Evidence map›Paper›PMID 29036902›Full record

ReviewInternational journal of molecular sciences2017

DNA Adducts Formed by Aristolochic Acid Are Unique Biomarkers of Exposure and Explain the Initiation Phase of Upper Urothelial Cancer.

Marie Stiborová, Volker M Arlt, Heinz H Schmeiser

Open access · goldAbstract readReview
In one paragraph

Review in International journal of molecular sciences, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 41 papers.

0numbers the graph read from it
0cells of the map it votes in
41citing papers in PubMed
6.6field-weighted citation impact, top 3% 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

41 citing papers in PubMed, 96 citations in OpenAlex.

  1. Article
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  5. CYP1B1- and CYP1A1-Template systems and their application to metabolism and inhibition.Genes and environment : the official journal of the Japanese Environmental Mutagen Society · 2025
    Article
  6. Article
  7. Mechanisms of DNA repair and mutagenesis induced by acetaldehyde, acrolein, aristolochic acids, and vinyl chloride.Journal of environmental science and health. Part C, Toxicology and carcinogenesis · 2025
    Review
  8. Article
  9. Overview of aristolochic acid nephropathy: an update.Kidney research and clinical practice · 2023
    Article
  10. Medicina (Kaunas, Lithuania) · 2023
    Article
  11. Article
  12. Article
  13. Article
  14. Chinese herbal medicines · 2022
    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

3 authors at 3 institutions in 3 countries.

Marie StiborováDepartment of Biochemistry, Faculty of Science, Charles University, Albertov 2030, CZ-12843 Prague 2, Czech Republic. stiborov@natur.cuni.cz.ORCID 0000-0001-5430-4403
Volker M ArltAnalytical and Environmental Sciences Division, MRC-PHE Centre for Environment and Health, King's College London, London SE1 9NH, UK. volker.arlt@kcl.ac.uk.ORCID 0000-0003-4314-9318
Heinz H SchmeiserDivision of Radiopharmaceutical Chemistry, German Cancer Research Center (DKFZ), Im Neuenheimer Feld 280, 69120 Heidelberg, Germany. h.schmeiser@dkfz-heidelberg.de.
Charles University · CZGerman Cancer Research Center · DEKing's College London · GB

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Aristolochic acid (AA) is a plant alkaloid that causes aristolochic acid nephropathy (AAN) and Balkan endemic nephropathy (BEN), unique renal diseases frequently associated with upper urothelial cancer (UUC). This review summarizes the significance of AA-derived DNA adducts in the aetiology of UUC leading to specific A:T to T:A transversion mutations (mutational signature) in AAN/BEN-associated tumours, which are otherwise rare in individuals with UCC not exposed to AA. Therefore, such DNA damage produced by AA-DNA adducts is one rare example of the direct association of exposure and cancer development (UUC) in humans, confirming that the covalent binding of carcinogens to DNA is causally related to tumourigenesis. Although aristolochic acid I (AAI), the major component of the natural plant extract AA, might directly cause interstitial nephropathy, enzymatic activation of AAI to reactive intermediates capable of binding to DNA is a necessary step leading to the formation of AA-DNA adducts and subsequently AA-induced malignant transformation. Therefore, AA-DNA adducts can not only be utilized as biomarkers for the assessment of AA exposure and markers of AA-induced UUC, but also be used for the mechanistic evaluation of its enzymatic activation and detoxification. Differences in AA metabolism might be one of the reasons for an individual's susceptibility in the multi-step process of AA carcinogenesis and studying associations between activities and/or polymorphisms of the enzymes metabolising AA is an important determinant to identify individuals having a high risk of developing AA-mediated UUC.

Indexed as

BiomarkersAnimalsAristolochic AcidsBalkan NephropathyCarcinogensCell Transformation, NeoplasticDisease SusceptibilityDNA AdductsHumansUrologic NeoplasmsAristolochic AcidsBiomarkersCarcinogensDNA Adductsaristolochic acidcarcinogenicityDNA adduct formationmutagenesisnephrotoxicity

Identifiers

PMID29036902
PMCPMC5666826
OpenAlexW2764282355

What Socratic holds

Textmetadata
LicenceCC BY
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 Socratic graph.