Evidence map›Paper›PMID 19362589›Full record

ReviewFree radical biology & medicine2009

Metabolic defects provide a spark for the epigenetic switch in cancer.

Michael J Hitchler, Frederick E Domann

Open access · greenAbstract readReview
In one paragraph

Review in Free radical biology & medicine, 2009. 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
4.2field-weighted citation impact, top 5% 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, 89 citations in OpenAlex.

  1. Review
  2. Review
  3. Article
  4. Article
  5. Article
  6. Article
  7. Review
  8. Review
  9. Review
  10. A c-Myc/miR-17-5p feedback loop regulates metastasis and invasion of hepatocellular carcinoma.Tumour biology : the journal of the International Society for Oncodevelopmental Biology and Medicine · 2016
    Article
  11. Article
  12. Review
  13. lnflammation-induced epigenetic switches in cancer.Cellular and molecular life sciences : CMLS · 2016
    Review
  14. Review
  15. Signaling and stress: The redox landscape in NOS2 biology.Free radical biology & medicine · 2015
    Review
  16. Article
  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.

Michael J HitchlerDepartment of Radiation Oncology, Free Radical and Radiation Biology Program, University of Iowa, Iowa City, IA 52242, USA.
Frederick E Domann
University of Iowa · US

Funding

Epigenetic factors governing SOD2 gene expressionR01CA073612 · NCI · UNIVERSITY OF IOWA · PI DOMANN, FREDERICK E · 2003 to 2007
$1.3M
Molecular Species Responsible for Tumor Supressive Effect of MnSODR01CA115438 · NCI · UNIVERSITY OF IOWA · PI DOMANN, FREDERICK E · 2007 to 2011
$1.2M
DNA METHYLATION AND SOD2/MNSOD GENE EXPRESSIONR29CA073612 · NCI · UNIVERSITY OF IOWA · PI DOMANN, FREDERICK E · 1998 to 2002
$321k
Chromatin Remodeling and SOD2 Expression in CancerR56CA073612 · NCI · UNIVERSITY OF IOWA · PI DOMANN, FREDERICK E · 2009 to 2009
$266k
NCI NIH HHS CA11543NCI NIH HHS CA73612NCI NIH HHS R01 CA073612NCI NIH HHS R01 CA115438NCI NIH HHS R29 CA073612NCI NIH HHS R56 CA073612
6 · The paper itself

Abstract

Cancer is a pathology that is associated with aberrant gene expression and an altered metabolism. Whereas changes in gene expression have historically been attributed to mutations, it has become apparent that epigenetic processes also play a critical role in controlling gene expression during carcinogenesis. Global changes in epigenetic processes, including DNA methylation and histone modifications, have been observed in cancer. These epigenetic alterations can aberrantly silence or activate gene expression during the formation of cancer; however, the process leading to this epigenetic switch in cancer remains unknown. Carcinogenesis is also associated with metabolic defects that increase mitochondrially derived reactive oxygen species, create an atypical redox state, and change the fundamental means by which cells produce energy. Here, we summarize the influence of these metabolic defects on epigenetic processes. Metabolic defects affect epigenetic enzymes by limiting the availability of cofactors like S-adenosylmethionine. Increased production of reactive oxygen species alters DNA methylation and histone modifications in tumor cells by oxidizing DNMTs and HMTs or through direct oxidation of nucleotide bases. Last, the Warburg effect and increased glutamine consumption in cancer influence histone acetylation and methylation by affecting the activity of sirtuins and histone demethylases.

Indexed as

Epigenesis, GeneticAcetylationAnimalsDNA MethylationFree RadicalsGlutathioneHistonesHumansNeoplasmsNucleosomesOxidation-ReductionS-AdenosylmethionineFree RadicalsGlutathioneHistonesNucleosomesS-Adenosylmethionine

Identifiers

PMID19362589
PMCPMC2728018
OpenAlexW2048189477

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.