Increased expression of stomatin-like protein 2 (STOML2) predicts decreased survival in gastric adenocarcinoma: a retrospective study

气孔素样蛋白 2 (STOML2) 表达增加预示胃腺癌生存率下降:一项回顾性研究

阅读:8
作者:Xiao-Hong Li, Fan He, Shu-Mei Yan, Yong Li, Yun Cao, Chun-Yu Huang, Zhi-Wei Zhou

Abstract

Stomatin-like protein 2 (STOML2), a member of the stomatin, has been reported to be upregulated in several human cancers. However, its role and clinical significance in gastric adenocarcinoma remains unclear to date. The purpose of this retrospective study was to explore whether there was a correlation between the expression of STOML2 by immunohistochemistry and the clinical outcome of a large group of patients with gastric adenocarcinoma. In this retrospective study, we performed immunohistochemistry to evaluation of STOML2 expression in a large panel of gastric adenocarcinoma samples. The receiver operating characteristic method was used to define the STOML2 immunoreactivity score cutoff value. The clinical/prognostic significance of STOML2 expression was analyzed statistically. Kaplan-Meier analysis was used to compare the postoperative survival between groups. STOML2 was overexpressed in gastric cancer compared with paracancerous normal mucosa. Increased STOML2 expression was associated with higher histologic grade (P = 0.047), T category (P < 0.001), and N category (P = 0.01). Patients with high expression of STOML2 demonstrated shortened overall survival compared with those with low expression of STOML2 (median of 38.9 vs. 64.0 months, P < 0.001). Furthermore, STOML2 expression could stratify patients survival in stage N0 (P < 0.001). Multivariate analysis showed that the level of STOML2 expression was an independent prognostic factor in gastric adenocarcinoma (RR = 1.920, P = 0.001). Increased expression of STOML2 suggests unfavorable prognosis for gastric adenocarcinoma patients. Further studies are warranted.

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。