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The aim of the study is to study the gender-age aspects of the incidence according to the materials of the Republican Oncologic Dispensary.Methods. For the observation period from 2010 to 2017 the incidence of lung cancer in men is more common – in some cities from 2 to 7 times in different age groups.Results. For the first time, lung cancer in men and women is mainly recorded in the age group of 30 – 39 years. In other age groups, no clear gender-age dependence has been identified, in addition to the upward trend in morbidity rates in persons over 40 years.Conclusion. It was found that the reduction of emissions of different groups of carcinogens in the air in Ufa and Sterlitamak led to a decrease in the incidence of respectively 9.72 and 31.17%, and an increase in emissions in Salavat and Oktyabrsky increased by 6.53 and 18.33%.

The aim of the present study was to investigate the association of COPD and frequent exacerbator COPD phenotype with CRP, CD14, and pro-inflammatory cytokines and their receptors (TNFA, LTA, TNFRSF1A, TNFRSF1B, IL1B, and IL6) genes. It was found that COPD was associated with allele A of the TNFA gene (rs1800629G>A) (P = 0.002, OR = 1.45); the association was established in the log-additive model (P = 0.0022, Pcor-FDR = 0.01705, OR = 1.47); this association was confirmed in the frequent exacerbator COPD phenotype group (P = 0.001, Pcor-FDR = 0.007, OR = 1.59). Allele G of the LTA gene (rs909253A>G) (P = 0.002, OR = 1.33) was also shown to be a marker for COPD risk; the association was established in the log-additive model (P = 0.0021, Pcor-FDR = 0.01705, OR = 1.31) and it was confirmed in patients with rare exacerbations (P = 0.003, Pcor-FDR = 0.0084, OR = 1.39). The genotype GG of the TNFRSF1B gene (rs1061622T>G) was a marker of resistance to the development of the frequent exacerbator COPD phenotype (P = 0.003, Pcor-FDR = 0.0084, OR = 0.46). The genotype CC of the CD14 gene (rs2569190T>C) was associated with higher forced expiratory volume in 1 s (P = 0.006); subjects with genotype AA of the TNFRSF1B gene (rs1061624A >G) and genotype GG of the LTA gene (rs909253A>G) exhibited lower forced expiratory volume in 1 s (P = 0.04 and P = 0.01, respectively). Genotype AA of the TNFRSF1A gene (rs767455A>G) was associated with higher smoking pack-years (P = 0.0036).

Chronic obstructive pulmonary disease (COPD) is a multifactorial chronic inflammatory disease of the respiratory system. A key phenomenon of COPD pathogenesis is inflammation. The goal of the present study was to investigate the association of COPD with alleles and genotypes of the genes that encode chemokines and chemokine receptors (CCL11, CX3CR1, CCR5, CCL5, CXCL12, CCL2, and CCL17), adhesion molecules (PECAM1 and ICAM1), and serum amyloid A1 (SAA1). It was found that COPD was associated with the C allele and the TC genotype of SAA1 (rs1136743C>T) (P = 0.0001, OR = 1.58 and P = 0.00001, OR = 2.15, respectively); this association was confirmed in the subgroups differentiated by smoking status. Markers of COPD risk were also the CG genotype of PECAM1 (rs281865545G>C) (P = 0.028, OR = 1.36) and the GG genotype of ICAM1 (rs5498A>G), which were significantly associated with the disease in smokers (P = 0.005, OR = 1.66). The AA genotype of CCL2 (rs1024611A>G) was associated with the disease in nonsmokers (P = 0.037, OR = 1.82). The GG genotype of PECAM1 (rs281865545G>C) and the AA genotype of CX3CR1 (rs3732378A>G) were associated with higher vital capacity (P = 0.014 and P = 0.04, respectively). Subjects with the GG genotype of ICAM1 (rs5498A>G) exhibited lower forced expiration volume in 1 s and lower forced vital capacity (P = 0.025 and P = 0.029, respectively).

