中青年与老年非吸烟女性肺癌危险因素的比较研究

目的 分析比较中青年和老年非吸烟女性肺癌的危险因素。方法 于1992年2月～1993年12月，在上海市区完成了一项大规模全人群女性肺癌病例对照研究，共调查了非吸烟女性肺癌病例504例及人群对照601例。根据年龄把研究对象分为两组，35～54岁和55～69岁组，并分析比较两组的结果。单因素分析采用Mantel—Haenszel分层分析法，进一步调整混杂因素采用多变量logistic回归模型。结果分析结果显示，中青年组危险因素是做饭时眼和喉烟雾刺激感，最高一组比数比为3．40；其次是肺癌家族史，比数为5．80。而保护因素是饮茶(OR：0．40)和活产次数(5次及以上组OR：0．39)。老年组的危险因素主要是：高身体指数(最高一组OR：1．69)、工作场所被动吸烟史(OR：1.55)、厨房在卧室内(OR：1．50)、做饭时厨房内烟雾较多(OR：2．43)、菜油为主要食用油(OR：1.94)等。此外。肺结核病史和肺癌家族史可能增加老年女性患肺癌的危险性。保护因素是维生素C(最高一组OR：0．45)，趋势检验有统计学意义。中青年组和老年组肺癌的结果比较表明，无论是危险因素还是保护因素，两者都有不同。结论 中青年和老年非吸烟女性肺癌的病因可能存在一定的差异。     

A practical approach to pulmonary risk assessment in the radiotherapy of lung cancer

The risk of lung injury is a significant limiting factor in the use of thoracic radiotherapy for lung cancer. Given the high mortality and local failure rates in patients with unresectable lung cancer, a goal has been to increase the dose to the tumor as much as possible while trying to limit the damage to normal tissue. Efforts have been made to predict the risks for lung injury pretreatment, based on the planned dose and volume of lung treated, with mixed results. Complicating factors include performance status, underlying medical conditions, possible genetic predisposition to injury, and tumor location-associated changes in lung function. Much as a thoracic surgeon stratifies a patient's risk for pulmonary morbidity before resection, radiation oncologists should perform an assessment of patient specific factors that will impact on the potential toxicity of a given course of treatment. We present a proposed approach to the evaluation, risk assessment, and follow-up of patients treated with thoracic radiotherapy for lung cancer.     

Association of genetic polymorphisms in the base excision repair pathway with lung cancer risk: a meta-analysis

Lung cancer is a major cause of cancer-related death in the developed countries and the overall survival rate has still an extremely poor. Although cigarette smoking is the main cause of lung cancer, not all smokers develop lung cancer, and a fraction of lifelong non-smokers will die from lung cancer. Genetic host factors have recently been implicated to account for some of the observed differences in lung cancer susceptibility. Various DNA alterations can be caused by exposure to environmental and endogenous carcinogens. Most of these alterations, if not repaired, may result in genetic instability, mutagenesis and cell death. DNA repair mechanisms are important for maintaining DNA integrity and preventing carcinogenesis. Recent genetic association studies on lung cancer risk have focused on identifying effects of single nucleotide polymorphisms (SNPs) in candidate genes, among which DNA repair genes are increasingly studied. Genetic variations in DNA repair genes are thought to modulate DNA repair capacity and are suggested to be related to lung cancer risk. We identified a sufficient number of epidemiologic studies on lung cancer to conduct a meta-analysis for genetic polymorphisms in nucleotide base repair (BER) pathway, focusing on 8-oxoguanine DNA glycosylase 1, X-ray cross-complementing group 1 (XRCC1) and apurinic/apyrimidinic endonuclease 1. The 399Gln/Gln genotype of the XRCC1 Arg399Gln polymorphism was associated with an increased risk of lung cancer among Asians (OR=1.34, 95% CI=1.16-1.54) but not among Caucasians. Little evidence of associations has been found between other BER genes and lung cancer risk. Considering the data available, it can be conjectured that if there is any risk association between single SNP and lung cancer, this risk increase/decrease will probably be minimal. Advances in identification of new polymorphisms and in high-throughput genotyping techniques will facilitate analysis of multiple genes in multiple DNA repair pathways. Therefore, it is likely that the defining feature of future epidemiologic studies will be the simultaneous analysis of large samples of cases and controls.     

