青岛市563例肺癌患者高危险因素的回顾性研究

目的筛查青岛地区肺癌高危险因素,以指导青岛地区人群进行肺癌综合预防工作。方法563例已确诊为原发性肺癌的患者作为病例组,按照1：1配对的方法,选择我院与病例组近亲属的同性别、同年龄的外伤患者作为健康对照组。所有病例均调查其发病前可能的危险因素,对于研究的项目,采用单因素条件Logistic回归分析和多因素条件Logistic回归分析,最终进入模型的项目为肺癌发病的独立危险因素或保护因素。结果单因素条件Logistic回归分析结果显示,共筛选出19项因素有统计学意义,最终进入模型有统计学意义的因素共6项,其中家族史、吸烟、生活应激强度大（5年内）、吃熟肉制品和抑郁等是肺癌发病的危险因素,而运动是肺癌发生的保护性因素。结论家族史、吸烟、生活应激强度大（5年内）、吃熟肉制品和抑郁等可引起青岛市人群肺癌发病增加,运动可以减少肺癌的发病风险。     

肺癌多阶段发病过程中的分子机制简述

肺癌是影响人类生存的重大疾病之一。全世界每年死于肺癌的患者约有110多万，占到了癌症死亡总数的17．8％。肺癌的发病过程是一个集遗传、环境及生活习惯等多因素于一体的复杂过程，但其确切机制仍不清楚，因此对其发病机制的探讨具有重要意义。     

被“气”出来的病——肺癌

导致肺癌发病的首要因素依然是吸烟,包括一手烟、二手烟和三手烟。其次,人口老龄化、空气污染、室内小环境污染、环境和职业致癌因素,以及性格心理因素等也是肺癌发病的重要相关因素。可以讲,肺癌就是一种＂被气出来的人造疾病＂。     

女性肺癌的临床特征及治疗策略

肺癌是全球恶性肿瘤死亡的首要原因，在我国，肺癌是男性和女性癌症死亡的第一原因。肺癌的发生是一个复杂的过程，涉及遗传、环境等多种因素，约90％的肺癌可能由吸烟引起。由于女性肺癌有其独特的分子表达谱、组织病理学及激素代谢特征，因此被认为是独立于男性肺癌的疾病。本文综述了女性肺癌的主要发病危险因素、临床特点及治疗策略。     

肺癌与大气污染关系的流行病学研究进展

随着我国肺癌负担的不断增加,对其危险因素的探讨显得十分迫切.环境污染,尤其室外空气污染可能在肺癌的发病和死亡过程中起重要作用.本文收集最近10年国内外相关文献,筛选出关于肺癌和室外空气污染的流行病学研究,并归纳不同地区主要的室外空气污染物对肺癌发病和死亡的影响,罗列出如气象因素、社会经济学状况、吸烟、职业等可能的混杂因素,为未来的相关研究提供信息.     

姜堰市男性肺癌危险因素的病例对照研究

目的 研究姜堰市男性肺癌危险因素,为肺癌的预防监测提供依据。方法 1999年8月-2000年6月间,对181例年龄范围在24-86岁肺癌生存病例进行问卷调查。按1：1配对,调查内容包括一般情况,居住环境、生活习惯、饮食嗜好、既往疾病及家族史等方面110个问题,采用比值比来估计各危险因素与肺癌的联系强度,用Logistic回归模型做单因素和多因素分析,筛选出专业上有意义的肺癌危险因素。结果 与肺癌发病有关的变量4个,分别为吸烟,呼吸系统疾病史、精神因素、饮酒,保护因素为良好的体质指数等,结论 吸烟、呼吸系统疾病、精神压抑、饮酒是具有统计学意义的肺癌危险因素,良好的体质指数是肺癌的保护因素。     

姜堰市男性肺癌危险因素的病例对照研究

目的　研究姜堰市男性肺癌危险因素 ,为肺癌的预防监测提供依据。方法　 1999年 8月～ 2 0 0 0年 6月间 ,对 181例年龄范围在 2 4～ 86岁肺癌生存病例进行问卷调查。按 1∶1配对 ,调查内容包括一般情况、居住环境、生活习惯、饮食嗜好、既往疾病及家族史等方面 110个问题。采用比值比来估计各危险因素与肺癌的联系强度 ,用Logistic回归模型做单因素和多因素分析 ,筛选出专业上有意义的肺癌危险因素。结果　与肺癌发病有关的变量 4个 ,分别为吸烟、呼吸系统疾病史、精神因素、饮酒。保护因素为良好的体质指数等。结论　吸烟、呼吸系统疾病、精神压抑、饮酒是具有统计学意义的肺癌危险因素 ,良好的体质指数是肺癌的保护因素。     

女性肺癌249例临床分析

目的 探讨女性肺癌的病因和病理类型的构成比和遗传因素对其的影响.方法 收集病理确诊的女性肺癌249例临床资料,从病因、病理类型、家族史及好发部位进行分析.结果 女性肺癌的致病因素与厨房油烟、大气污染及被动吸烟有密切关系.结论 女性肺癌的临床特点为发病年龄早,就诊时病期晚,转移快,预后差.病理类型以腺癌多见,周围型肺癌居多,肺下叶居多,与遗传因素有关.     