Aim. To study the dynamics of lung cancer (LC) morbidity among the population of five cities of the Republic of Bashkortostan over the period from 2010 to 2016 and the structure of industrial emissions for grounding of adequate integral index, connected with LC morbidity and development of preventive measures to decrease malignant neoplasms. Materials and methods. The structure of gross emissions of industrial enterprises and ecologohygienic assessment of atmospheric air was conducted according to the materials of the Department of Rospotrebnadzor in Bashkortostan for 2010-2016. Lung cancer morbidity in the above mentioned territories was studied by the materials of Republican Clinical Oncological Dispensary. To estimate the influence of gross emissions on LC morbidity, modeling technique, adequate to panel analysis of spatially dynamic structural data, was applied. Results. The assessment of carcinogenic risk of atmospheric air emissions, taking into account not separate carcinogens, but their combined effect as substances with similarly directed impact, detected accurate correlation of dependence of high LC morbidity on the resultant carcinogens action. Conclusions. High LC morbidity in the cities of Bashkortostan is connected with high gross emission of carcinogens into the atmospheric air. Information on gross emissions of carcinogens and their structure can serve as an integral criterion of atmospheric pollution impact on lung cancer morbidity.

In the paper there is presented a review of foreign and literature data, documented in electronic search system PubMed regarding epidemiology, early and prenosological diagnosis, carcinogenic factors for development of malignant respiratory neoplasms, lung cancer.

Chronic obstructive pulmonary disease (COPD) is a complex chronic inflammatory disease of the respiratory system that affects primarily distal respiratory pathways and lung parenchyma. Smoking tobacco is a major risk factor for COPD. The relationship of HTR4 (rs3995090), HTR2A (rs6313), GRIK5 (rs8099939), GRIN2B (rs2268132), and CHRNB4 (rs1948) gene polymorphisms and COPD, as well as the contribution of these polymorphisms to the variations in quantitative characteristics that describe respiratory function, smoking behavior, and nicotine dependence was assessed in an ethnically homogeneous Tatar population. The polymorphisms of HTR2A (rs6313) (P = 0.026, OR = 1.42 for the CC genotype) and GRIN2B (rs2268132) (P = 0.0001, OR = 2.39 for the TT genotype) were significantly associated with increased risk of COPD. The AA genotype of GRIK5 (rs8099939) had a protective effect (P = 0.02, OR = 0.61). Importantly, the HTR2A (rs6313), GRIN2B (rs2268132), and GRIK5 (rs8099939) polymorphisms were only associated with COPD in smokers. Smoking index (pack-years) was significantly higher in carriers of the GRIK5 genotype AC (rs8099939) (P = 0.0027). The TT genotype of GRIN2B (rs2268132) was associated with COPD in subjects with high nicotine dependence according to the Fagerstrom test (P = 0.002, OR = 2.98). The TT genotype of HTR2A (rs6313) was associated with a reduced risk of the disease in the group with moderate nicotine dependence (P = 0.02, OR = 0.22). The CC genotype of HTR2A (rs6313) and the TT genotype of GRIN2B (rs2268132) were associated with higher levels of nicotine dependence according to the Fagerstrom test (P = 0.0011 and P = 0.037). Our results may provide insight into potential molecular mechanisms that involve the glutamate (GRIK5, GRIN2B) and serotonin (HTR2A) receptor genes in the pathogenesis of COPD.

Chronic obstructive pulmonary disease (COPD) is a complex chronic inflammatory disease of the respiratory system that affects primarily distal respiratory pathways and lung parenchyma. Smoking tobacco is a major risk factor for COPD. The relationship of HTR4 (rs3995090), HTR2A (rs6313), GRIK5 (rs8099939), GRIN2B (rs2268132), and CHRNB4 (rs1948) gene polymorphisms and COPD, as well as the contribution of these polymorphisms to the variations in quantitative characteristics that describe respiratory function, smoking behavior, and nicotine dependence was assessed in an ethnically homogeneous Tatar population. The polymorphisms of HTR2A (rs6313) (P = 0.026, OR = 1.42 for the CC genotype) and GRIN2B (rs2268132) (P = 0.0001, OR = 2.39 for the TT genotype) were significantly associated with increased risk of COPD. The AA genotype of GRIK5 (rs8099939) had a protective effect (P = 0.02, OR = 0.61). Importantly, the HTR2A (rs6313), GRIN2B (rs2268132), and GRIK5 (rs8099939) polymorphisms were only associated with COPD in smokers. Smoking index (pack-years) was significantly higher in carriers of the GRIK5 genotype AC (rs8099939) (P = 0.0027). The TT genotype of GRIN2B (rs2268132) was associated with COPD in subjects with high nicotine dependence according to the Fagerstrom test (P = 0.002, OR = 2.98). The TT genotype of HTR2A (rs6313) was associated with a reduced risk of the disease in the group with moderate nicotine dependence (P = 0.02, OR = 0.22). The CC genotype of HTR2A (rs6313) and the TT genotype of GRIN2B (rs2268132) were associated with higher levels of nicotine dependence according to the Fagerstrom test (P = 0.0011 and P = 0.037). Our results may provide insight into potential molecular mechanisms that involve the glutamate (GRIK5, GRIN2B) and serotonin (HTR2A) receptor genes in the pathogenesis of COPD.

