Quantitative assessment of the diagnostic role of FHIT promoter methylation in non-small cell lung cancer
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Xin Geng1,*, Weilin Pu2,*, Yulong Tan1, Zhouyi Lu3, An Wang3, Lixing Tan2, Sidi Chen2, Shicheng Guo4, Jiucun Wang2, Xiaofeng Chen1
1Department of Cardiothoracic Surgery, Huashan Hospital, Fudan University, Shanghai 200032, China
2State Key Laboratory of Genetic Engineering, Collaborative Innovation Center for Genetics and Development, School of Life Sciences, Fudan University, Shanghai 200433, China
3Department of Chest Surgery, Shanghai Pulmonary Hospital, Shanghai 200433, China
4Department of Bioengineering, University of California at San Diego, La Jolla, CA 92093, USA
*These authors have contributed equally to this work
Shicheng Guo, email: email@example.com
Xiaofeng Chen, email: firstname.lastname@example.org
Jiucun Wang, email: email@example.com
Keywords: FHIT, DNA methylation, non-small cell lung cancer, NSCLC, diagnosis
Received: April 28, 2016 Accepted: December 12, 2016 Published: December 27, 2016
Aberrant methylation of CpG islands acquired in promoter regions plays an important role in carcinogenesis. Accumulated evidence demonstrates FHIT gene promoter hyper-methylation is involved in non-small cell lung cancer (NSCLC). To test the diagnostic ability of FHIT methylation status on NSCLC, thirteen studies, including 2,119 samples were included in our meta-analysis. Simultaneously, four independent DNA methylation datasets from TCGA and GEO database were analyzed for validation. The pooled odds ratio of FHIT promoter methylation in cancer samples was 3.43 (95% CI: 1.85 to 6.36) compared with that in controls. In subgroup analysis, significant difference of FHIT gene promoter methylation status in NSCLC and controls was found in Asians but not in Caucasian population. In validation stage, 950 Caucasian samples, including 126 paired samples from TCGA, 568 cancer tissues and 256 normal controls from GEO database were analyzed, and all 8 CpG sites near the promoter region of FHIT gene were not significantly differentially methylated. Thus the diagnostic role of FHIT gene in the lung cancer may be relatively limited in the Caucasian population but useful in the Asians.
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