The results show a higher percentage of males (64%) compared to females (36%) in the lung cancer group. The larger percentage in men may suggest that there are sex-specific risk factors for lung cancer development, as more men than women engage in risky behaviors like smoking or occupational exposures that are associated with the disease[18, 19].
The variations in mean BMI between the control group and lung cancer patients could point to an association between a higher risk of developing lung cancer and an elevated BMI. While obesity is an established risk factor for several malignancies, it's vital to remember this. There are several factors that could contribute to the observed variation in BMI, including age, sex, and lifestyle choices [20, 21].
Our results reported that the mean age of patients with lung cancer is 65.15 years. This suggests that the study's lung cancer patients are older than those in the control group. The variation in mean age suggests that being older might be a risk factor for lung cancer. This discovery is consistent with the well accepted notion that the risk of cancer rises with age [19]. The correlation between smoking and lung cancer is well-established, and this is supported by the higher percentage of smokers among patients with lung cancer. According to Hecht [22], tobacco smoke contains carcinogens that can harm lung cells and raise the risk of developing cancer. It is not always the case that lung cancer patients who smoke have a larger percentage of smoking among them [11]. A significant majority of individuals may be diagnosed with lung cancer at an advanced stage, as indicated by the increased percentage of patients in stage IV. This is problematic because advanced phases frequently present more difficult treatment and prognostic situations. Prognosis and treatment outcomes are typically better with early discovery (stages I and II) [23].
Large-scale research is needed to validate our findings, as serum leptin and resistin levels play a crucial role as pro-inflammatory cytokines in lung cancer. Nevertheless, their application as diagnostic or prognostic indicators is still viable. Leptin was detected high in our patients, particularly in patients with NSCLC. This might explain that leptin hormone is secreted from many adenomatous structures in the body, particularly from adipose tissue. Therefore, leptin secretion may be induced by paraneoplastic events or cytokine effects in lung carcinoma [7, 24]. Our results agree with [25] who indicated that mean of leptin increase in lung cancer group contrast with control. The results of present study disagree with results by Tas, [26]; Hong, [27] who they recorded that the mean of leptin decrease in lung cancer compared with control. In Chine, according to the meta-analysis, leptin levels in serum and tissue may have a role in the etiology of lung cancer and tumor metastasis [28]. An earlier investigation revealed that leptin stimulation increases the growth of lung cancer by stimulating the production of immunoinflammatory cytokines, such as TNF-a and IL-6, and by causing resistance to apoptosis [27].
In one study, increased leptin in lung tissue was found to be associated with impairment in lung tissue, along with increased risk of NSCLC [7]. Many studies have concluded that elevated blood leptin levels may be predictive of lung cancer diagnosis and progression, suggesting that leptin plays a significant role in the pathophysiology of lung cancer [28, 29]. Additionally, the current study's findings along with those of earlier research may enable us to pinpoint a novel marker for the diagnosis of lung cancer as well as a therapeutic target. A large number of studies have suggested that leptin has potential as an anticancer drug target [30, 31]. While, Resistin hormone had been significant increase in SCLC and NSCLC group compared with control group. These results agree with results by Demiray et al., [11] who indicated that lung cancer Patients' serum resistin levels were noticeably elevated (6.3 ± 1.9) ng/ml at (P = .025) than the control group (4.4 ± 0.5) ng/ml. It was stated that tissue inflammation and organ failure were linked to this increase[14]. Study by Nigro et al., [32] indicated that NSCLC patients showed significantly higher serum resistin levels than healthy volunteers and they found that resistin might be involved in the pathophysiology of weight reduction in NSCLC patients. Our results disagree with[14] when who indicated that no significant correlation between the resistin level in the lung cancer and control groups. There aren't many studies looking into the connection between resistin and cancer. Peripheral blood monocytes, macrophages and adipose tissue produce resistin in tumor tissues[13]. Lung cancer patients may have elevated resistin levels due to both adipose tissue involvement and monocyte activation as a component of the greater inflammatory process33,34. The results by Gong et al., [13] implied that resistin could increase the migration and invasion of lung adenocarcinoma cells. In the borderline regions of human lung cancer tissue, there is more resistin than in the non-cancerous portions reported by Kuo et al. [35].
These results show mean of Irisin significant increase in SCLC and NSCLC groups compared with control group. These results agree with results by Nowinska et al., [36] who indicated that the Irisin level increase in NSCLC patients (2.25 ± 0.09) ng/ml compared with in control (1 ± 0.97)ng/ml. The results by Tsiani et al., [37] consistent with our results increase Irisin levels in NSCLC tissue and in stromal fibroblasts, and they suggest that Irisin expression in stromal fibroblasts may be a separate predictor of survival for NSCLC patients as well as a possible link to enhanced cancer cell proliferation. In China, study by Shao et al., [38] found that Irisin dramatically reduced NSCLC cell proliferation at concentrations of 20–50 nM, and decreased the migration and invasiveness of NSCLC cells at values greater than 20 nM [15, 39]. Irisin is expressed in the greatest energy-demanding cells in normal bodily tissues, such as hepatocytes, cardiac muscle cells, and skeletal muscle fibers [37]. Furthermore, irisin enhances glucose absorption and is linked to glucose homeostasis. This could account for the increased production of irisin in lung cancer cells, which also have a high glucose absorption need as a result of tumor growth [39]. Many researches have observed that increased irisin expression in fibroblasts may function as an independent prognostic factor and is linked to a worse patient prognosis [37, 38]. Perhaps only lung cancer exhibits irisin expression in the malignant stromal. No other form of cancer has been shown to express irisin in the stromal cells. This may just be a feature of lung tumors[16, 37]. In tumor cells, Irisin expression levels were decreased with higher grades of malignancy and in larger tumors (T)[39].