Evidence map›Paper›PMID 18957495›Full record

ArticleThe Journal of clinical endocrinology and metabolism2009

Effect of tumor necrosis factor-alpha on estrogen metabolism and endometrial cells: potential physiological and pathological relevance.

Salama A Salama, Marwa W Kamel, Concepcion R Diaz-Arrastia, Xia Xu, Timothy D Veenstra, Sana Salih, Shaleen K Botting, Raj Kumar

Open access · bronzeAbstract read
In one paragraph

Article in The Journal of clinical endocrinology and metabolism, 2009. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 31 papers.

0numbers the graph read from it
0cells of the map it votes in
31citing papers in PubMed
1.6field-weighted citation impact, top 18% 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

31 citing papers in PubMed, 72 citations in OpenAlex.

  1. Trial
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  7. Article
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  9. Article
  10. Review
  11. CYP1B1 as a therapeutic target in cardio-oncology.Clinical science (London, England : 1979) · 2020
    Article
  12. Review
  13. Review
  14. The Impact of Obesity on Breast Cancer.Current oncology reports · 2018
    Review
  15. Article
  16. Article
  17. Obesity and Cancer: Concepts and Challenges.Indian journal of surgical oncology · 2015
    Article
  18. Article
  19. Article
  20. Estrogen signaling in metabolic inflammation.Mediators of inflammation · 2014
    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

8 authors at 5 institutions in 2 countries.

Salama A SalamaDivision of Gynecologic Oncology, Department of Obstetrics and Gynecology, University of Texas Medical Branch at Galveston, 300 University Boulevard, Galveston, Texas 77555, USA. sasalama@utmb.edu
Marwa W Kamel
Concepcion R Diaz-Arrastia
Xia Xu
Timothy D Veenstra
Sana Salih
Shaleen K Botting
Raj Kumar
The University of Texas Medical Branch at Galveston · USCairo University · EGNational Cancer Institute · USScience Applications International Corporation (United States) · USUniversity of Wisconsin–Madison · US

Funding

NCI NIH HHS N01 CO012400NCI NIH HHS N01-CO-12400PHS HHS E506676
6 · The paper itself

Abstract

contextEstrogen and its metabolites play a critical role in the pathophysiology of the endometrium. The bioavailability of estrogen and estrogen metabolites in endometrial tissues depends on the expression of enzymes involved in estrogen biosynthesis and metabolism. Substantial evidence indicates that estrogen-dependent endometrial disorders are also associated with proinflammatory milieu. However, the mechanism whereby inflammation contributes to these conditions is not known.

objectiveThe objective of the study was to investigate the effect of TNF-alpha on estrogen metabolism and the expression of estrogen-metabolizing genes in human endometrial glandular epithelial cells (EM1).

designEM1 were treated with 17beta-estradiol (E2) with or without TNF-alpha. Capillary liquid chromatography-tandem mass spectrometry analysis was used for quantitative measurement of estrogens and estrogen metabolites. Western blot analysis, reporter gene assay, and real-time RT-PCR were used to assess the expression of estrogen-metabolizing genes.

resultsTNF-alpha treatment significantly increased the level of total estrogen and estrogen metabolites and significantly increased the rate of conversion of estrone (E1) into E2. TNF-alpha also enhanced the oxidative metabolism of estrogen into catecholestrogens with concomitant inhibition of their conversion into methoxyestrogens. Gene expression analysis revealed that TNF-alpha induced the expression of genes involved in E2 biosynthesis (steroidogenic factor-1 and aromatase) and activation (17beta- hydroxysteroid dehydrogenase type 1 and cytochrome P-450, 1B1) with simultaneous repression of genes involved in estrogen inactivation (17beta-hydroxysteroid dehydrogenase type 2; catechol O-methyltransferase; and nicotinamide adenine dinucleotide phosphate-quinone oxidoreductase 1).

conclusionTNF-alpha increases the local estrogen biosynthesis in human endometrial glandular cells and directs estrogen metabolism into more hormonally active and carcinogenic metabolites. These effects may impact many physiological and pathological processes that occur within the endometrium.

Indexed as

AromataseAryl Hydrocarbon HydroxylasesCatechol O-MethyltransferaseCell LineCytochrome P-450 CYP1A1Cytochrome P-450 CYP1B1Cytochrome P-450 Enzyme SystemEndometriumEstradiolEstradiol DehydrogenasesEstrogensFemaleGene Expression RegulationHumansNAD(P)H Dehydrogenase (Quinone)Steroidogenic Factor 1AromataseAryl Hydrocarbon HydroxylasesCatechol O-MethyltransferaseCYP1B1 protein, humanCytochrome P-450 CYP1A1Cytochrome P-450 CYP1B1Cytochrome P-450 Enzyme SystemEstradiolEstradiol DehydrogenasesEstrogensHSD17B1 protein, humanHSD17B2 protein, humanNAD(P)H Dehydrogenase (Quinone)NQO1 protein, humanNR5A1 protein, humanSteroidogenic Factor 1Tumor Necrosis Factor-alpha

Identifiers

PMID18957495
PMCPMC2630861
OpenAlexW1967280402

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.