TGFB1 and TGFBR2 functional polymorphisms and risk of esophageal squamous cell carcinoma: a case–control analysis in a Chinese population

Abstract

These results are consistent with our previous findings in gastric cancer and support the hypothesis that genetic variants in TGFB1 and TGFBR2 may modulate the risk of ESCC.

A functional polymorphism of TGFBR2 is associated with risk of breast cancer with ER+, PR+, ER+PR+ and HER2− expression in women

“…However, results of the present study have shown that the -875A allele was marginally associated with a decreased risk of breast cancer. These findings are consistent with previous ones indicating that the TGFBR2 G-875A polymorphism significantly correlates with a decreased risk of gastric and esophageal squamous cell carcinomas in the Chinese population (22,23 -. Activation of the TGF-β-mediated signal transduction is subject to hormonal regulation (24).…”

Influence of TGFB1+869T>C functional polymorphism in non-small cell lung cancer (NSCLC) risk

“…TGFß1 plays a key role in cell cycle control and carcinogenesis (Elliott and Blobe 2005;Jin et al 2008). TGFß1 binds to type II TGFß1 receptor (TßRII), phosphorylates the type I TGFß1 receptor (TßRI) and activates downstream kinases of the TGFß1-signaling pathway (Bierie and Moses 2006).…”

Association between the TGFBR2 G-875A Polymorphism and Cancer Risk: Evidence from a Meta-analysis

“…As one of the key effectors of TGF-β signaling, TGFBR2 mediates the growth-inhibitory signals from TGF-β through a complex with TGFBR1 (Derynck and Zhang, 2003;Ikushima and Miyazono, 2010). Though the functional role of the TGFBR2 G-875A variant in TGF-β pathway has not yet to be well interpreted, several published clinic studies reported this variant was at decreased risk of developing various cancer Zhou et al, 2007;Jin et al, 2008;Xu et al, 2011;Zhang et al, 2011;Guo et al, 2012;Teixeira et al, 2013). However, two published clinic studies reported this variant was not involved in the risk of cancer (Seijo et al, 2001;Jin et al, 2004).…”