Pounds against breast cancer has been suggested on the basis of in vitro and in

Pounds against breast cancer has been suggested on the basis of in vitro and in vivo observations, indicating for the regulatory activity of Se on estrogen receptors expression [53?5]. In the light of epidemiological data however, including our study, link between Se and breast cancer remains still elusive.Limitations of the studyConclusions Up to date, no studies have been conducted on the association between individual genetic background and markers of prooxidative effects in breast cancer. The results of this study suggest that GPX1 polymorphism may be an important factor that modifies oxidative stress response in breast cancer. The potential link may have great significance in terms of potential implication in tumor progression or treatment thus these findings, if replicated elsewhere, require further investigation. Additional fileAdditional file 1: Table S1. Functional SNPs selected for the study. Table S2. Restriction fragment analysis for BRCA1 mutations. Table S3. Oxidative stress parameters in breast cancer cases according to treatment. (DOCX 31 kb)Results of this study could have been biased by nonrandom selection of the control subjects. It should be noted that the study presented here was not a typical case control study. Thus, we were not able to assign theAbbreviations BMI: Body mass index; BRCA1: Breast cancer 1, early onset (gene); BRCA2: Breast cancer 2, early onset (gene); Cat: Catalase; Cp: Ceruloplasmin; GPX1: Cytosolic glutathione peroxidase (gene); GPx1: Cytosolic glutathione PubMed ID:https://www.ncbi.nlm.nih.gov/pubmed/26795252 peroxidase; GPx2: Gastrointestinal glutathione peroxidase; GPX3: Plasma glutathione peroxidase (gene); GPx3: Plasma glutathione peroxidase; GPX4: Phospholipid hydroperoxide glutathione peroxidase (gene); GPx4: phospholipid hydroperoxide glutathione peroxidase; HR: Hazard ratio; HRM: High resolution melting; Leu: Leucine; MDA: Malondialdehyde; OR: Odds ratio; PCR: Polymerase chain reaction; Pro: Proline; ROS: Reactive oxygen species; Se: Selenium; SEP15: 15-kDa selenoprotein (gene); SEPP1: Selenoprotein P (gene); SelP: Selenoprotein P; SNP: Single nucleotide polymorphism; SOD2: Mitochondrial superoxide dismutase (gene); SOD1: Cytosolic superoxide dismutase; SOD2: Mitochondrial superoxide dismutase; SOD3: Extracellular superoxide disumutase; TBARS: Thiobarbituric acid reactive substances. Competing interests The authors declare that they have no competing interests.Jablonska et al. BMC Cancer (2015) 15:Page 11 ofAuthors’ contributions EJ and ER designed the study. EJ, PG, EW and KMB performed genetic analyses. JG supervised biochemical analyses. OZQ, MG and ZM collected blood, questionnaire data and clinical data from the patients. BP and AB collected blood, questionnaire data and mammographic density data from the healthy controls. WF performed the statistical analysis. WW supervised the whole project and provided materials, reagents and analysis tools. EJ, WF and ER contributed to the writing of the manuscript. JG, BP, WF, ER, AB, PG, WW revised the manuscript. All the authors have read and approved the final manuscript. Acknowledgements This work was supported by NIOM Internal Grants IMP 1.3/2012 and IMP 1.13/2014. Author details 1 Department of Toxicology and Carcinogenesis, Nofer Institute of Peficitinib structure Occupational Medicine, 8 Sw. Teresy Str, Lodz, Poland. 2Department of Environmental Epidemiology, Nofer Institute of Occupational Medicine, 8 Sw. Teresy Str, Lodz, Poland. 3Department of Pediatrics, Oncology, Hematology and Diabetology, Medical Univers.