Title of article :
Expression of 14-3-3γ in patients with breast cancer: Correlation with clinicopathological features and prognosis
Author/Authors :
Song، نويسنده , , Yulan and Yang، نويسنده , , Zheng and Ke، نويسنده , , Zunfu and Yao، نويسنده , , Yunhong and Hu، نويسنده , , Xinrong and Sun، نويسنده , , Yanqin and Li، نويسنده , , Hongmei and Yin، نويسنده , , Jinbao and Zeng، نويسنده , , Chao، نويسنده ,
Issue Information :
روزنامه با شماره پیاپی سال 2012
Pages :
4
From page :
533
To page :
536
Abstract :
Aim n 14-3-3γ is an important member of the 14-3-3 family that play important roles in the regulation of various cellular processes. The aim of the study is to investigate the association between 14-3-3γ expression and the clinicopathological features of patients with breast cancer. s pression of 14-3-3γ was detected by Western blot in both foci of breast cancer and adjacent non-cancerous tissues. In addition, 14-3-3γ expression was analyzed by immunohistochemistry in 60 clinicopathologically characterized breast cancer cases. The association of 14-3-3γ expression with survival of the patients were analyzed. s pression level of 14-3-3γ protein in breast cancer were significantly higher than that in non-cancerous mammary gland tissues. Moreover, high expression of 14-3-3γ correlated with tumor size and tumor grade (all P < 0.05). Patients with high 14-3-3γ expression had worse overall survival rate than that with low expression (P < 0.05). Furthermore, multivariate analysis showed that 14-3-3γ expression was an independent predictor of overall survival (HR, 0.196; 95%CI, 0.043–0.892; P = 0.035). sions ta suggest for the first time that the increased expression of 14-3-3γ in breast cancer is associated significantly with tumor progression and poor prognosis. 14-3-3γ may be a novel and potential prognostic marker for breast cancer.
Keywords :
breast cancer , immunohistochemistry , 14-3-3? , Prognosis
Journal title :
Cancer Epidemiology
Serial Year :
2012
Journal title :
Cancer Epidemiology
Record number :
1765904
Link To Document :
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