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Prognostic value of β-catenin, c-myc, and cyclin D1 expressions in patients with esophageal squamous cell carcinoma

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Abstract

Esophageal squamous cell carcinoma (ESCC) is one of the most frequently diagnosed malignant tumors in North China. We have identified that Wnt2/β-catenin pathway is activated in ESCC cells and sodium nitroprusside (SNP) and siRNA against β-catenin not only inhibit the expressions of β-catenin and its major downstream effectors including c-myc and cyclin D1 but induce cell cycle arrest and apoptosis. The purpose of the present study was to analyze the relationship between pathological parameters including invasion depth and lymph node metastasis and the expressions of β-catenin, c-myc, and cyclin D1 in order to evaluate their values of prognosis in patients with ESCC. The expressions of β-catenin, c-myc, and cyclin D1 were detected immunohistochemically in the resected cancer tissues from 40 patients with ESCC. The β-catenin expression was reduced in 22 (55.0%) patients, which was closely correlated with invasion depth (P = 0.023) and lymph node metastasis (P = 0.003). There was the positive c-myc expression in 21 (52.5%), which was significantly correlated with invasion depth (P = 0.009) and lymph node metastasis (P = 0.001). Furthermore, the results of survival rates analyzed by Kaplan–Meier curve revealed that patients with the reduced expression of β-catenin had a poorer prognosis than those with the preserved expression (P = 0.031), and patients with the positive expression of c-myc also had a significantly poorer prognosis than those with the negative expression (P = 0.008). These findings demonstrate that β-catenin pathway plays a crucial role in the progression of ESCC, suggesting that both β-catenin and c-myc may be used as markers for predicting the prognosis of patients with ESCC.

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Correspondence to Lexun Xue.

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Wang, W., Xue, L. & Wang, P. Prognostic value of β-catenin, c-myc, and cyclin D1 expressions in patients with esophageal squamous cell carcinoma. Med Oncol 28, 163–169 (2011). https://doi.org/10.1007/s12032-010-9436-0

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  • DOI: https://doi.org/10.1007/s12032-010-9436-0

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