Authors’ contributions All authors read and approved the final manuscript. CO prepared the design of the manuscript and made the contouring of the target volume and organs at risk; ET and EO collected the samples; AY gave advise on the work and MY helped in the interpretation of the data; GA made the treatment planning; CO wrote the paper together with BP.”
“Introduction In gastric caner, patients with the same clinicopathologic characteristics and the same treatment regimens may have different clinical outcomes. Although stage is the best available clinical measure of tumor aggression and prognosis, there are clearly important differences

even within the same tumor stage [1, 2]. Therefore, it would be helpful to improve the prognostic accuracy by identifying readily accessible molecular markers that predict Tideglusib manufacturer some of the variation in clinical outcomes. In recent decades, many studies have shown that genetic alterations play roles in the development and progression of gastric cancer [3]. Among

these molecular markers, single nucleotide polymorphisms (SNPs) are the most commonly investigated genetic variation that may contribute to patients’ clinical outcomes [4]. Epidemiologic and clinical BTK inhibitor cost investigations have suggested that both TGF-β1 and VEGF may play an important role in the oncogenesis of the stomach [5, 6]. For example, TGFB1 and VEGF variants are associated with altered protein products, which may contribute to variation in individual susceptibility to cancer and clinical outcomes [4]. Both TGFB1 and VEGF genes are highly polymorphic, reportedly having 168 and 140 variants, respectively, but only few of these variants are within the promoter or coding regions that may be potentially 6-phosphogluconolactonase functional http://​www.​ncbi.​nlm.​nih.​gov/​SNP/​.

Of these variants, several SNPs have been described as important in modulation of gene functions [7–9] and reportedly involved in the etiology of various cancers [10–13]. The TGF-β1 pathway is critically involved in tumor development and progression. In tumor cell cultures, TGF-β1 has anti-proliferative effects and can block tumor progression in its early stages, whereas it can also accelerates invasion and metastasis in the later stages of tumor progression [14, 15]. One experimental study reported that TGF-β1-mediated activation of the ALK5-Smad 3 pathway is essential for the Shh protein to promote motility and invasiveness in gastric cancer cells [16]. Mouse experiments also showed that altered TGF-β1 was associated with the latent TGF-β1 binding proteins that can cause inflammation and tumors [17] and that the disrupted TGF-β1 pathway can lead to tumor growth by increasing the tumor angiogenesis induced by decreased expression of p38 MAPK inhibitor thrombospondin-1 [18].