The serum activity of thioredoxin reductases 1 (TrxR1) is correlated with the poor prognosis in EGFR wild-type and ALK negative non-small cell lung cancer

血清硫氧还蛋白还原酶1 (TrxR1) 活性与EGFR野生型和ALK阴性非小细胞肺癌的不良预后相关

阅读:1

Abstract

BACKGROUND: The thioredxin reductases 1 (TrxR1) is one of the major antioxidant and redox regulators in mammalian cells. Studies have shown that TrxR1 is over expressed in many malignancy diseases. However, few studies have evaluated the role of TrxR1 in non-small cell lung cancer (NSCLC). METHODS: Serum levels of TrxR1 and CEA in 142 patients with EGFR wild type and ALK negative advanced NSCLC was measured by ELISA assay before first line standard doublet chemotherapy from June 2013 to February 2016 in Hunan Cancer Hospital. Clinical characteristics and Survival data were collected and analyzed according to serum TrxR1 levels. RESULTS: No significant differences were founded from clinic pathological variables. With the cut-off value of 12U/mL, the lower serum TrxR1 activity patients had long progression-free survival (PFS) and overall survival (OS) compared with higher patients (PFS: 5.3m vs. 3.6m p=0.044, OS: 14.5m vs. 11m p<0.001). In subgroup, lower serum TrxR1 activity patients had long OS both in adenocarcinoma (ADC) (17m vs. 8m, p=0.003) and squamous cell carcinoma (SCC) (13m vs. 11m, p=0.035). While combining with TrxR1 activity and serum CEA concentrations, we founded that patients with lower serum TrxR1 activity and serum CEA concentrations had long OS compared with higher group patients (20m vs. 7m, p<0.001). CONCLUSIONS: Serum TrxR1 activity was not affected by clinic pathological variables. Measurement of serum TrxR1 activity might be an independent prognostic factor for EGFR wild type and ALK negative advanced NSCLC patients. Combination of serum TrxR1 activity and serum CEA concentrations need to be further profiled from bench to beside.

特别声明

1、本页面内容包含部分的内容是基于公开信息的合理引用;引用内容仅为补充信息,不代表本站立场。

2、若认为本页面引用内容涉及侵权,请及时与本站联系,我们将第一时间处理。

3、其他媒体/个人如需使用本页面原创内容,需注明“来源:[生知库]”并获得授权;使用引用内容的,需自行联系原作者获得许可。

4、投稿及合作请联系:info@biocloudy.com。