The single nucleotide polymorphism +936 C/T VEGF is associated with human epidermal growth factor receptor 2 expression in Moroccan breast cancer women

The vascular endothelial growth factor (VEGF), a potent regulator of angiogenesis, is involved in the development and progression of breast cancer (BC). The functional +936C/T polymorphism of the VEGF-A gene has been implicated in BC susceptibility; however, published data are conflicting. In the cu...

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Veröffentlicht in:Medical oncology (Northwood, London, England) London, England), 2014-12, Vol.31 (12), p.336-336, Article 336
Hauptverfasser: Rahoui, Jalila, Sbitti, Yassir, Touil, Nadia, Laraqui, Abdelilah, Ibrahimi, Azeddine, Rhrab, Brahim, Al Bouzidi, Abderrahman, Moussaoui Rahali, Driss, Dehayni, Mohamed, Ichou, Mohamed, Zaoui, Fatima, Mrani, Saad
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Sprache:eng
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Zusammenfassung:The vascular endothelial growth factor (VEGF), a potent regulator of angiogenesis, is involved in the development and progression of breast cancer (BC). The functional +936C/T polymorphism of the VEGF-A gene has been implicated in BC susceptibility; however, published data are conflicting. In the current case–control study, we analyzed the association of the +936C/T polymorphism with BC risk and tumor markers expression, human epidermal growth factor receptor 2 (HER2/neu) and caner antigen 15.3 (CA 15.3) in Moroccan women. We genotyped the DNA of 70 BC patients and 70 healthy women by TaqMan SNP assays. The χ 2 test and Fisher’s exact test were used for statistical analyses. The overall results revealed that there is no association between the +936C/T polymorphism and BC risk [ p  = 0.8; OR 0.87, 95 % CI (0.32–2.42)]. However, when we stratified the group of patients according to the status of tumor markers, a statistical significant association of +936C/T SNP and HER2/neu expression was observed ( p  = 0.009). In contrast, no association with the other tumor marker, CA 15.3, was found ( p  = 0.090). Thus, the +936C/T polymorphism seems to have a correlation with HER/neu expression in BC disease.
ISSN:1357-0560
1559-131X
DOI:10.1007/s12032-014-0336-6