胃癌主要诱因就在“吃”

胃癌是我国的常见恶性肿瘤,其发病率仅次于肺癌,排在我国十大恶性肿瘤第二位。胃癌发病原因不明,可能与多种因素有关,如生活习惯、饮食种类、环境因素、遗传素质和精神因素等。根据流行病学资料可见,胃癌是可以在饮食上进行预防的肿瘤,只要养成健康的饮食习惯,避免进食有害食物,就有可能降低胃癌的发生。     

广州市男性肺癌危险因素的病例对照研究

目的：研究广州市肺癌危险因素,为进一步的肺癌危险因素监测提供依据。方法：１９９７ 年１６ 月采用问卷调查,对２５８ 例年龄范围在３０７４ 岁肺癌生存病例,按１ ∶１ 配对,调查了包括一般情况、生活居住环境、饮食习惯、生活方式、疾病及家族史等５ 个方面３５ 项１７３ 个问题。用相对危险度的近似估计值比值比来估计各危险因素与肺癌的联系强度,用Ｌｏｇｉｓｔｉｃ 回归模型做单因素和多因素分析筛选出专业上有意义的肺癌危险因素。结果：与肺癌发病有关的主要变量４ 个,分别为吸烟、精神压抑、呼吸系统疾病史、１０ 年前以煤为生活燃料。保护因素为体育锻炼、１０ 年前肉类月均消耗量高、１０ 年前动物油月均消耗量高、１０ 年前住房为木地板、喜欢酸性食品、良好的体质指数等６ 个因素。结论：吸烟和精神压抑是具有统计学意义的肺癌危险因素,良好的体质指数是肺癌的保护因素。     

非吸烟人群肺癌危险因素的病例对照研究

目的探讨中国非吸烟人群肺癌的危险因素,为防癌措施提供依据。方法采用病例对照研究的方法,按频数匹配收集非吸烟肺癌新发病例306例及非吸烟对照306例,利用统一编制的调查表对调查对象进行面访,收集病例和对照危险因素的暴露史等。结果单因素分析发现25个因素与非吸烟人群肺癌的发病有关联;多因素分析后发现：非吸烟人群肺癌发病的危险因素是体重指数(body mass index,BMI)＜18.5,居住地周围有污染企业、装修刺激性气味、家庭被动吸烟、工作场所被动吸烟、使用农药、性格内向、食用油炸食品、肺部手术史、癌症家族史,而保护因素是BMI≥24、常吃蛋类、常吃水果、饮茶、常以散步作为锻炼(2年前),经广义多因子降维法（GWDR）拟合的最优的交互作用模型是居住地企业+装修刺激性气味+家庭被动吸烟+工作场所被动吸烟+农药接触史+癌症家族史。结论非吸烟者发生肺癌的影响因素较多,仍需进一步识别。     

Patterns of allelic loss differ in lung adenocarcinomas of smokers and nonsmokers

Cigarette smoking is the most important cause of lung cancer, however approximately 10% of patients with lung cancer have no history of smoking. While the molecular pathogenesis of smoking associated lung carcinogenesis is becoming well characterized, the pathogenesis of lung cancer in nonsmokers is not. We designed a study to examine the pathogenesis of adenocarcinoma in nonsmokers by determining if loss of heterozygosity (LOH) in tumors of nonsmokers differs from those of smokers. We evaluated six cases of primary adenocarcinoma in never smokers and six selected cases in smokers, matched by clinical and histological criteria. LOH in tumor DNA relative to nonmalignant lung DNA was determined at 52 microsatellites located on ten chromosomal loci. The extent of allelic loss in smokers, as measured by fractional allelic loss (FAL), was compared with nonsmokers. LOH was more frequent in the tumors of nonsmokers than of smokers with mean FAL of 46% in nonsmokers and 28% in smokers (P<0.05). Increased LOH in nonsmokers was most pronounced at chromosomes: 3p, 8p, 9p, 10p, and 18q. Since this study compared allelic loss between lung and tumor-bearing lung, less frequent LOH in smokers' tumors can be interpreted to suggest LOH was already present in the nonmalignant lung of smokers and fewer additional instances of allelic loss were present in the tumors of smokers. Our results suggest that the early steps of lung carcinogenesis differ in nonsmokers compared with smokers. In addition, the chromosomal sites of LOH may identify genes important for lung carcinogenesis in nonsmokers.     