宣威肺癌遗传因素作用大小的估算与分析

目的 探讨肺癌的遗传方式,估算肺癌肺癌发病过程中遗传因素作用的大小,以期进一步完善宣威肺癌的病因学研究。方法 利用遗传流行病学的理论与方法,选择了370例肺癌先证者,同时以每位肺癌先证者的配偶为对照且形成对照组。结果 肺癌的分离比为0．15,肺癌的遗传度为24．6％,其中男性为14．6％,女性为37．8％。结论 遗传因素与肺癌的发病密切相关,是肺癌的重要危险因素。肺癌遗传属多基因遗传。遗传因素在女性产生肺癌的过程中作用较大;但不论是男性还是女性发生肺癌,遗传因素都不是宣威肺癌高发的主要危险因素。     

中国人群肺癌、肝癌、乳腺癌危险因素的综合研究

[目的]探讨目前我国人群肺癌、肝癌和乳腺癌发生的主要危险因素，为预防决策提供依据。[方法]利用综合分析方法估计我国人群三种肿瘤的主要危险因素的相对危险度及人群归因危险度百分比。[结果]三种肿瘤的主要危险因素分别为，肺癌包括精神因素、室内环境污染、香烟烟雾、遗传因素和饮食中蔬菜水果的摄入少；乳腺癌包括女性生育和生理因素、疾病史、生活精神刺激、家庭史、体重；肝癌包括病毒感染、家庭肝癌史、摄入黄曲霉毒素污染食物、饮水污染和心理因素。[结论]在影响三种肿瘤发生的因素中，除了各自的特点外，其共同的因素如相应系统疾病史、精神因素等应引起重视。     

武汉市城区居民肺癌危险因素研究

 目的 探讨武汉市肺癌主要危险因素,为采取切实可行的防治措施提供依据。方法 采用病例对照研究方法,收集370例肺癌病例和符合条件的对照740例进行问卷调查,应用条件Logistic回归分析方法进行单因素和多因素的分析,并计算每个危险因素的PAR%。结果 武汉市城区肺癌主要危险因素有室内化学物污染、吸烟、被动吸烟、精神压抑、肺部疾患史、新鲜蔬菜和水果摄入少等。男性肺癌归因于吸烟的比例为最高;女性肺癌主要归因于新鲜蔬菜摄入少、体重指数、体育锻炼、厨房油烟。结论精神压抑、室内化学物污染、吸烟、被动吸烟、新鲜蔬菜摄入少、呼吸系统疾病史、厨房油烟等因素可以解释武汉市城区90%左右的肺癌发病。而吃蔬菜较多、参加体育锻炼、心理健康等为肺癌发病的保护因素。     

我国肺癌流行现状及其预防对策

文章描述了当前我国肺癌发病和死亡现状及其主要危险因素,强调了肺癌是可以预防和控制的,提出了我国肺癌的流行趋势与预防要点.     

Lung cancer risk in never-smokers: An overview of environmental and genetic factors

