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Mitotic arrest deficient-like 1 is correlated with poor prognosis in small-cell lung cancer after surgical resection

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Tumor Biology

Abstract

Mitotic arrest deficient-like 1 (MAD1L1) whose dysfunction is associated with chromosomal instability plays a pathogenic role in a few human cancers. However, the status of MAD1L1 expression in small-cell lung cancer (SCLC) remains unknown. Immunohistochemistry was used to determine the expression of MAD1L1 protein in 32 lymph node metastasis (LN-M) tissues and 88 primary SCLCs compared with 32 adjacent noncancerous tissues. The associations of MAD1L1 protein expression with the clinicopathologic features and clinical outcomes in patients with SCLC were analyzed. The ratio of MAD1L1 positive expression was higher in primary SCLC tissues (39.8 %) and LN-M tissues (46.9 %) compared with adjacent noncancerous tissues (9.4 %). MAD1L1 positive expression was associated with tumor-node-metastasis (TNM) stage (P = 0.003), International Association for the Study of Lung Cancer (IASLC) stage (P = 0.004), tumor size (P = 0.015), lymph node metastasis (P = 0.014), and recurrence (P < 0.001). Multivariate analysis suggested that MAD1L1 positive expression was an independent factor for overall survival (hazard ratio (HR) 2.002; 95 % confidence interval (CI) 1.065–3.763; P = 0.031) and recurrence-free survival (HR 2.263; 95 % CI 1.197–4.276; P = 0.012). To sum up, MAD1L1 positive expression may be associated with tumour progression and metastasis in SCLCs and may thus serve as a new biomarker for prognosis in these patients.

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Acknowledgments

This work is supported by a grant from the National Natural Science Foundation of China (No.30772540 and No.81172214).

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Correspondence to Li Cai.

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This study was approved by the Medical Ethics Committee of Harbin Medical University, and informed consent was obtained from the participating patients.

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Li, D., Meng, Q., Zhang, H. et al. Mitotic arrest deficient-like 1 is correlated with poor prognosis in small-cell lung cancer after surgical resection. Tumor Biol. 37, 4393–4398 (2016). https://doi.org/10.1007/s13277-015-4302-5

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  • DOI: https://doi.org/10.1007/s13277-015-4302-5

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