Authors’ VX-680 contributions KZ participated in the collection of clinical data, performed patient follow-ups, and drafted the manuscript. CT made substantial contributions to conception and design of this research and has reviewed the manuscript for important intellectual content and given final approval of the version to be published. HD assisted during patient follow-ups and collection of data. ZX participated in project coordination and assisted with

manuscript. Each author has participated sufficiently in this work to take public responsibility for the appropriate portions of the manuscript. All authors read and approve of the final manuscript.”
“Backgrounds Nasopharyngeal cancer (NPC), a fast-growing tumour, characterized by a high frequency of nodal and distant

metastasis at diagnosis, Smad2 phosphorylation is rare in many areas of the world but common in Southeast Asia [1]. Evidence suggests that Epstein-Barr virus (EBV) infection is a major risk factor contributing to its tumorigenesis [2]. Besides, cigarette Erismodegib molecular weight smoking and alcohol consumption are probably important etiological factors increasing the risk of developing NPC [3]. Moreover, environmental chemical pollutions, widely spread carcinogens, are difficult to be degraded in the environment and thus may have a long-term effect on human health. Despite many individuals exposed to EBV infection, environmental risk factors and/or with ADP ribosylation factor extensive tobacco and alcohol consumption, NPC develops only in a small group of exposed people, which suggests that genetic host factors might contribute to the carcinogenic mechanisms. Recent evidence indicates that carcinogen-metabolizing genes and DNA-repair genes may play critical roles in determining individual susceptibility to cancers. Polymorphisms in these genes encoding the enzymes, possibly by altering their expression and function, may increase or decrease carcinogen activation/detoxication and modulate DNA repair. Xenobiotics can be detoxified by phase II enzymes, such

as GSTM1 and GSTT1 which have been suggested to be involved in detoxification of polycyclic aromatic hydrocarbons (PAHs) and benzo(a)pyrene [4]. Evidence suggests that genetic polymorphisms of these genes might increase individual susceptibility to NPC. Therefore, a number of published studies have focused on GSTM1 and GSTT1 genetic variation with respect to NPC and have yielded conflicting results. Whether GSTM1 or GSTT1 polymorphism is a risk factor for NPC remains largely uncertain. Since a single study may have been underpowered to clarify the associations of GSTM1 or GSTT1 polymorphisms with NPC susceptibility, in the present study we aimed to perform evidence-based quantitative meta-analyses that might increase statistical power to address this controversy.