APEX1 promotes transcriptional activation of HIF-1 and its reduced levels are related to a decrease in tumour volume and FDG uptake, suggesting that it affects glucose metabolism and cellular proliferation [41]. Homozygosity (TT genotype) for the rs1130409 APEX1 SNP was significantly associated with a poor overall cancer survival [15]. Here, this genotype was not significantly associated with SUV, compared with the GG/TG genotypes, as previously shown by by Kim SJ et al. [15]. HIF1a itself has an SNP (rs11549465) that we studied for possible association with FDG uptake. However, we observed no association in BC disease, in agreement with data previously
obtained in NSCLC [15]. VEGFA rs3025039 polymorphism has been related with BC risk and a C > T polymorphism at position 936 in the 3’ untranslated region of the VEGFA gene has been associated with VEGF Tipifarnib supplier plasma levels. Specifically, the T-variant is linked to lower VEGF level and associated with increased BC risk [13] and worse outcome [17] compared Cabozantinib to the wildtype allele. Wolf G. and co-workers [13] suggested a potential role of this VEGFA polymorphism on the variability of FDG uptake in tumour tissue. However, our study and data reported by Lorenzen S. et al. [17] do not confirm this association. The MTHFR rs1801133 SNP is highly represented
in the Caucasian population [46] and it is related to increased BC risk [36–38]. Nevertheless, its role in PET has not been studied yet. Here, we evaluated its importance in FDG uptake, for the first time, finding no associations. Considering its great importance in BC, we still believe that additional studies are needed to clarify its relevance. Unfortunately, the genotype distributions for the remaining HIF1a: rs11549467, EPAS1: rs137853037 and rs137853036 SNPs did not allow us to evaluate Olopatadine their possible association with SUV. The possible association between FDG uptake and SNPs is described by a limited number of studies,
due to the need for multidisciplinary team and expertise. Moreover, this research field is characterized by controversial reports. Moreover a strong variability of FDG-PET uptake on BC tissue has been reported [13], but the reason for this variability is not fully understood and may involve various cellular processes and risk factors such as genetic predisposition. Overall, our analysis succeeded to reproduce some previous findings, while we failed to confirm others, which still need to be further investigated. These discrepancies can be explained by the shortage of patients assayed both in our work and previous studies [13–15]. In addition these works looked at different groups of people from various European countries.