NFKB1 -94insertion/deletion ATTG polymorphism and cancer risk: Evidence from 50 case-control studies
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Wen Fu1,*, Zhen-Jian Zhuo2,*, Yung-Chang Chen3,*, Jinhong Zhu4, Zhang Zhao1, Wei Jia1, Jin-Hua Hu1, Kai Fu1, Shi-Bo Zhu1, Jing He1, Guo-Chang Liu1
1Department of Pediatric Urology, Department of Pediatric Surgery, Guangzhou Institute of Pediatrics, Guangzhou Women and Children’s Medical Center, Guangzhou Medical University, Guangzhou 510623, Guangdong, China
2School of Chinese Medicine, Faculty of Medicine, The Chinese University of Hong Kong, Hong Kong 999077, China
3Department of Gastroenterology, The First People’s Hospital of Foshan (Affiliated Foshan Hospital of Sun Yat-sen University), Foshan 528000, Guangdong, China
4Molecular Epidemiology Laboratory and Department of Laboratory Medicine, Harbin Medical University Cancer Hospital, Harbin 150040, Heilongjiang, China
*These authors have contributed equally to this work
Guo-Chang Liu, email: email@example.com
Jing He, email: firstname.lastname@example.org
Keywords: NFKB1, -94ins/delATTG, polymorphism, cancer risk, meta-analysis
Received: August 15, 2016 Accepted: November 22, 2016 Published: December 26, 2016
Nuclear factor-kappa B1 (NF-𝛋B1) is a pleiotropic transcription factor and key contributor to tumorigenesis in many types of cancer. Numerous studies have addressed the association of a functional insertion (I)/deletion (D) polymorphism (-94ins/delATTG, rs28362491) in the promoter region of NFKB1 gene with the risk of various types of cancer; however, their conclusions have been inconsistent. We therefore conducted a meta-analysis to reevaluate this association. PubMed, EMBASE, China National Knowledge infrastructure (CNKI), and WANFANG databases were searched through July 2016 to retrieve relevant studies. After careful assessment, 50 case-control studies, comprising 18,299 cases and 23,484 controls were selected. Crude odds ratios (ORs) and 95% confidence intervals (CIs) were used to determine the strength of the association. The NFKB1 -94ins/delATTG polymorphism was associated with a decreased risk of overall cancer in the homozygote model (DD vs. II): OR = 0.75, 95% CI = 0.64-0.87); heterozygote model (ID vs. II): OR = 0.91, 95% CI = 0.83-0.99; recessive model (DD vs. ID/II): OR = 0.81, 95% CI = 0.71-0.91; dominant model (ID/DD vs. II): OR = 0.86, 95% CI = 0.78-0.95; and allele contrast model (D vs. I): OR = 0.88, 95% CI = 0.81-0.95). Subgroup and stratified analyses revealed decreased risks for lung cancer, nasopharyngeal carcinoma, prostate cancer, ovarian cancer, and oral squamous cell carcinoma, and this association held true also for Asians (especially Chinese subjects) in hospital-based studies, and in studies with quality scores less than nine. Well-designed, large-scale case-control studies are needed to confirm these results.
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