期刊文献+

SASH1基因在非小细胞肺癌中表达的临床和预后意义 被引量:1

Clinical and prognostic significance of SASH1 expression in non-small cell lung cancer
下载PDF
导出
摘要 目的:探讨候选抑癌基因SASH1(SAM-and SH3-domain containing 1)在非小细胞肺癌(NSCLC)组织中的表达及其与临床病理特征和预后的关系。方法:应用免疫组织化学法检测202例NSCLC组织及110例癌旁组织中SASH1蛋白的表达,并分析与临床病理参数及预后的相关性。结果:(1)SASH1蛋白在癌组织阳性表达率为35.64%,显著低于癌旁组织的62.73%,差异具有统计学意义(P<0.001)。(2)SASH1蛋白阳性表达率远处转移组较非远处转移组明显降低,差异具有统计学意义(P=0.034),与肿瘤TNM分期相关(P=0.028)。(3)单因素Cox回归分析显示SASH1表达(P<0.001)、淋巴结转移(P=0.003)及TNM分期(P=0.001)与NSCLC的预后相关;多因素Cox回归分析显示SASH1表达(P<0.001)及TNM分期(P=0.026)是独立的预后指标。结论:SASH1基因在NSCLC中表达下调,该基因可能是NSCLC的抑癌基因,可能作为分子标记而用于NSCLC的诊断和治疗。 Objective:To investigate the expression of SASH1(SAM-and SH3-domain containing 1) in non-small cell lung cancer(NSCLC),and to analyze the correlations of SASH1 expression with clinicopathological factors and prognosis in NSCLC.Methods:The expression of SASH1 was detected by immunohistochemistry in 202 NSCLC samples and 110 benign tumor-adjacent samples.STATA12.0 software was used for χ2 test,and SPSS20.0 software for Cox regression analysis and Kaplan-Meier survival analysis.Results:(1)The positive rate of SASH1 protein expression in NSCLC was significantly lower than that in adjacent noncancerous tissues(35.64% vs 62.73%,P0.001).(2)SASH1 expression was significantly correlated with TNM stage(P=0.028) and distant metastasis(M)(P=0.034).(3)Univariate analyses indicated that low SASH1 expression(P0.001),lymph node metastasis(N)(P=0.003) and tumor TNM stage(P =0.001) were associated with the 5-year survival rate of NSCLC patients.Multivariate analyses further revealed that low SASH1 expression(P0.001) and TNM stage(P=0.026) were independent prognostic factors.Conclusion:SASH1 was significantly downregulated in NSCLC SASH1 could be used as an independent biomarker for the diagnosis and treatment of NSCLC.
出处 《交通医学》 2017年第5期418-421,共4页 Medical Journal of Communications
关键词 非小细胞肺癌 候选抑癌基因SASH1 免疫组织化学 预后 non-small cell lung cancer SAM- and SH3 - domain containing 1 immunohistochemistry prognosis
  • 相关文献

参考文献3

二级参考文献23

共引文献22

同被引文献2

引证文献1

相关作者

内容加载中请稍等...

相关机构

内容加载中请稍等...

相关主题

内容加载中请稍等...

浏览历史

内容加载中请稍等...
;
使用帮助 返回顶部