Evidence map›Paper›PMID 24919441›Full record

ArticleJournal of cancer research and clinical oncology2014

Polymorphisms of NRF2 and NRF2 target genes in urinary bladder cancer patients.

Edyta Reszka, Zbigniew Jablonowski, Edyta Wieczorek, Ewa Jablonska, Magdalena Beata Krol, Jolanta Gromadzinska, Adam Grzegorczyk, Marek Sosnowski, Wojciech Wasowicz

Open access · hybridAbstract read
In one paragraph

Article in Journal of cancer research and clinical oncology, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 19 papers, 5 of them syntheses that pooled it.

0numbers the graph read from it
0cells of the map it votes in
19citing papers in PubMed, 5 pooled it
1.7field-weighted citation impact, top 16% 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

19 citing papers in PubMed, 5 syntheses or guidelines pooled it, 32 citations in OpenAlex.

  1. Pooled it
  2. Association betweenDisease markers · 2018
    Pooled it
  3. Pooled it
  4. Pooled it
  5. Pooled it
  6. Medicina (Kaunas, Lithuania) · 2023
    Article
  7. Article
  8. Article
  9. The Association of Polymorphisms inOxidative medicine and cellular longevity · 2021
    Article
  10. Article
  11. Review
  12. Article
  13. Article
  14. Changes ofOxidative medicine and cellular longevity · 2018
    Article
  15. Article
  16. Journal of Cancer · 2016
    Article
  17. Review
  18. Article
  19. 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

9 authors at 2 institutions in 1 country.

Edyta ReszkaDepartment of Toxicology and Carcinogenesis, Nofer Institute of Occupational Medicine, Teresy St. 8, 91-348, Lodz, Poland, edyta@imp.lodz.pl.
Zbigniew Jablonowski
Edyta Wieczorek
Ewa Jablonska
Magdalena Beata Krol
Jolanta Gromadzinska
Adam Grzegorczyk
Marek Sosnowski
Wojciech Wasowicz
Nofer Institute of Occupational Medicine · PLMedical University of Lodz · PL

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

purposeNRF2 transcription factor is involved in modulation of various antioxidant and metabolic genes and, therefore, may modulate anti-carcinogenic potential. Association between polymorphisms of NRF2 and five NRF2-regulated genes and urinary bladder cancer (BC) risk was analyzed.

methodsThe study group included 244 BC patients, while the control group comprised 365 individuals with no evidence of malignancy. Genotyping of GSTM1 (deletion), GSTT1 (deletion), GSTA1 -69C/T (rs3957357), GSTP1 Ile105Val (rs1695), SOD2 Ala16Val (rs4880) and NRF2 -617C/A (rs6721961) in blood genomic DNA was performed by means of real-time PCR assays. The associations between gene polymorphism and BC risk were computed by logistic regression.

resultsThe frequency of GSTA1, GSTP1, SOD2 and NRF2 genotypes did not differ in both groups. A significantly higher BC risk was associated with GSTM1 null genotype after adjusting to age, sex and smoking habit (OR 1.85, 95 % CI 1.30-2.62; P = 0.001). GSTT1 null (OR 0.50, 95 % CI 0.31-0.81; P = 0.005) and GSTP1 Val105Val (OR 0.52, 95 % CI 0.27-0.98; P = 0.04) genotypes were associated with reduced BC risk separately or in combination (OR 0.24, 95 % CI 0.11-0.51; P < 0.0001) (P heterogeneity = 0.01). Combined GSTT1 null and SOD2 with at least one 16Val allele among never smokers encompass reduced BC risk (OR 0.14, 95 % CI 0.03-0.63; P = 0.01) (P heterogeneity = 0.04).

conclusionsThis study supports hypothesis that GSTM1 null genotype may be a moderate BC risk factor. The gene-gene and gene-environment interactions associated with combined GSTP1/GSTT1 and combined GSTT1/SOD2 genetic polymorphisms along with cigarette smoking habit may play a significant role in BC risk modulation.

Indexed as

Polymorphism, Single NucleotideAdultAgedAged, 80 and overAge FactorsAlanineEpistasis, GeneticFemaleGene DeletionGene-Environment InteractionGenotypeGlutathione S-Transferase piGlutathione TransferaseHumansIsoleucineMaleAlanineGlutathione S-Transferase piglutathione S-transferase T1Glutathione TransferaseGSTP1 protein, humanIsoleucineNFE2L2 protein, humanNF-E2-Related Factor 2Superoxide DismutaseSuperoxide Dismutase 2Valine

Identifiers

PMID24919441
PMCPMC4160566
OpenAlexW2165566015

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.