Lung cancer is the leading cause of cancer-related mortality globally, accounting for 1.8 million deaths in 2020. While the vast majority are caused by tobacco smoking, 15%−25% of all lung cancer cases occur in lifelong never-smokers. The International Agency for Research on Cancer (IARC) has classified multiple agents with sufficient evidence for lung carcinogenesis in humans, which include tobacco smoking, as well as several environmental exposures such as radon, second-hand tobacco smoke, outdoor air pollution, household combustion of coal and several occupational hazards. However, the IARC evaluation had not been stratified based on smoking status, and notably lung cancer in never-smokers (LCINS) has different epidemiological, clinicopathologic and molecular characteristics from lung cancer in ever-smokers. Among several risk factors proposed for the development of LCINS, environmental factors have the most available evidence for their association with LCINS and their roles cannot be overemphasized. Additionally, while initial genetic studies largely focused on lung cancer as a whole, recent studies have also identified genetic risk factors for LCINS. This article presents an overview of several environmental factors associated with LCINS, and some of the emerging evidence for genetic factors associated with LCINS. An increased understanding of the risk factors associated with LCINS not only helps to evaluate a never-smoker’s personal risk for lung cancer, but also has important public health implications for the prevention and early detection of the disease. Conclusive evidence on causal associations could inform longer-term policy reform in a range of areas including occupational health and safety, urban design, energy use and particle emissions, and the importance of considering the impacts of second-hand smoke in tobacco control policy.     

肺癌静脉血栓栓塞的危险因素及生物标志物的研究进展

癌症是引起静脉血栓栓塞(venous thromboembolism,VTE)的重要危险因素,而VTE是引起肿瘤患者死亡的重要原因。肺癌患者VTE的发生率在不同的研究中结果有所差别,发生率从7%~13%不等,其中还包括大量可疑肺栓塞病例。肺癌患者VTE发生的危险因素可以分为三类:患者自身特征、肿瘤相关因素以及治疗相关的因素。此外,许多生物标志物也被发现可以作为VTE发生的危险因素(例如D-二聚体)。了解肺癌VTE发生的危险因素对于预防血栓并发症的发生、改善肺癌患者的治疗方面具有重要的意义。本文就VTE危险因素及生物标志物进行综述。     

大厂锡矿肺癌高发原因的条件Logistic回归分析

An increased risk of lung cancer in Dachang Tin Mine of Guangxi has been reported. To investigate the factors of the excessive risk of lung cancer, the authors conducted a matched pair case-control study in the mine area and analysed the effect of multiple factors, such as condition of living and housing, occupational exposure and smoking by statistical method of conditional logistic regression. The patients group consisted of 69 patients with primary bronchogenic cancer including 55 deceased. The control group consisted of 138 persons also including 55 deceased. The results showed that the factors of the excessive risk of lung cancer in the mine area were mainly related to the occupational exposure. The risk factors with statistical significance in conditional logistic regression analysis were exposure time of smelting, time of underground drilling, and age of beginning mining underground. In the study model of all cases matched against living controls, daily number of cigarette also was a risk factor besides the above three factors. Furthermore, there was a synergic action among the factors. The relationship between the risk factors and lung cancer is discussed.     

Molecular epidemiology to better predict lung cancer risk

Although it is clear that smoking causes lung cancer, it is not known why some smokers develop the disease while others do not. Little is also known regarding risk factors for lung cancer among never-smokers, particularly women, or why women with lung cancer are more likely to have a family history of cancer, to be diagnosed at a young age, or to have adenocarcinoma. The application of molecular epidemiology to the study of lung cancer risk might facilitate elucidation of these questions. In this review, the molecular epidemiology of lung cancer is discussed, with an emphasis on studies of genetic variability in metabolic pathways as a means for determining susceptibility. Work that has assessed intermediate markers of risk, such as DNA adducts, is also presented, as are studies of tumor tissue alterations, such as mutations and DNA methylation, in relation to risk of lung cancer. Finally, approaches to evaluating factors that might explain the differing epidemiology of lung cancer between men and women are also presented. It is likely that, by incorporating biomarkers of susceptibility, exposure, and effect, molecular epidemiologic approaches might better define factors that explain some of the variability in lung cancer risk.     

