Evidence map›Paper›PMID 27694624›Full record

ArticleNucleic acids research2016

Adaptive upregulation of DNA repair genes following benzo(a)pyrene diol epoxide protects against cell death at the expense of mutations.

Markus Christmann, Catherine Boisseau, Rebekka Kitzinger, Christian Berac, Sebastian Allmann, Tina Sommer, Dorthe Aasland, Bernd Kaina, Maja T Tomicic

Open access · goldAbstract read
In one paragraph

Article in Nucleic acids research, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 30 papers.

0numbers the graph read from it
0cells of the map it votes in
30citing papers in PubMed
2.7field-weighted citation impact, top 10% 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

30 citing papers in PubMed, 69 citations in OpenAlex.

  1. Review
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  10. Mapping the influence of hydrocarbons mixture on molecular mechanisms, involved in breast and lung neoplasms: in silico toxicogenomic data-mining.Genes and environment : the official journal of the Japanese Environmental Mutagen Society · 2024
    Article
  11. Article
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  13. Review
  14. Metabolic Activation of Benzo[International journal of molecular sciences · 2022
    Article
  15. Article
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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

9 authors at 2 institutions in 1 country.

Markus ChristmannDepartment of Toxicology, University Medical Center Mainz, Obere Zahlbacher Strasse 67, D-55131 Mainz, Germany mchristm@uni-mainz.de.
Catherine BoisseauDepartment of Toxicology, University Medical Center Mainz, Obere Zahlbacher Strasse 67, D-55131 Mainz, Germany.
Rebekka KitzingerDepartment of Toxicology, University Medical Center Mainz, Obere Zahlbacher Strasse 67, D-55131 Mainz, Germany.
Christian BeracDepartment of Toxicology, University Medical Center Mainz, Obere Zahlbacher Strasse 67, D-55131 Mainz, Germany.
Sebastian AllmannDepartment of Toxicology, University Medical Center Mainz, Obere Zahlbacher Strasse 67, D-55131 Mainz, Germany.
Tina SommerDepartment of Toxicology, University Medical Center Mainz, Obere Zahlbacher Strasse 67, D-55131 Mainz, Germany.
Dorthe AaslandDepartment of Toxicology, University Medical Center Mainz, Obere Zahlbacher Strasse 67, D-55131 Mainz, Germany.
Bernd KainaDepartment of Toxicology, University Medical Center Mainz, Obere Zahlbacher Strasse 67, D-55131 Mainz, Germany.
Maja T TomicicDepartment of Toxicology, University Medical Center Mainz, Obere Zahlbacher Strasse 67, D-55131 Mainz, Germany tomicic@uni-mainz.de.
University Medical Center of the Johannes Gutenberg University Mainz · DEJohannes Gutenberg University Mainz · DE

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

A coordinated and faithful DNA damage response is of central importance for maintaining genomic integrity and survival. Here, we show that exposure of human cells to benzo(a)pyrene 9,10-diol-7,8-epoxide (BPDE), the active metabolite of benzo(a)pyrene (B(a)P), which represents a most important carcinogen formed during food preparation at high temperature, smoking and by incomplete combustion processes, causes a prompt and sustained upregulation of the DNA repair genes DDB2, XPC, XPF, XPG and POLH. Induction of these repair factors on RNA and protein level enhanced the removal of BPDE adducts from DNA and protected cells against subsequent BPDE exposure. However, through the induction of POLH the mutation frequency in the surviving cells was enhanced. Activation of these adaptive DNA repair genes was also observed upon B(a)P treatment of MCF7 cells and in buccal cells of human volunteers after cigarette smoking. Our data provide a rational basis for an adaptive response to polycyclic aromatic hydrocarbons, which occurs however at the expense of mutations that may drive cancer formation.

Indexed as

ApoptosisDNA RepairTranscriptional Activation7,8-Dihydro-7,8-dihydroxybenzo(a)pyrene 9,10-oxideCell SurvivalDNA AdductsDNA DamageDNA-Directed DNA PolymeraseFeedback, PhysiologicalHumansMCF-7 CellsMutagensTranscription Factor AP-1Tumor Suppressor Protein p53Up-RegulationY-Family DNA Polymerases7,8-Dihydro-7,8-dihydroxybenzo(a)pyrene 9,10-oxideDNA AdductsDNA-Directed DNA PolymeraseMutagensRad30 proteinTP53 protein, humanTranscription Factor AP-1Tumor Suppressor Protein p53Y-Family DNA Polymerases

Identifiers

PMID27694624
PMCPMC5159553
OpenAlexW2524109626

What OpenQuestion holds

Textmetadata
LicenceCC BY-NC
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.