Résumé
Objective:To analyze the expression and clinical significance of lymphoid enhancer factor-1 (LEF-1) and P53 protein in hilar cholangiocarcinoma.Methods:A total of 50 cases with hilarcholangiocarcinoma in the Tangshan People′s Hospital from March 2010 to December 2017 were retrospectively analyzed.P53 protein mutation was detected by immunohistochemistry.At the same time, the expression of LEF1 protein in cholangiocarcinoma and adjacent normal tissues was detected.The expression of LEF1 and its correlation with clinicopathological parameters were analyzed.At the same time, the relationship between p53 protein mutation and LEF1 protein expression and the prognosis of patients were discussed.Results:The positive expression rate of LEF1 in tumor tissues were 62.00%(31/50), which was higher than in adjacent tissues 36.00% (18/50). The difference was statistically significant (χ 2=6.763, P=0.016). There were 28 patients with TP53 protein mutation and 22 patients with wild type.The positive rate of LEF1 in TP53 mutant group was 75.00% (21/28), which was significantly higher than that in TP53 wild type group(45.45%, 10/22), and the difference was statistically significant(χ 2=4.565, P=0.03). The LEF1 expression was associated with tumor differentiation, TNM stage, lymph node metastasis and TP53 protein mutation (all P<0.05). LEF-1 expression was positively correlated with TP53 protein mutation ( r=0.294, P=0.04). The 1-year cumulative survival rate of patients with TP53 protein mutation was significantly lower than that of patients with TP53 protein wild type (60% vs.81%, P=0.0416). The 1-year cumulative survival rate of patients with LEF1 positive expression was also significantly lower than that of patients with negative expression (53% vs.82%, P=0.0180). Conclusion:LEF-1 is highly expressed in hilar cholangiocarcinoma, and patients with high expression have poor prognosis.The positive expression of LEF-1 in hilar cholangiocarcinoma patients with TP53 protein mutation was increased, and the prognosis of patients with TP53 protein mutation was poor.