Lung cancer susceptibility from GSTM1 deletion and air pollution with smoking status: a meta-prediction of worldwide populations
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Pojui Yu1,2, Joyce D. Kusuma3, Maria Aurora R. Suarez4 and Shyang-Yun Pamela Koong Shiao5
1Department of Nursing, Fu Jen Catholic University Hospital, New Taipei City, Taiwan (R.O.C.)
2School of Nursing, College of Medicine, National Taiwan University, Taipei, Taiwan (R.O.C.)
3Heritage Victor Valley Medical Group, Big Bear Lake, CA, USA
4Department of Critical Care and Telemetry, Citrus Valley Health Partners, West Covina, CA, USA
5College of Nursing and Medical College of Georgia, Augusta University, Augusta, GA, USA
Shyang-Yun Pamela Koong Shiao, email: firstname.lastname@example.org
Keywords: Glutathione S transferase mu 1; lung cancer; meta-prediction; air pollution; smoking
Received: May 15, 2018 Accepted: June 13, 2018 Published: July 24, 2018
Glutathione S transferase mu 1 (GSTM1) gene has been associated with lung cancer (LC) risk, for GSTM1 enzyme playing a vital role in detoxification pathway and protective against toxic insults. The major objective of this study was to investigate GSTM1 deletion pattern and its association with LC in the world’s population by using meta-prediction techniques. The secondary objective was to examine the effects of air pollution, smoking status, and other factors for gene-environment interactions with GSTM1 deletion and LC risk. We completed a comprehensive search to yield a total of 170 studies (40,296 cases and 48,346 controls) published from 1999 to 2017 for meta-analyses. The results revealed that GSTM1 deletion type was associated with increased risk of LC, while GSTM1 present type provided protective effect for all populations combined worldwide. Subgroup analysis on the rank order of risks from highest to lowest, among racial–ethnic groups, were Chinese, South East Asian, other North Asian, European, and finally American. Additional predictive analyses presented that air pollution played a significant role with increased risks of GSTM1 deletion and LC susceptibility, and the risks increased for smokers with higher levels of air pollution. Based on the findings of meta-predictive analysis, increased air pollution levels and smoking status presented additive effects to the LC risk susceptibilities and GSTM1 gene polymorphisms, for gene-environment interactions. Future studies are needed to examine gene-environment interactions for GSTM1 interacting with environmental factors and dietary interventions to mitigate the toxic effects, for LC prevention.
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