Abstract

Genetic factors can contribute to both the occurrence and development of lung cancer. This study aimed to investigate endothelial nitric oxide synthase (eNOS) G894T and T-786C polymorphisms and plasma asymmetric dimethylarginine (ADMA) levels of lung cancer patients in comparison with healthy subjects. A total of 200 subjects, 100 patients with lung cancer and 100 healthy volunteers were included in this study. To determine eNOS gene polymorphisms, we collected and analyzed blood samples with polymerase chain reaction (PCR). Plasma ADMA levels were evaluated by high-performance liquid chromatography (HPLC). The difference in gene polymorphisms between lung cancer patients and healthy controls were insignificant. However, lung cancer patients had statistically significantly higher plasma ADMA levels than healthy controls. The patients and control groups with CC polymorphisms and TT polymorphisms on eNOS T-786C and G894T gene regions had higher plasma ADMA levels. The CC polymorphisms and plasma ADMA levels were higher in patients with small-cell lung cancer compared to those in patients with non-small-cell lung cancer. Although eNOS gene polymorphisms had no significant difference between lung cancer patients and healthy controls, plasma ADMA levels were higher in lung cancer patients compared to healthy controls. Our study suggests that CC genotypes and elevated plasma ADMA levels might be associated with small-cell lung cancer.

Highlights

  • Among cancers, lung cancer has the highest mortality rate and is the most common among cancers globally and in our country

  • The CC polymorphisms and plasma asymmetric dimethylarginine (ADMA) levels were higher in patients with small-cell lung cancer compared to those in patients with nonsmall-cell lung cancer

  • Conclusion: endothelial nitric oxide synthase (eNOS) gene polymorphisms had no significant difference between lung cancer patients and healthy controls, plasma ADMA levels were higher in lung cancer patients compared to healthy controls

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Summary

Introduction

Lung cancer has the highest mortality rate and is the most common among cancers globally and in our country. Several factors can cause lung cancer; smoking is the primary cause. In the United States, 75-80% of women and 90% of men who die from lung cancer are smokers [1, 2]. Less than 20% of smokers have lung cancer. Various factors other than smoking can contribute in lung cancer formation. Asbestos, past pulmonary diseases, and family history are some of them [3]. The contribution of various gene polymorphisms and other factors as well as smoking and other toxic exposures to lung cancer ethiopathogenesis have been shown [4, 5]

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