Increased B4GALT1 expression associates with adverse outcome in patients with non-metastatic clear cell renal cell carcinoma

B4GALT1 表达增加与非转移性透明细胞肾细胞癌患者的不良预后相关

阅读:13
作者:Huyang Xie, Yu Zhu, Huimin An, Hongkai Wang, Yao Zhu, Hangcheng Fu, Zewei Wang, Qiang Fu, Jiejie Xu, Dingwei Ye

Abstract

B4GALT1 is one of seven beta-1, 4-galactosyltransferase (B4GALT) genes, which has distinct functions in various malignances. Here, we evaluate the association of B4GALT1 expression with oncologic outcome in patients with non-metastatic clear cell renal cell carcinoma (ccRCC). A retrospective analysis of 438 patients with non-metastatic ccRCC at two academic medical centers between 2005 and 2009 was performed. The first cohort with 207 patients was treated as training cohort and the other as validation cohort. Tissue microarrays (TMAs) were created in triplicate from formalin-fixed, paraffin embedded specimens. Immunohistochemistry (IHC) was performed and the association of B4GALT1 expression with standard pathologic features and prognosis were evaluated. B4GALT1 expression was significantly associated with tumor T stage (P<0.001 and P<0.001, respectively), Fuhrman grade (P<0.001 and P<0.001, respectively) and necrosis (P=0.021 and P=0.002, respectively) in both training and validation cohorts. And high B4GALT1 expression indicated poor overall survival (OS) (P<0.001 and P<0.001, respectively) in the two cohorts. Furthermore, B4GALT1 expression was identified as an independent adverse prognostic factor for survival (P=0.007 and P=0.002, respectively). Moreover, the accuracy of established prognostic models was improved when B4GALT1 expression was added. Therefore, a predictive nomogram was generated with identified independent prognosticators to assess patients' OS at 5 and 10 years. Increased B4GALT1 expression is a potential independent adverse prognostic factor for OS in patients with non-metastatic ccRCC.

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。