Evidence map›Paper›PMID 24278510›Full record

ReviewToxicological research2010

Modulation of MnSOD in Cancer:Epidemiological and Experimental Evidence.

Aekyong Kim

Open access · bronzeAbstract readReview
In one paragraph

Review in Toxicological research, 2010. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 13 papers.

0numbers the graph read from it
0cells of the map it votes in
13citing papers in PubMed
–field-weighted citation impact, top 90% 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

13 citing papers in PubMed, 28 citations in OpenAlex.

  1. Review
  2. Review
  3. Assessment of the Impact of Trace Essential Metals on Cancer Development.International journal of molecular sciences · 2024
    Review
  4. Insights into Manganese Superoxide Dismutase and Human Diseases.International journal of molecular sciences · 2022
    Review
  5. Article
  6. Review
  7. Article
  8. Extracellular superoxide dismutase and its role in cancer.Free radical biology & medicine · 2017
    Review
  9. Article
  10. Article
  11. Preliminary neutron diffraction analysis of challenging human manganese superoxide dismutase crystals.Acta crystallographica. Section F, Structural biology communications · 2017
    Article
  12. Article
  13. 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

1 author at 1 institution in 1 country.

Aekyong KimSchool of Pharmacy, Catholic University of Daegu, Gyeongbuk 712-702, Korea.
Catholic University of Daegu · KR

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Since it was first observed in late 1970s that human cancers often had decreased manganese superoxide dismutase (MnSOD) protein expression and activity, extensive studies have been conducted to verify the association between MnSOD and cancer. Significance of MnSOD as a primary mitochondrial antioxidant enzyme is unquestionable; results from in vitro, in vivo and epidemiological studies are in harmony. On the contrary, studies regarding roles of MnSOD in cancer often report conflicting results. Although putative mechanisms have been proposed to explain how MnSOD regulates cellular proliferation, these mechanisms are not capitulated in epidemiological studies. This review discusses most recent epidemiological and experimental studies that examined the association between MnSOD and cancer, and describes emerging hypotheses of MnSOD as a mitochondrial redox regulatory enzyme and of how altered mitochondrial redox may affect physiology of normal as well as cancer cells.

Indexed as

CancerCarcinogenesisEpidemiologyHydrogen peroxideMitochondriaMnSODOxidative stressRedoxSuperoxide anion

Identifiers

PMID24278510
PMCPMC3834467
OpenAlexW2030033321

What OpenQuestion holds

Textmetadata
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.