Evidence map›Paper›PMID 20646321›Full record

ArticleBMC cancer2010

Toll-like receptor (TLR) and nucleosome-binding oligomerization domain (NOD) gene polymorphisms and endometrial cancer risk.

Katie A Ashton, Anthony Proietto, Geoffrey Otton, Ian Symonds, Mark McEvoy, John Attia, Rodney J Scott

Open access · goldAbstract readComparative Study
In one paragraph

Article in BMC cancer, 2010. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 35 papers, 3 of them syntheses that pooled it.

0numbers the graph read from it
0cells of the map it votes in
35citing papers in PubMed, 3 pooled it
2.4field-weighted citation impact, top 10% 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

35 citing papers in PubMed, 3 syntheses or guidelines pooled it, 65 citations in OpenAlex.

  1. Pooled it
  2. Pooled it
  3. Pooled it
  4. Article
  5. Review
  6. Article
  7. Article
  8. Article
  9. The role of toll-like receptors (TLRs) and their therapeutic applications in endometrial cancer.Clinical & translational oncology : official publication of the Federation of Spanish Oncology Societies and of the National Cancer Institute of Mexico · 2023
    Review
  10. Article
  11. Review
  12. Article
  13. Article
  14. Review
  15. Endometrial cancer: a genetic point of view.Translational cancer research · 2020
    Article
  16. Article
  17. Toll-like receptor 9 polymorphisms andWorld journal of gastrointestinal oncology · 2019
    Article
  18. Article
  19. Article
  20. TLR4 Polymorphisms and Expression in Solid Cancers.Molecular diagnosis & therapy · 2018
    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

7 authors at 2 institutions in 1 country.

Katie A AshtonDiscipline of Medical Genetics, School of Biomedical Sciences, Faculty of Health, University of Newcastle, Australia.
Anthony Proietto
Geoffrey Otton
Ian Symonds
Mark McEvoy
John Attia
Rodney J Scott
University of Newcastle Australia · AUJohn Hunter Hospital · AU

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

backgroundEndometrial cancer is the most common gynaecological malignancy in women of developed countries. Many risk factors implicated in endometrial cancer trigger inflammatory events; therefore, alterations in immune response may predispose an individual to disease. Toll-like receptors (TLRs) and nucleosome-binding oligomerization domain (NOD) genes are integral to the recognition of pathogens and are highly polymorphic. For these reasons, the aim of the study was to assess the frequency of polymorphic variants in TLR and NOD genes in an Australian endometrial cancer population.

methodsTen polymorphisms were genotyped in 191 endometrial cancer cases and 291 controls using real-time PCR: NOD1 (rs2075822, rs2907749, rs2907748), NOD2 (rs5743260, rs2066844, rs2066845), TLR2 (rs5743708), TLR4 (rs4986790) and TLR9 (rs5743836, rs187084).

resultsHaplotype analysis revealed that the combination of the variant alleles of the two TLR9 polymorphisms, rs5743836 and rs187084, were protective for endometrial cancer risk: OR 0.11, 95% CI (0.03-0.44), p = 0.002. This result remained highly significant after adjustment for endometrial cancer risk factors and Bonferroni correction for multiple testing. There were no other associations observed for the other polymorphisms in TLR2, TLR4, NOD1 and NOD2.

conclusionsThe variant 'C' allele of rs5743836 causes greater TLR9 transcriptional activity compared to the 'T' allele, therefore, higher TLR9 activity may be related to efficient removal of microbial pathogens within the endometrium. Clearly, the association of these TLR9 polymorphisms and endometrial cancer risk must be further examined in an independent population. The results point towards the importance of examining immune response in endometrial tumourigenesis to understand new pathways that may be implicated in disease.

Indexed as

AgedAustraliaCase-Control StudiesEndometrial NeoplasmsFemaleGenetic Predisposition to DiseaseGenotypeHaplotypesHumansLinkage DisequilibriumMiddle AgedNod1 Signaling Adaptor ProteinNod2 Signaling Adaptor ProteinPolymorphism, GeneticPrognosisRisk FactorsNOD1 protein, humanNod1 Signaling Adaptor ProteinNOD2 protein, humanNod2 Signaling Adaptor ProteinTLR2 protein, humanTLR4 protein, humanTLR9 protein, humanToll-Like Receptor 2Toll-Like Receptor 4Toll-Like Receptor 9

Identifiers

PMID20646321
PMCPMC2918576
OpenAlexW2167404844

What OpenQuestion holds

Textmetadata
LicenceCC BY
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.