肺癌患者合并肺部真菌感染的临床分析

目的 分析肺癌患者并发肺部真菌感染的影响因素及临床特点,以有效预防和控制感染。方法收集新疆肿瘤医院2007年1月~12月出院的872例肺癌患者的临床资料,对其中合并肺部真菌感染的87例资料总结,分析真菌感染的影响因素及真菌种类特点。结果 872例肺癌患者中,肺部真菌感染87例,感染发生率9.9%。真菌类型主要为念珠菌菌属（96.6%）,其中白色念珠菌（81%）为主要菌种,主要影响因素有年龄≥50岁,Ⅲ～Ⅳ期的中晚期肺癌患者、住院时间≥14天、化疗、放疗,侵袭性操作、白细胞减少≥Ⅲ度,长时间使用抗生素及激素(P＜0.05)。而患者的性别,肺癌的病理分型,是否行手术治疗与肺部真菌感染无关(P＞0.05)。结论 减少易感因素,及时治疗是降低肺癌患者真菌感染的有效措施。     

Relationships of TP53 codon 72 and HRAS1 polymorphisms with lung cancer risk in an ethnically diverse population.

Tobacco smoking is a strong cause of lung cancer. However, because only a small proportion of smokers develop the disease, other factors, including genetic susceptibility, may be important in determining lung cancer risk. Polymorphisms in the TP53 tumor suppressor gene and HRAS1 proto-oncogene have been associated in some studies with this cancer; we sought to replicate these associations in an ethnically diverse population in Hawaii. We conducted a population-based case-control study among 334 incident lung cancer cases and 446 controls of Caucasian, Japanese, or Native Hawaiian origin. In-person interviews collected detailed information on lifestyle risk factors. DNA was extracted from peripheral blood leukocytes, and genotyping was performed using a PCR-based assay for the TP53 codon 72 polymorphism and Southern blot analysis and PCR for allelic polymorphisms in the HRAS1 minisatellite. Logistic regression analyses were used to compute odds ratios (ORs) and 95% confidence intervals (CIs) adjusting for smoking and other risk factors. The presence of two rare HRAS1 alleles was associated with a 2.2-fold (95% CI, 1.0-5.0) increased lung cancer risk for all ethnic groups combined. The association was present in Native Hawaiians (OR, 5.2; 95% CI, 1.1-24.4) and was suggested for Japanese (OR, 2.8; 95% CI, 0.6-12.5); no association was observed in Caucasians (OR, 0.8; 95% CI, 0.2-3.6). This association was also observed for each lung cancer cell type. The presence of only one rare allele did not increase risk for any ethnic group or cell type. No significant association was found between the TP53 codon 72 polymorphism and lung cancer [OR, 1.4 (95% CI, 0.8-2.4) for the Pro/Pro genotype compared with the Arg/Arg genotype]. This study suggests that the presence of two rare HRAS1 alleles confers an increased lung cancer risk in Native Hawaiians and Japanese but possibly not in Caucasians. The amino acid replacement of arginine by proline at codon 72 of TP53 appears not to be important in determining lung cancer risk in this population.     

Gender and lung cancer.

Although lung cancer is the leading cause of cancer death among men and women in the United States, female smokers appear to be at increased risk. After controlling for the number of cigarettes smoked, female sex imparts a significant, independent risk for most histologic types of lung cancer. Cigarette smoking, genetics, and endocrine factors may interact to contribute to the disparity in lung cancer risk between the sexes. Estrogens have direct and indirect actions in the lung, and estrogen has been implicated in lung carcinogenesis in female smokers. This review of the literature will focus on endocrine factors and tobacco carcinogens as risk factors for lung cancer in women.     

