Evidence map›Paper›PMID 23483552›Full record

ArticleInternational journal of cancer2013

Mechanisms of oral carcinogenesis induced by dibenzo[a,l]pyrene: an environmental pollutant and a tobacco smoke constituent.

Kun-Ming Chen, Joseph B Guttenplan, Shang-Min Zhang, Cesar Aliaga, Timothy K Cooper, Yuan-Wan Sun, Joseph DelTondo, Wieslawa Kosinska, Arun K Sharma, Kun Jiang and 4 more

Open access · bronzeAbstract read
In one paragraph

Article in International journal of cancer, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 28 papers.

0numbers the graph read from it
0cells of the map it votes in
28citing papers in PubMed
1.6field-weighted citation impact, top 17% of its field
1 · What the graph read from it

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.

2 · The registry

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.

3 · Its place in the literature

Who cites it

28 citing papers in PubMed, 43 citations in OpenAlex.

  1. Trial
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  12. Review
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  14. Effects of the Tobacco CarcinogensChemical research in toxicology · 2019
    Article
  15. Observational
  16. Article
  17. Effects of Black Raspberry on Dibenzo[Cancer prevention research (Philadelphia, Pa.) · 2018
    Article
  18. Article
  19. Effects of chronic alcohol consumption on DNA damage and immune regulation induced by the environmental pollutant dibenzo[a,l]pyrene in oral tissues of mice.Journal of environmental science and health. Part C, Environmental carcinogenesis & ecotoxicology reviews · 2017
    Article
  20. Article
4 · The record

Corrections and comments

PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.

5 · Who and what money

Authors and funding

14 authors at 3 institutions in 1 country.

Kun-Ming ChenDepartment of Biochemistry and Molecular Biology, Penn State College of Medicine, Hershey, PA, USA.
Joseph B Guttenplan
Shang-Min Zhang
Cesar Aliaga
Timothy K Cooper
Yuan-Wan Sun
Joseph DelTondo
Wieslawa Kosinska
Arun K Sharma
Kun Jiang
Richard Bruggeman
Kwangmi Ahn
Shantu Amin
Karam El-Bayoumy
Penn State Milton S. Hershey Medical Center · USNew York University · USPennsylvania State University · US

Funding

TOBACCO CARCINOGENESIS AND CHEMOPREVENTIONP01CA070972 · NCI · PENNSYLVANIA STATE UNIV HERSHEY MED CTR · PI EL-BAYOUMY, KARAM E · 1996 to 2005
$6.9M
Chemoprevention by Black Raspberry of Oral Cancer Induced by Tobacco Carcinogens: Translational StudiesR01CA173465 · NCI · PENNSYLVANIA STATE UNIV HERSHEY MED CTR · PI EL-BAYOUMY, KARAM E · 2013 to 2024
$3.1M
NCI NIH HHS P01 CA070972NCI NIH HHS R01 CA173465NCI NIH HHS R01-CA173465
6 · The paper itself

Abstract

We previously reported that dibenzo[a,l]pyrene (DB[a,l]P), the most potent known environmental carcinogen among polycyclic aromatic hydrocarbons (PAH) congeners, is carcinogenic in the oral tissues of mice. We have now developed a new mouse model which employs the oral application of the fjord region diol epoxide, (±)-anti-11,12-dihydroxy-13,14-epoxy-11,12,13,14-tetrahydrodibenzo[a,l]pyrene (DB[a,l]PDE), a metabolite of the tobacco smoke constituent DB[a,l]P, and we show its specific induction of oral squamous cell carcinoma (OSCC) in both tongue and other oral tissues. Groups of B6C3F1 mice (20/group) received 6 or 3 nmol of (±)-anti-DB[a,l]PDE administered into the oral cavity; 3 times per week for 38 weeks. Additional groups received the vehicle alone or were left untreated. Mice were sacrificed 42 weeks after the first carcinogen administration. The high dose induced 74 and 100% OSCC in the tongue and other oral tissues, respectively; the corresponding values at the lower dose were 45 and 89%. Using immunohistochemistry, we showed that DB[a,l]PDE resulted in overexpression of p53 and COX-2 proteins in malignant tissues when compared to normal oral tissues and tongues. Consistent with the carcinogenicity, we demonstrated powerful mutagenicity in cII gene in B6C3F1 (Big Blue) mouse tongue. The mutational profile in lacI reporter gene is similar to those detected in human head and neck cancer, and p53 mutations were observed in mouse oral tumor tissues. Taken together, we conclude that the formation of diol epoxides plays a major role among the mechanisms by which DB[a,l]P exerts its oral mutagenicity and tumorigenicity.

Indexed as

AnimalsBenzopyrenesCarcinogens, EnvironmentalFemaleGenes, p53ImmunohistochemistryMiceMouth NeoplasmsMutationSmokeBenzopyrenesCarcinogens, Environmentaldibenzo(a,l)pyreneSmokecarcinogenesisCOX-2mutagenesisoral cancerp53

Identifiers

PMID23483552
PMCPMC3707976
OpenAlexW1592333946

What OpenQuestion holds

Textmetadata
LicenceTDM
Read underepoch 390

Registered trials

None linked

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.