Diet, reproductive factors and lung cancer risk among Chinese women in Singapore: evidence for a protective effect of soy in nonsmokers.

The factors associated with risk of lung cancer among nonsmokers have not been fully elucidated, but dietary factors have consistently been shown to play a role. Chinese women are unique in having a high incidence of lung cancer despite a low smoking prevalence. This population is also known to have a high intake of soy, a dietary source of phytoestrogens. We conducted a hospital-based case-control study among Singapore Chinese women, comprising 303 cases and 765 age-matched controls, of whom 176 cases and 663 controls were lifetime nonsmokers. Data on demographic background, reproductive factors and dietary intake of fruit, vegetables and soy foods were obtained by in-person interview. We observed an inverse association between intake of total, cruciferous and non-cruciferous vegetables and risk of lung cancer among smokers. Although smokers in the highest tertile of fruit intake also had a lower risk, this was not statistically significant. Higher intake of soy foods significantly reduced risk of lung cancer among lifetime nonsmokers, but not among smokers. When soy isoflavonoid intake in mg/week was computed based on frequency and portion size of intake of eight common local soy foods, the adjusted OR among nonsmokers for the highest tertile compared to the lowest was 0.56, 95% CI 0.37-0.85 (p for trend <0.01). Fruit intake was also significantly associated with reduced lung cancer risk among nonsmokers, but the effect was not significant after adjustment for soy intake. On the other hand, soy intake remained an independent predictor of risk after controlling for fruit intake. Reproductive effects were also primarily confined to lifetime nonsmokers, among whom having 3 or more livebirths (adjusted OR 0.65, 0.44-0.96) and a menstrual cycle length of more than 30 days (OR 0.46, 0.25-0.84) accorded a significantly reduced risk of lung cancer. Place of birth was significantly associated with risk among nonsmokers (OR 2.6, 1.7-3.9 for China-born vs. local born) but not among smokers. When analysis was restricted to nonsmokers with adenocarcinomas, the dietary effects were consistent or enhanced. On stepwise regression, soy intake and cycle length emerged as the independent dietary and reproductive predictors of lung cancer risk in nonsmokers. These findings are consistent with other evidence suggesting an involvement of estrogen-related pathways in lung cancer among non-smoking women.     

CEA levels in serum and BAL in patients suffering from lung cancer

Background Carcinoembryonic antigen (CEA) is a tumor marker belonging to the immunoglobulin gene superfamily of adhesion molecules. CEA is synthesized by epithelial and tumor cells. In this study, CEA levels in sera and bronchoalveolar lavage fluid (BAL) were measured in patients with malignant lung cancer and benign lung diseases. Methods In the present study CEA was measured in serum using IRMA methods and in bronchoalveolar lavage of individuals undergoing fiberoptic bronchoscopy. Fifty patients with lung cancer (G1), 20 patients with benign lung lesions (G2), and a control group consisted of 20 individuals (G3) were enrolled in the study. Results We found that serum CEA levels were significantly higher in G1 compared to G2 and G3 (p < 0.01). No significant difference in serum CEA levels was found between smokers and nonsmokers in any of the three groups studied. CEA was significantly higher in G1 BAL (p < 0.05) compared to G2 and G3 BAL. Furthermore, a statistically significant difference was found in CEA levels in BAL between smokers and nonsmokers of G2. Conclusions CEA levels in BAL of normal individuals may be influenced by smoking and other factors that affect lung epithelial cell function. Thus, CEA measurement in BAL alone has little value in the diagnosis of malignancy. BAL CEA levels in smokers of G2 are found significantly higher compared with nonsmokers of the same group and healthy individuals. Smokers of G2 have to be followed up carefully for the possibility of lung cancer growth.     