Relationship between ERCC2 Polymorphism and Risk of Lung Cancer in Chinese Nonsmoker

Objective: Excision repair cross-complimentary group 2 (ERCC2) is one of the important DNA repair genes. ERCC2 codon 751 polymorphism has been shown to modulate cancer risk. We therefore assessed the relationship between the ERCC2 polymorphism and the susceptibility to lung cancer in nonsmoking females via a hospital-based case-control study. Methods: There were 105 lung cancer cases and matched healthy controls in this study. Information concerning demographic and risk factors was obtained, each person donated 2 ml blood for biomarker testing. ERCC2 genotypes were determined by PCR-RFLP method. All of the statistical analyses were performed with SPSS (v 12.0). Results: All of the subjects in this study were nonsmoking females in Shenyang. There was significant difference between the frequencies of ERCC2 polymorphism in cancer cases and controls (P<0.05). The frequencies of ERCC2 751 Gln allele were 6.2% in controls and 13.8% in cancer cases. The individuals with Lys/Gln Gln/Gln combined genotype were at an increased risk for lung cancer as compared with those carrying the Lys/Lys genotype (adjusted OR=2.80, 95%=CI 1.21?6.48). We analyzed the environmental risk factors for lung cancer in nonsmoking females. The cancer patients showed a higher prevalence of exposure to cooking fumes compared with controls (OR=2.44, P<0.05). Furthermore, an interaction between exposure to cooking fumes and the variant ERCC2 751 Gln allele on the risk of lung cancer was observed. Individuals with both risk genotype and exposure to cooking fumes had a higher risk of cancer than those with only one of them. Conclusion: The above findings indicate that the genetic polymorphism in the ERCC2 codon 751 is associated with the risk of lung cancer in nonsmoking females.     

Lung cancer risk in Venice: a population-based case-control study.

Populations resident in the historical town of Venice and in the inland industrial city of Mestre are at different risk of exposure to environmental pollutants. This case-control study compares the risk of developing lung cancer in the two populations in relation to known risk factors for this neoplasm. A retrospective study of 305 incident cases of lung and 447 frequency-matched population controls was conducted through a standard questionnaire on main risk factors for lung cancer. Completeness of cases was checked against the Venetian Cancer Registry files. The results indicate that lung cancer risk associated with tobacco smoking was high in both areas, although more elevated in Venice islands among heavy smokers. An elevation of risk was associated with housing without a heating system, possibly suggesting a role of worse hygienic conditions. An increased risk associated with exposure to occupational carcinogens was detected in the inland area. In conclusion, lung cancer risk due to tobacco smoking largely affects both the populations, while other risks such as occupation or housing conditions appear to be more population-specific.     

Nutrition Habits,Physical Activity,and Lung Cancer: An Authoritative Review

Lung cancer is the leading cause of cancer death worldwide. Because of high incidence rates and low survival rates, it is important to study the risk factors that may help prevent the disease from developing. It has been well established that cigarette smoking is the most important risk factor for lung cancer. Nonetheless it is likely that there are other modifiable risk factors that would assist in the prevention of lung cancer. Research on factors such as nutrition and physical activity and their influence on lung cancer has been carried out for nearly 3 decades. A systematic review in the MEDLINE database of published studies was conducted, focusing on systematic reviews, meta-analyses, and large prospective studies. The association between physical activity and lung cancer has been conflicting. Among the researched studies, 10 showed an inverse association, whereas 11 reported no association. A meta-analysis that was conducted from 1996 to October 2003 showed that leisure physical activity (LPA) prevents lung cancer. Data from 11 cohort and case-control studies showed an inverse relationship between fruit and vegetable consumption and lung cancer. Evidence from case-control studies suggests a positive association between meat intake and risk of lung cancer, although several more recent studies have presented doubts about these findings. The possible association of physical activity, nutrition, and the risk of lung cancer development remains controversial. Further prospective studies should be conducted to determine the potential influence of these 2 risk factors.     

