278P - Association of ERP29 genetic polymorphism with breast cancer risk and prognosis

Date 29 September 2014
Event ESMO 2014
Session Poster Display session
Topics Translational Research
Breast Cancer
Basic Principles in the Management and Treatment (of cancer)
Presenter Gustavo Lourenco
Citation Annals of Oncology (2014) 25 (suppl_4): iv85-iv109. 10.1093/annonc/mdu327
Authors G.J. Lourenco1, C.B.M. Oliveira1, C. Cardoso-Filho2, L.S. Bossi2, C. Oliveira1, L.O.Z. Sarian2, M.S. Costa-Gurgel2, C.S.P. Lima1
  • 1Department Of Internal Medicine, Faculty of Medical Sciences, University of Campinas, 13083888 - Campinas/BR
  • 2Center Of Integral Attention To Women’s Health, University of Campinas, 13083888 - Campinas/BR



ERP29, a tumor suppressor gene, was related with the onset of tumors. The influence of ERP29 c.*293A > G (rs7114) polymorphism in breast cancer (BC) risk and prognosis has never been performed before and was the aim of this study.


We analyzed 737 BC patients and 742 healthy women. The BC patients were treated by conventional procedures. ERP29 c.*293A > G genotypes were obtained from genomic DNA by TaqMan® genotyping assays. The expression of ERP29 mRNA was determined by quantitative PCR using total RNA from blood leukocytes of healthy individuals with distinct genotypes (15 individuals with AA, 17 with AG, and six with GG). Overall survival (OS) was obtained from date of first diagnosis until the date of death or last follow-up. The differences in frequencies of distinct genotypes in patients and controls were analyzed by logistic regression model, serving to obtain age, ethnic origin and adjusted crude odds ratios (ORs), considering a confidence interval (CI) of 95%. OS time was calculated using the Kaplan-Meier estimate probabilities and differences between survival curves were analyzed by the log-rank test. Statistical significance was established at a P< 0.05. All computations analyses were done using the SPSS 21.0 software (SPSS Incorporation).


The frequency of ERP29 AG + GG combined genotypes was higher in BC patients than in controls (36.5% vs. 30.7%, P= 0.03). Carriers of G allele were under a 1.32 (95% CI: 1.02-1.70)-fold increased risk for the tumor. The mRNA expression was lower in carriers of G allele than those with ERP29 AA genotype (0.75 arbitrary units (AUs) vs. 1.30 AUs; P= 0.008). The median of observation of BC patients enrolled in the study was 54 months (1-325). OS of BC patients with the ERP29 AG + GG combined genotypes was higher than that observed in those with the ERP29 AA wild genotype (67.5% vs. 59.0% at 120 months of follow up; P= 0.04).


Our data suggest, for the first time, that ERP29 c.*293A > G polymorphism alters the risk and prognosis of BC possibly due to variation in the protein production.


All authors have declared no conflicts of interest.