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Pharmacogenetic role of ERCC1 genetic variants in treatment response of platinum-based chemotherapy among advanced non-small cell lung cancer patients

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Tumor Biology

Abstract

The excision repair cross-complementation group 1 (ERCC1) plays an essential role in DNA repair and has been linked to resistance to platinum-based anticancer drugs among advanced non-small cell lung cancer (NSCLC) patients. We systematically evaluate whether ERCC1 Asn118Asn and C8092A genetic variants are associated with treatment response of platinum chemotherapy. We preformed a meta-analysis using ten eligible cohort studies (including 11 datasets) with a total of 1,252 NSCLC patients to summarize the existing data on the association between the ERCC1 Asn118Asn and C8092A polymorphisms and response to platinum regiments. Odds ratio or hazard ratio with 95% confidence interval were calculated to estimate the correlation. We found that neither ERCC1 C8092A polymorphism nor Asn118Asn variant is associated with different response of platinum-based treatment among advanced NSCLC patients. Additionally, these two genetic variants are not related to treatment response in either Caucasian patients or Asian patients. Our meta-analysis indicates that the ERCC1 Asn118Asn and C8092A polymorphisms may not be good prognostic biomarkers for platinum-based chemotherapy in patients with stage III–IV NSCLC.

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Acknowledgments

This work was supported by Beijing Nova Program (no. 2010B013 to M. Yang), the Fundamental Research Funds for the Central Universities (no. ZZ1234 to M. Yang) and National Natural Science Foundation of China (no. 30872968).

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Correspondence to Qipeng Yuan or Ming Yang.

Additional information

Dianke Yu and Juan Shi contributed equally to this work.

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ESM 1

Treatment characteristics and genotyping methods of studies included in the meta-analysis (PDF 30 kb)

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Yu, D., Shi, J., Sun, T. et al. Pharmacogenetic role of ERCC1 genetic variants in treatment response of platinum-based chemotherapy among advanced non-small cell lung cancer patients. Tumor Biol. 33, 877–884 (2012). https://doi.org/10.1007/s13277-011-0314-y

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  • DOI: https://doi.org/10.1007/s13277-011-0314-y

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