Evidence map›Paper›PMID 26446998›Full record

ArticleBMC cancer2015

Lipid peroxidation and glutathione peroxidase activity relationship in breast cancer depends on functional polymorphism of GPX1.

Ewa Jablonska, Jolanta Gromadzinska, Beata Peplonska, Wojciech Fendler, Edyta Reszka, Magdalena B Krol, Edyta Wieczorek, Agnieszka Bukowska, Peter Gresner, Michal Galicki and 3 more

Open access · goldAbstract read
In one paragraph

Article in BMC cancer, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 53 papers, 4 of them syntheses that pooled it.

0numbers the graph read from it
0cells of the map it votes in
53citing papers in PubMed, 4 pooled it
2.6field-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

53 citing papers in PubMed, 4 syntheses or guidelines pooled it, 95 citations in OpenAlex.

  1. The Role of rs713041 Glutathione Peroxidase 4 (International journal of molecular sciences · 2022
    Pooled it
  2. Pooled it
  3. Selenium for preventing cancer.The Cochrane database of systematic reviews · 2018
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  4. Association betweenDisease markers · 2018
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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

13 authors at 3 institutions in 1 country.

Ewa JablonskaDepartment of Toxicology and Carcinogenesis, Nofer Institute of Occupational Medicine, 8 Sw. Teresy Str, Lodz, Poland. ewa@imp.lodz.pl.
Jolanta GromadzinskaDepartment of Toxicology and Carcinogenesis, Nofer Institute of Occupational Medicine, 8 Sw. Teresy Str, Lodz, Poland. jola@imp.lodz.pl.
Beata PeplonskaDepartment of Environmental Epidemiology, Nofer Institute of Occupational Medicine, 8 Sw. Teresy Str, Lodz, Poland. beatap@imp.lodz.pl.
Wojciech FendlerDepartment of Pediatrics, Oncology, Hematology and Diabetology, Medical University of Lodz, 36/50 Sporna Str, Lodz, Poland. fendler.wojciech@gmail.com.
Edyta ReszkaDepartment of Toxicology and Carcinogenesis, Nofer Institute of Occupational Medicine, 8 Sw. Teresy Str, Lodz, Poland. edyta@imp.lodz.pl.
Magdalena B KrolDepartment of Toxicology and Carcinogenesis, Nofer Institute of Occupational Medicine, 8 Sw. Teresy Str, Lodz, Poland. lena@imp.lodz.pl.
Edyta WieczorekDepartment of Toxicology and Carcinogenesis, Nofer Institute of Occupational Medicine, 8 Sw. Teresy Str, Lodz, Poland. edytaw@imp.lodz.pl.
Agnieszka BukowskaDepartment of Environmental Epidemiology, Nofer Institute of Occupational Medicine, 8 Sw. Teresy Str, Lodz, Poland. bukowska@imp.lodz.pl.
Peter GresnerDepartment of Toxicology and Carcinogenesis, Nofer Institute of Occupational Medicine, 8 Sw. Teresy Str, Lodz, Poland. pgresner@imp.lodz.pl.
Michal GalickiDepartment of Surgical Oncology, Regional Cancer Center, Copernicus Memorial Hospital in Lodz, 62 Pabianicka Str, Lodz, Poland. faber@toya.net.pl.
Oskar Zambrano QuispeDepartment of Surgical Oncology, Regional Cancer Center, Copernicus Memorial Hospital in Lodz, 62 Pabianicka Str, Lodz, Poland. ozambran@op.pl.
Zbigniew MorawiecDepartment of Surgical Oncology, Regional Cancer Center, Copernicus Memorial Hospital in Lodz, 62 Pabianicka Str, Lodz, Poland. z.morawiec@op.pl.
Wojciech WasowiczDepartment of Toxicology and Carcinogenesis, Nofer Institute of Occupational Medicine, 8 Sw. Teresy Str, Lodz, Poland. wojciech@imp.lodz.pl.
Nofer Institute of Occupational Medicine · PLCopernicus Memorial Hospital · PLMedical University of Lodz · PL

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

backgroundSince targeting oxidative stress markers has been recently recognized as a novel therapeutic target in cancer, it is interesting to investigate whether genetic susceptibility may modify oxidative stress response in cancer. The aim of this study was to elucidate whether genetic polymorphism in the antioxidant enzymes is associated with lipid peroxidation in breast cancer.

methodsWe conducted a study among Polish women, including 136 breast cancer cases and 183 healthy controls. The analysis included genetic polymorphisms in five redox related genes: GPX1 (rs1050450), GPX4 (rs713041), SOD2 (rs4880), SEPP1 (rs3877899) and SEP15 (rs5859), lipid peroxidation, the activities of antioxidant enzymes determined in blood compartments as well as plasma concentration of selenium - an antioxidant trace element involved in cancer. Genotyping was performed using the Real Time PCR. Lipid peroxidation was expressed as plasma concentration of thiobarbituric acid reactive substances (TBARS) and measured with the spectrofluorometric method. Glutathione peroxidase activity was spectrophotometrically determined in erythrocytes (GPx1) and plasma (GPx3) by the use of Paglia and Valentine method. Spectrophotometric methods were employed to measure activity of cytosolic superoxide dismutase (SOD1) in erythrocytes (Beauchamp and Fridovich method) and ceruloplasmin (Cp) in plasma (Sunderman and Nomoto method). Plasma selenium concentration was determined using graphite furnace atomic absorption spectrophotometry.

resultsBreast cancer risk was significantly associated with GPX1 rs1050450 (Pro198Leu) polymorphism, showing a protective effect of variant (Leu) allele. As compared to the control subjects, lipid peroxidation and GPx1 activity were significantly higher in the breast cancer cases, whereas ceruloplasmin activity was decreased. After genotype stratification, both GPx1 activity and TBARS concentration were the highest in GPX1 Pro/Pro homozygotes affected by breast cancer. At the same time, there was a significant correlation between the level of lipid peroxidation and GPx1 activity among the cancer subjects possessing GPX1 Pro/Pro genotype (r = 0.3043; p = 0.0089), whereas such a correlation was completely absent in the cases carrying at least one GPX1 Leu allele as well as in the controls (regardless of GPX1 genotype).

conclusionsGPX1 polymorphism may be an important factor modifying oxidative stress response in breast cancer subjects. Further studies are needed to elucidate its potential clinical significance.

Indexed as

Lipid PeroxidationPolymorphism, Single NucleotideAdultBiomarkers, TumorBreast NeoplasmsCase-Control StudiesEnzyme ActivationFemaleGenes, BRCA1Glutathione PeroxidaseGlutathione Peroxidase GPX1HumansMiddle AgedMutationNeoplasm GradingNeoplasm StagingBiomarkers, TumorGlutathione PeroxidaseGlutathione Peroxidase GPX1GPX1 protein, humanSelenoproteinsSuperoxide DismutaseThiobarbituric Acid Reactive Substances

Identifiers

PMID26446998
PMCPMC4597452
OpenAlexW1949515053

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Registered trials

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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.