Chronic obstructive pulmonary disease (COPD) is a complex chronic inflammatory disease of the respiratory system affecting primarily distal respiratory pathways and lung parenchyma. This work was designed as a case–control study aimed at investigating the association of COPD with polymorphisms in inflammatory and immune response genes (JAK1, JAK3, STAT1, STAT3, NFKB1, IL17A, ADIPOQ, ADIPOR1, etc.) in Tatar population from Russia. Ten SNPs (rs310216, rs3212780, rs12693591, rs2293152, rs28362491, rs4711998, rs1974226, rs1501299, rs266729, and rs12733285) were genotyped by the real-time polymerase chain reaction (TaqMan assays) in a case–control study (425 COPD patients and 457 in the control group, from Ufa, Russia). Logistic regression was used to detect the association of SNPs in different models. Linear regression analyses were performed to estimate the relationship between SNPs and lung function parameters and pack-years. In Tatar population, significant associations of JAK1 (rs310216) (P = 0.0002, OR 1.70 in additive model), JAK3 (rs3212780) (P = 0.001, OR 1.61 in dominant model), and IL17A (rs1974226) (P = 0.0037, OR 2.31 in recessive model) with COPD were revealed. The disease risk was higher in carriers of insertion allele of NFKB1 (rs28362491) (P = 0.045, OR 1.22). We found a significant gene-by-environment interaction of smoking status and IL17A (rs1974226) (P interact = 0.016), JAK3 (rs3212780) (P interact = 0.031), ADIPOQ (rs266729) (P interact = 0.013), and ADIPOR1 (rs12733285) (P interact = 0.018). The relationship between the rs4711998, rs1974226, rs310216, rs3212780, rs28362491, and smoking pack-years was found (P = 0.045, P = 0.004, P = 0.0005, P = 0.021, and P = 0.042). A significant genotype-dependent variation of forced vital capacity was observed for NFKB1 (rs28362491) (P = 0.017), ADIPOR1 (rs12733285) (P = 0.043), and STAT1 (rs12693591) (P = 0.048). The genotypes of STAT1 (rs12693591) (P = 0.013) and JAK1 (rs310216) (P = 0.048) were associated with forced expiratory volume in 1 s.

Polymorphisms of the CHRNA5/A3, CYP2A6, NQO1, XPC, XRCC1, CRCC3, XPD, and XPA genes were tested for association with the development and progression of chronic obstructive pulmonary disease (COPD) in ethnic Tatars. CHRNA5 (rs16969968) (P = 0.0001, OR = 2.24) and CHRNA3 (rs1051730) (P = 0.0001, OR = 2.72) polymorphisms were associated with COPD development in the recessive model. The nondeletion variant of CYP2A6 (del) was associated with COPD risk (P = 0.00001, OR = 2.77). NQO1 (rs113341), XRCC1 (rs25487), XRCC3 (rs86539), XPC (rs2228001), and XPA (rs1800975) were associated with COPD in the additive model (P = 0.000001, OR = 2.67; P = 0.00001, OR = 0.51; P = 0.0003, OR = 1.76; P = 0.0004, OR = 0.54; and P = 0.007, OR = 0.74, respectively). A gene-by-environment interaction was observed for XPA (rs1800975) and the smoking status (P interact = 0.002), and the rs16969968 and rs1051730 polymorphisms of the CHRNA3/5 gene cluster showed an association with COPD only in smokers. Carriers of the CYP2A6 deletion (CYP2A6*4) had a lower smoking index (P = 0.0019). XRCC3 (rs861539) genotype TT was characterized by lower indices of pulmonary function, including vital capacity (VC) (P = 0.0487), forced vital capacity (FVC) (P = 0.0032), and forced expiratory volume in 1 second (FEV1) (P = 0.02). FVC was found to depend on the genotype at XPA (rs1800975) (P = 0.0028).