Evidence map›Paper›PMID 20842114›Full record

ArticleBritish journal of cancer2010

Arsenic-related DNA copy-number alterations in lung squamous cell carcinomas.

V D Martinez, T P H Buys, M Adonis, H Benítez, I Gallegos, S Lam, W L Lam, L Gil

Abstract read
In one paragraph

Article in British journal of cancer, 2010. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 20 papers.

0numbers the graph read from it
0cells of the map it votes in
20citing papers in PubMed
–field-weighted citation impact
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

20 citing papers in PubMed.

  1. Genomic alterations in oral multiple primary cancers.International journal of oral science · 2024
    Article
  2. Article
  3. Update of the risk assessment of inorganic arsenic in food.EFSA journal. European Food Safety Authority · 2024
    Article
  4. Review
  5. Article
  6. Review
  7. Review
  8. Review
  9. Review
  10. Article
  11. Article
  12. DNA Copy Number Variations as Markers of Mutagenic Impact.International journal of molecular sciences · 2019
    Review
  13. Article
  14. Review
  15. Arsenic is cytotoxic and genotoxic to primary human lung cells.Mutation research. Genetic toxicology and environmental mutagenesis · 2014
    Article
  16. Review
  17. Arsenic, asbestos and radon: emerging players in lung tumorigenesis.Environmental health : a global access science source · 2012
    Review
  18. Article
  19. 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

8 authors.

V D MartinezDepartment of Molecular and Cell Biology, Faculty of Medicine, Biomedical Sciences Institute, University of Chile, Independencia 1027, Santiago 8380453, Chile. vmartinez@med.uchile.cl
T P H Buys
M Adonis
H Benítez
I Gallegos
S Lam
W L Lam
L Gil

Funding

Canadian Institutes of Health Research MOP 77903Canadian Institutes of Health Research MOP 86731
6 · The paper itself

Abstract

backgroundLung squamous cell carcinomas (SqCCs) occur at higher rates following arsenic exposure. Somatic DNA copy-number alterations (CNAs) are understood to be critical drivers in several tumour types. We have assembled a rare panel of lung tumours from a population with chronic arsenic exposure, including SqCC tumours from patients with no smoking history.

methodsFifty-two lung SqCCs were analysed by whole-genome tiling-set array comparative genomic hybridisation. Twenty-two were derived from arsenic-exposed patients from Northern Chile (10 never smokers and 12 smokers). Thirty additional cases were obtained for comparison from North American smokers without arsenic exposure. Twenty-two blood samples from healthy individuals from Northern Chile were examined to identify germline DNA copy-number variations (CNVs) that could be excluded from analysis.

resultsWe identified multiple CNAs associated with arsenic exposure. These alterations were not attributable to either smoking status or CNVs. DNA losses at chromosomes 1q21.1, 7p22.3, 9q12, and 19q13.31 represented the most recurrent events. An arsenic-associated gain at 19q13.33 contains genes previously identified as oncogene candidates.

conclusionsOur results provide a comprehensive approach to molecular characteristics of the arsenic-exposed lung cancer genome and the non-smoking lung SqCC genome. The distinct and recurrent arsenic-related alterations suggest that this group of tumours may be considered as a separate disease subclass.

Indexed as

AlgorithmsAllelic ImbalanceArsenicCarcinoma, Non-Small-Cell LungCase-Control StudiesChromosomes, HumanComparative Genomic HybridizationDNA Copy Number VariationsEnvironmental ExposureGene Expression ProfilingGene FrequencyHumansLung NeoplasmsOligonucleotide Array Sequence AnalysisArsenic

Identifiers

PMID20842114
PMCPMC2967055

What OpenQuestion holds

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LicenceCC BY-NC-SA
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Registered trials

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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.