GSTM1 and GSTT1 polymorphisms and nasopharyngeal cancer risk: an evidence-based meta-analysis

The associated literature was acquired through deliberate searching and selected based on the established inclusion criteria for publications, then the extracted data were further analyzed using systematic meta-analyses.A total of 85 articles were identified, of which eight case-control studies concerning NPC were selected. The results showed that the overall OR was 1.42 (95%CI = 1.21–1.66) for GSTM1 polymorphism. While for GSTT1 polymorphism, the overall OR was 1.12 (95% CI = 0.93–1.34).The data were proven stable via sensitivity analyses. The results suggest GSTM1 deletion as a risk factor for NPC and failed to suggest a marked correlation of GSTT1 polymorphisms with NPC risk.Nasopharyngeal cancer (NPC), a fast-growing tumour, characterized by a high frequency of nodal and distant metastasis at diagnosis, 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 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 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