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  • The diverse complex molecular events

    2018-10-23

    The diverse, complex molecular events involved in the initiation and development of malignant neoplasm require functional changes not only in the tumor cell growth-related genes and/or tissue-specific genes but also in the body\'s immune response-related genes. Accordingly, there should be multiple miRNAs targeting those genes involved in tumorigenesis. Circulating miRNAs can derive from the tumor itself or from host responses to the tumor (Pritchard et al., 2012; Chen et al., 2012b). Therefore, functionally dysregulated miRNAs in circulation can be classified into three groups: (i) tissue-specific, (ii) tumor cell growth/cycle-related, and (iii) immune response-related. Of the five members of our predictive biomarker, miR-7 is a tissue-specific miRNA, because it has been found to be directly involved in NSCLC (Chou et al., 2010). miR-25, miR-483-5p and miR-193a-3p are tumor cell growth/cycle-related miRNAs (Zhang et al., 2013; Soon et al., 2009; Yu et al., 2015; Uhlmann et al., 2012). Finally, miR-214 may be categorized as an immune response-related miRNA because it has been found to play a dominant role in endothelial cell function, angiogenesis and exosome-mediated communication between endothelial toxins (van Balkom et al., 2013; Ghalali et al., 2014; Schwarzenbach et al., 2012). Therefore, the combination of the identified five serum miRNAs in our study should be more reliable and specific than the single miRNA for the detection of NSCLC.
    Conflicts of Interest
    Author Contributions
    Introduction Neuropathic pain is defined by the International Association for the Study of Pain as pain arising as a direct consequence of a lesion or a disease affecting the somatosensory system (Jensen et al., 2011). The prevalence of neuropathic pain is estimated to be around 7% in a general population while in a diabetic population around 1 in 4 patients will suffer from this disorder (van Hecke et al., 2014; Abbott et al., 2011). The current treatment of neuropathic pain is far from satisfactory, with fewer than 30% of patients achieving satisfactory relief of diabetic neuropathic pain (Barrett et al., 2007). Compared to people without pain and patients with non-neuropathic pain, diabetic neuropathic pain has a significant negative effect on patients\' quality of life (Davies et al., 2006). In addition, the disorder represents a significant economic burden to healthcare systems (Tarride et al., 2006; Dworkin et al., 2010). Cross-sectional epidemiological studies have identified multiple risk factors for neuropathic pain. These include older age, female gender, manual occupation, lower educational attainment, and living in a rural area or in poor accommodation (Smith et al., 2007; Torrance et al., 2006). These risk factors are difficult to modify and are not suitable for clinical intervention, though they are still of academic and political interest. Specifically for diabetic neuropathic pain, modifiable risk factors including smoking, hypertension, obesity, hypercholesterolemia and duration of diabetes have been identified (Jensen et al., 2006; Tesfaye et al., 2005). Unfortunately, there are no published clinical trials that suggest a reduction in the incidence or severity of neuropathic pain through addressing these modifiable risk factors. Further effort is required in this area. Studies have found that, although glycaemic control can reduce the incidence of diabetic neuropathy, there is limited impact in decreasing the incidence of accompanying neuropathic pain, even with long-term excellent glycaemic control (Callaghan et al., 2012; Marti et al., 2006). Epidemiological studies, such as genetic association studies, can identify independent risk factors which are clinically important, and offer these risk factors as covariates for basic research studies, or as new factors to address clinically. Diabetic neuropathic pain is considered as a complex trait which is affected by both environmental risk factors and genetic risk factors. Unlike well documented environmental risk factors, the understanding of the genetic contributors to neuropathic pain is rather poor, though evidence from animal models and human studies have both confirmed that it is a heritable trait (Devor et al., 2005; Meng et al., 2015). Studies on animal models have proposed candidate genes for neuropathic pain such as P2X7, P2X4, TLR4, and CACNG2 (Chessell et al., 2005; Trang et al., 2009; Nissenbaum et al., 2010; Wang et al., 2013). The first genome-wide association study (GWAS) on diabetic neuropathic pain in humans reported that GFRA2 might be associated with a subgroup of this disorder (Meng et al., 2015). All these candidate genes need further replications to validate their biological roles.