Evidence map›Paper›PMID 23389288›Full record

ArticleCarcinogenesis2013

Contrasting roles of dietary selenium and selenoproteins in chemically induced hepatocarcinogenesis.

Marina V Kasaikina, Anton A Turanov, Andrei Avanesov, Ulrich Schweizer, Sandra Seeher, Roderick T Bronson, Sergey N Novoselov, Bradley A Carlson, Dolph L Hatfield, Vadim N Gladyshev

Open access · bronzeAbstract read
In one paragraph

Article in Carcinogenesis, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 17 papers, 2 of them syntheses that pooled it.

0numbers the graph read from it
0cells of the map it votes in
17citing papers in PubMed, 2 pooled it
3.7field-weighted citation impact, top 7% 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

17 citing papers in PubMed, 2 syntheses or guidelines pooled it, 33 citations in OpenAlex.

  1. Selenium for preventing cancer.The Cochrane database of systematic reviews · 2018
    Pooled it
  2. Pooled it
  3. Article
  4. Review
  5. Article
  6. The Effect of tRNAInternational journal of molecular sciences · 2021
    Article
  7. Article
  8. Article
  9. Review
  10. Environmental Selenium and Human Health: an Update.Current environmental health reports · 2018
    Review
  11. Review
  12. Selenoprotein H is an essential regulator of redox homeostasis that cooperates with p53 in development and tumorigenesis.Proceedings of the National Academy of Sciences of the United States of America · 2016
    Article
  13. Article
  14. Review
  15. Article
  16. Article
  17. Review
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

10 authors at 6 institutions in 2 countries.

Marina V KasaikinaDivision of Genetics, Department of Medicine, Brigham and Women's Hospital and Harvard Medical School, Boston, MA 02115, USA.
Anton A Turanov
Andrei Avanesov
Ulrich Schweizer
Sandra Seeher
Roderick T Bronson
Sergey N Novoselov
Bradley A Carlson
Dolph L Hatfield
Vadim N Gladyshev
Harvard University · USBrigham and Women's Hospital · USCharité - Universitätsmedizin Berlin · DECenter for Cancer Research · USNational Cancer Institute · USUniversity of Nebraska–Lincoln · US

Funding

Selenoproteins as Targets for Cancer PreventionR01CA080946 · NCI · UNIVERSITY OF NEBRASKA LINCOLN · PI GLADYSHEV, VADIM N. · 2001 to 2018
$4.5M
Role of Selenium in Development and HealthZIABC005317 · NCI · DIVISION OF BASIC SCIENCES - NCI · PI HATFIELD, DOLPH · 2009 to 2014
$2.7M
Intramural NIH HHSNCI NIH HHS CA080946NCI NIH HHS R01 CA080946
6 · The paper itself

Abstract

Selenium (Se) has long been known for its cancer prevention properties, but the molecular basis remains unclear. The principal questions in assessing the effect of dietary Se in cancer are whether selenoproteins, small molecule selenocompounds, or both, are involved, and under which conditions and genotypes Se may be protective. In this study, we examined diethylnitrosamine-induced hepatocarcinogenesis in mice lacking a subset of selenoproteins due to expression of a mutant selenocysteine tRNA gene (Trsp (A37G) mice). To uncouple the effects of selenocompounds and selenoproteins, these animals were examined at several levels of dietary Se. Our analysis revealed that tumorigenesis in Trsp (A37G) mice maintained on the adequate Se diet was increased. However, in the control, wild-type mice, both Se deficiency and high Se levels protected against tumorigenesis. We further found that the Se-deficient diet induced severe neurological phenotypes in Trsp A37G mice. Surprisingly, a similar phenotype could be induced in these mice at high dietary Se intake. Overall, our results show a complex role of Se in chemically induced hepatocarcinogenesis, which involves interaction among selenoproteins, selenocompounds and toxins, and depends on genotype and background of the animals.

Indexed as

AnimalsCell Transformation, NeoplasticDietFemaleGenotypeLiver NeoplasmsMiceMice, Inbred C57BLPhenotypeRNA, Transfer, Amino Acid-SpecificSeleniumSelenoproteinsRNA, Transfer, Amino Acid-SpecificSeleniumSelenoproteinstRNA, selenocysteine-

Identifiers

PMID23389288
PMCPMC3643414
OpenAlexW2148890167

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.