ± 1.02 adducts/108 dG). Likewise, levels of DBPDE-N6-dA in smokers (5.49 ± 3.41 adducts/108 dA) were significantly higher (P = 0.019) than non-smokers (2.76 ± 2.29 adducts/108 dA). Collectively, the results of this clinical study support that PAHs in tobacco smoke can contribute to the development of oral cancer in humans.
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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.