腹腔镜下根治性胃癌切除术后并发肺炎的危险因素分析

目的:探究腹腔镜下根治性胃癌切除术后并发肺炎的危险因素。方法:收集2017年9月1日至2019年5月1日期间在我院行腹腔镜下根治性胃癌切除术的患者。详细统计所有患者入院后一般资料、病理资料、手术及术后相关资料，将出现肺部感染患者与未出现肺部感染患者分为两组，先通过单因素分析得出影响腹腔镜下根治胃癌切除术后患者肺部感染的危险因素。进一步将有意义的因素纳入多因素分析，得出患者的独立危险因素。结果:本研究共纳入319例患者，其中术后发生肺部感染患者有13例。单因素分析提示术前是否合并有糖尿病、术前是否有肺部疾病、是否有肺功能不全、是否有术前低蛋白血症或者贫血、手术方式、手术时间、是否入住ICU治疗、是否有术后护理协助患者排痰为术后并发肺部感染的危险因素。多因素分析发现术前是否合并有糖尿病、既往是否有肺部疾病病史、手术时间为腹腔镜下根治性胃癌切除术后并发肺部感染的独立危险因素。且术后并发肺部感染与不良预后相关。结论:胃癌术后并发肺部感染的危险因素存在于围术期每个环节，医护人员需从多个角度出发，积极干预，预防术后并发肺部感染的可能。     

Previous pulmonary disease and family cancer history increase the risk of lung cancer among Hong Kong women

Chinese women in Hong Kong have among the highest incidence and mortality of lung cancer in the world, in spite of a low prevalence of smoking. We carried out this population-based case–control study to evaluate the associations of previous lung disease and family cancer history with the occurrence of lung cancer among them. We selected 212 cases that were newly diagnosed with primary lung cancer, and randomly sampled 292 controls from the community, frequency matched by age group. All the cases and controls were lifetime nonsmokers. We estimated the main effects of preexisting asthma, pulmonary tuberculosis, pneumonia, chronic bronchitis, and family lung/all cancer history, using unconditional logistic regression, accounting for various potential risk factors and confounders. All of the previous lung diseases, except chronic bronchitis, were related to an elevated risk for lung cancer, and the association with asthma was significant. Those who had more than one previous lung disease tended to be at higher risk than those with only one of them. Positive family history of any cancer was associated with over 2-fold risk than negative family history. The joint effect of positive history of previous pulmonary diseases and positive family cancer history appeared to be additive, indicating the two factors acted independently. The results support an etiological link of preexisting lung disease and family cancer history to the risk of lung cancer.     

人口老龄化对重庆市肺癌发病影响的定量分析

[目的]了解重庆市肺癌发病变化人口老龄化与其他危险因素的贡献率,为制定肺癌的防治策略提供依据.[方法]收集整理2006～2015年重庆市11个肿瘤登记点ICD-10编码为C33、C34的所有气管、支气管、肺癌的个案资料.计算粗发病率、中国人口标化发病率(中标率)、年度变化百分比.发病率趋势变化的比较采用曲线估计指数分布回归模型进行判别.利用恶性肿瘤发病率差别分解法计算出人口老龄化和其他危险因素对2006年与2015年肺癌发病变化的贡献值与贡献率.[结果]重庆市肺癌发病率由2006年的37.52/10万上升至2015年的68.17/10万,APC为5.23％,变化趋势差异有统计学意义(F=31.14,P=0.001).中标率由2006年的32.86/10万上升至2015年的41.04/10万,变化趋势差异无统计学意义(F=1.75,P=0.223).男、女性以及农村地区肺癌发病率均呈上升的趋势,APC分别为5.23％、5.02％、7.04％,变化趋势差异均有统计学意义(F值分别为27.25、17.57、61.64,P均＜0.05).2006年与2015年肺癌发病率变化中人口老龄化与其他危险因素的贡献率分别为65.50％与34.50％,男性人口老龄化的贡献率(83.58％)高于其他危险因素(16.42％),女性肺癌发病率的变化其他危险因素的贡献率(56.63％)高于人口老龄化的贡献率(43.37％),城市与农村人口老龄化的贡献率(55.44％、69.83％)均高于其他危险因素的贡献率(44.56％、30.17％).[结论]重庆市肺癌发病率高并呈持续上升的趋势,肺癌发病率上升受人口老龄化与其他危险因素的协同作用,但人口老龄化是主要因素.