Evidence map›Paper›PMID 22989067›Full record

ReviewCritical reviews in toxicology2012

Genomic impact of cigarette smoke, with application to three smoking-related diseases.

M Talikka, N Sierro, N V Ivanov, N Chaudhary, M J Peck, J Hoeng, C R E Coggins, M C Peitsch

Abstract readReview
In one paragraph

Review in Critical reviews in toxicology, 2012. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 35 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
35citing papers in PubMed, 1 pooled it
–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

35 citing papers in PubMed, 1 synthesis or guideline pooled it.

  1. Pooled it
  2. Trial
  3. Evaluation of Biomarkers of Exposure in Smokers Switching to a Carbon-Heated Tobacco Product: A Controlled, Randomized, Open-Label 5-Day Exposure Study.Nicotine & tobacco research : official journal of the Society for Research on Nicotine and Tobacco · 2016
    Trial
  4. Article
  5. Review
  6. Review
  7. Article
  8. Review
  9. Article
  10. Article
  11. Article
  12. Relationships of Long-Term Smoking and Moist Snuff Consumption With a DNA Methylation Age Relevant Smoking Index: An Analysis in Buccal Cells.Nicotine & tobacco research : official journal of the Society for Research on Nicotine and Tobacco · 2019
    Article
  13. Article
  14. Article
  15. Article
  16. Article
  17. Epigenetic Inheritance: Concepts, Mechanisms and Perspectives.Frontiers in molecular neuroscience · 2018
    Article
  18. Review
  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.

M TalikkaPhilip Morris International R&D, Philip Morris Products S.A., Neuchâtel, Switzerland.
N Sierro
N V Ivanov
N Chaudhary
M J Peck
J Hoeng
C R E Coggins
M C Peitsch

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

There is considerable evidence that inhaled toxicants such as cigarette smoke can cause both irreversible changes to the genetic material (DNA mutations) and putatively reversible changes to the epigenetic landscape (changes in the DNA methylation and chromatin modification state). The diseases that are believed to involve genetic and epigenetic perturbations include lung cancer, chronic obstructive pulmonary disease (COPD), and cardiovascular disease (CVD), all of which are strongly linked epidemiologically to cigarette smoking. In this review, we highlight the significance of genomics and epigenomics in these major smoking-related diseases. We also summarize the in vitro and in vivo findings on the specific perturbations that smoke and its constituent compounds can inflict upon the genome, particularly on the pulmonary system. Finally, we review state-of-the-art genomics and new techniques such as high-throughput sequencing and genome-wide chromatin assays, rapidly evolving techniques which have allowed epigenetic changes to be characterized at the genome level. These techniques have the potential to significantly improve our understanding of the specific mechanisms by which exposure to environmental chemicals causes disease. Such mechanistic knowledge provides a variety of opportunities for enhanced product safety assessment and the discovery of novel therapeutic interventions.

Indexed as

AnimalsCardiovascular DiseasesChromatinDisease Models, AnimalDNA MethylationEpigenesis, GeneticEpigenomicsHumansInhalation ExposureLung NeoplasmsNicotianaPulmonary Disease, Chronic ObstructiveSmokeSmokingChromatinSmoke

Identifiers

PMID22989067
PMCPMC3491444

What OpenQuestion holds

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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.