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  • The protein biomarkers described in this

    2018-11-05

    The protein biomarkers described in this study have all been associated with lung cancer, and characterized previously for cancer diagnostic potential. The elevated CRP preceded lung cancer diagnosis by several years (Chaturvedi et al., 2010), and were associated with increasing lung cancer risk (Xu et al., 2013). Elevation of serum prolactin could be served as diagnostic biomarkers for lung cancer (Bigbee et al., 2012; Nolen et al., 2011). Sera HGF were significantly elevated in lung cancer patients (Tanaka et al., 2011), and a high level of blood HGF exhibited a poor prognosis of metastatic disease in primary lung cancer patients (Hosoda et al., 2012). NY-ESO-1 autoantibody frequencies in lung cancer have been reported to range from 4 to 23% (Chapman et al., 2008; Tureci et al., 2006; Stockert et al., 1998). More importantly, NY-ESO-1 autoantibody was detected in patients with small primary tumors and more frequently before distant ipi-145 occurred, suggesting that NY-ESO-1 antibody is an early event (Tureci et al., 2006). Although the biomarker panel we described here could not detect every lung cancer patient, it offers a high specificity in detecting healthy controls as well as the patients with benign lung diseases. After the appropriate confirmatory clinical trials, one could envision that the most immediate scenario in which this panel could be used is to improve interpretation of CT images in the setting of a suspicious pulmonary nodule. In this context, a diagnostic biomarker panel must perform at a maximal level of specificity in order to reduce the number of false positive results rendered by CT. Actually, of the 80 prospective patients, the 4-biomarker predictor produced 82.6% sensitivity and 98.2% specificity as determined by post-surgery histologic results or 2years clinical follow-up. Therefore, as a supplementary diagnostic approach to CT scan, such a strategy could significantly reduce the number of futile invasive procedures. Upon further validation and optimization, these serum biomarkers could provide an effective means to further assess the malignant patients designated as having a high risk for lung cancer by LDCT scanning.
    Conclusions
    Authors Contributions
    Funding The study was supported by grants from the Major Science and Technology Innovation Project of Hangzhou (20112312A01), the National Natural Science Foundation (81172072), the Science Foundation for Distinguished Young Scholars of Zhejiang (R2101405), the International Science and Technology Cooperation Project of Zhejiang (2012C24008), and the Collaborative Innovation Projects of Science and Technology Department of Zhejiang (2014F50014), China. The funders had no role in study design, data collection, data analysis, interpretation and writing of the report.
    Conflict of Interest
    Introduction Cigarette smoking is the leading modifiable risk for cancer and multiple major chronic illnesses. Growing evidence identifies that genetic variation in the α5 nicotinic cholinergic receptor subunit (CHRNA5) gene plays a key role in both heavy smoking and nicotine dependence (Bierut et al., 2007; Bierut et al., 2008a). Multiple large meta-analyses demonstrated the association with smoking quantity, defined by number of cigarettes smoked per day (CPD) (Liu et al., 2010; Saccone et al., 2010; TAG, 2010; Thorgeirsson et al., 2010), with the most robust signal for two highly correlated genetic variants, rs16969968 and rs1051730 in subjects of European ancestry (TAG, 2010). The coding variant, rs16969968, results in an amino acid change in the α5 nicotinic cholinergic receptor subunit, and subsequently alters nicotinic receptor conductance in vitro (Bierut et al., 2008b; Kuryatov et al., 2011). Genetic variation in CHRNA5 increases risk for smoking-related disorders such as lung cancer and chronic obstructive pulmonary disease (COPD) (Amos et al., 2008; Pillai et al., 2009; Thorgeirsson et al., 2008). Research suggests that the association between CHRNA5 and lung cancer may be mediated by COPD (Young et al., 2011; Brennan et al., 2011; Wang et al., 2010). Further, CHRNA5 has been reported to predict smoking cessation in both cessation trials (Baker et al., 2009; Bergen et al., 2013; Chen et al., 2012; Munafo et al., 2011; Sarginson et al., 2011) and general population studies (TAG, 2010; Chen et al., 2012; Chen et al., 2015a). The CHRNA5 variant rs16969968 was recently shown to be a marker of delayed smoking cessation in a meta-analysis (Chen et al., 2015a). Smokers with the high-risk genotype had delayed age of smoking cessation compared with those with the low-risk genotype (age 56 versus age 52). Similarly, those with the high-risk genotype had a 4-year earlier age of lung cancer diagnosis compared to those with the low-risk genotypes (age 61 vs. age 65).