Evidence map›Paper›PMID 22009064›Full record

ReviewCancer metastasis reviews2011

Cyclooxygenase- and lipoxygenase-mediated DNA damage.

N Speed, I A Blair

Abstract readReview
In one paragraph

Review in Cancer metastasis reviews, 2011. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 27 papers.

0numbers the graph read from it
0cells of the map it votes in
27citing papers in PubMed
3.8field-weighted citation impact, top 8% 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

27 citing papers in PubMed, 57 citations in OpenAlex.

  1. Article
  2. Review
  3. Review
  4. Article
  5. Review
  6. Optogenetics in Alzheimer's Disease: Focus on Astrocytes.Antioxidants (Basel, Switzerland) · 2023
    Review
  7. Article
  8. Review
  9. Article
  10. Review
  11. Article
  12. Review
  13. Review
  14. Obesity, DNA Damage, and Development of Obesity-Related Diseases.International journal of molecular sciences · 2019
    Review
  15. Review
  16. Review
  17. Review
  18. Article
  19. Review
  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

2 authors at 1 institution in 1 country.

N SpeedCenters for Cancer Pharmacology and Excellence in Environmental Toxicology, University of Pennsylvania Perelman School of Medicine, 854 BRB II/III, 421 Curie Boulevard, Philadelphia, PA 19104-6160, USA.
I A Blair
University of Pennsylvania · US

Funding

Translational Research Support CoreP30ES013508 · NIEHS · UNIVERSITY OF PENNSYLVANIA · PI Rebecca A Simmons · 2006 to 2026
$35.3M
Training Program in Cancer PharmacologyR25CA101871 · NCI · UNIVERSITY OF PENNSYLVANIA · PI BLAIR, IAN ALEXANDER · 2003 to 2013
$4.3M
Molecular Dosimetry of Endogenous GenotoxinsR01CA091016 · NCI · UNIVERSITY OF PENNSYLVANIA · PI BLAIR, IAN ALEXANDER · 2001 to 2010
$2.6M
NCI NIH HHS R01CA091016NCI NIH HHS R25 CA101871NCI NIH HHS R25CA101871NIEHS NIH HHS P30 ES013508NIEHS NIH HHS P30ES013508
6 · The paper itself

Abstract

Cancer is a disease of aging, and so with the increasing age of the US population, the incidence of cancer is also increasing. Furthermore the global burden of cancer continues to increase largely because of aging and growth of the world population together with increasing smoking rates in economically developing countries. Tumor formation is critically dependent upon two processes--initiation and progression. The initiation step is mediated by DNA damage, which causes activating mutations in proto-oncogenes and inactivation of tumor suppressor genes in many cancers. This is then thought to facilitate tumor progression and metastasis. Cyclooxygenase-2 (COX-2) is upregulated at an early stage in tumorigenesis and has been implicated as an important mediator of proliferation through the increased formation of bioactive arachidonic acid (AA) metabolites such as prostaglandin E(2). Significantly, we have found that COX-2-mediated AA metabolism also results in the formation of heptanone-etheno (Hε)-DNA adducts. Furthermore, we showed that the Hε-DNA adducts arose from the reaction of DNA with the lipid hydroperoxide-derived bifunctional electrophile, 4-oxo-2(E)-nonenal (ONE). Similarly, 5-lipoxoygenase-mediated AA metabolism also results in the formation of ONE-derived DNA adducts. The resulting Hε-DNA adducts are highly mutagenic in mammalian cell lines suggesting that these pathways could be (in part) responsible for the somatic mutations observed in tumorigenesis. As approximately 80% of cancers arise from somatic mutations, this provides an additional link between the upregulation of COX-2 and tumorigenesis.

Indexed as

MutagenesisAnimalsDNA AdductsDNA RepairHumansLipid PeroxidationLipoxygenasesNeoplasmsOxidation-ReductionOxidative StressProstaglandin-Endoperoxide SynthasesDNA AdductsLipoxygenasesProstaglandin-Endoperoxide Synthases

Identifiers

PMID22009064
PMCPMC3237763
OpenAlexW1986706355

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.