美国吸烟者与非吸烟者肺癌流行病学概况

人们已清楚知道，吸烟是肺癌的主要危险因素，也知道吸烟和职业暴露以外的因素在某些肺癌特别是腺癌中起作用。本文以医院病例为基础进行大样本的病冽对照研究来分析肺癌与吸烟因素（吸烟量，过滤咀烟，黑白人种的吸烟习惯）及非吸烟因素（ＥＴＳ暴露，原发性肿瘤和治疗，生殖和内分泌因素，躯体指数）的联系。虽然吸烟与所有主要细胞类型的肺癌都有剂量－效应关系，但与腺癌的联系强度较弱，提示吸烟以外的因素对腺癌的重要性。在白人和黑人中，无论男、女，肺癌的ＯＲ值均随香烟焦油摄入量的增加而增加，并随戒烟年限的延长而减少。是否吸含薄荷香烟，对肺癌的危险性影响不大。未见到ＥＴＳ与肺癌的联系，即使丈夫吸烟也未能使不吸烟妻子患肺癌的危险性增加。生殖系统原发性肿瘤和放射治疗，可使不吸烟女性患肺癌的危险性增加４倍。曾观察到身体瘦弱与现在吸烟、以前吸烟和从不吸烟的女性肺癌之间的联系。以上结果在本文中分别加以讨论。总的来说，人群中肺癌患病率的不同，可能由于：（１）香烟烟雾中的致癌物不同；（２）香烟烟雾的作用因素不同，包括受到机体敏感性及对致癌物的代谢的影响；（３）暴露于吸烟以外的其他各种危险因素     

Oxidative DNA damage and antioxidant vitamin level: comparison among lung cancer patients, healthy smokers and nonsmokers

In the present study, we examined whether the level of 8-oxo-7,8-dihydro-2'-deoxyguanosine (8-oxodGuo) in leukocyte DNA is higher in lung cancer patients compared to controls. Factors that may influence oxidative stress, such as antioxidant vitamins, were also determined. These parameters were analyzed in 4 groups of subjects: smokers with lung cancer, ex-smokers with lung cancer, healthy smokers with comparable smoking status and healthy nonsmokers. The 8-oxodGuo mean level in leukocytes of lung cancer patients reached values of 9.22/10(6) dGuo molecules (smokers) and 11.16/10(6) dGuo molecules (ex-smokers). These values were significantly higher than in DNA of healthy smokers and nonsmokers, where mean levels reached 6.99/10(6) dGuo molecules and 5.98/10(6) dGuo molecules, respectively. Mean levels of vitamin C in the plasma of controls and lung cancer patients were 56.17 microM (nonsmokers), 26.34 microM (healthy smokers), 23.83 microM (cancer patients, smokers) and 29.19 microM (cancer patients, ex-smokers). The difference between nonsmokers and the 3 other groups was statistically significant. Vitamin E level was significantly reduced in the plasma of cancer patients (smokers 19.94 microM, ex-smokers 19.59 microM) compared to healthy smokers (28.93 microM). No changes in vitamin A concentration were found. Our results suggest that a high level of 8-oxodGuo in leukocyte DNA and a low concentration of vitamin E in the blood may predict lung cancer risk. However, it is also possible that these phenomena may simply result from disease development.     

Familial lung cancer and aggregation of smoking habits: a simulation of the effect of shared environmental factors on the familial risk of cancer.

BACKGROUND: Tobacco smoking is the principal cause of lung cancer. The risk of lung cancer in the offspring of lung cancer patients is about twice higher than the risk in the general population. The present study investigated the contribution of shared smoking habits to the familial clustering of lung cancer. METHODS: We estimated the relative risk of lung cancer attributable to smoking according to the extent to which smokers transmit their smoking habits to the offspring (heritability of smoking), the prevalence of smoking in the general population, and the risk of lung cancer for smokers compared with nonsmokers. FINDINGS: The relative risk of lung cancer for the offspring of lung cancer patients attributable to smoking was 1.19 when published data on smoking practice were modeled (i.e., assuming that the heritability of smoking was 0.5, the smoking prevalence 40%, and the odds ratio of lung cancer for smokers versus nonsmokers was 20). INTERPRETATION: Most familial cases of lung cancer cannot be attributed to shared smoking habits. The example of smoking can be used for other familial cancers, for which no strong environmental risk factors are usually known, to infer the primary role for heritable genes.     

A study on chronologic change of the relationship between cigarette smoking and lung cancer based on autopsy diagnosis

Human cases autopsied at the Department of Pathology, University of Tokyo, were studied to investigate the chronologic changes in the relationship between cigarette smoking and lung cancer occurrence. The results obtained were as follows: (1) it was confirmed that the incidence of lung cancer was significantly higher among cigarette smokers than among nonsmokers, and that there was a definite dose-response relationship between the quantity of cigarettes smoked and the occurrence of lung cancer; and (2) over the time span studied, the incidence of lung cancer among autopsies showed a remarkable increase. However, this tendency was seen in both cigarette smokers and nonsmokers, and in fact, the increase was comparatively higher in the latter group. It should be stressed that the relative importance of cigarette smoking in human pulmonary carcinogenesis seems to have decreased in the past 40 years or so, and factors other than cigarette smoking seems to have become more important.     

Dose-response relationship between cooking fumes exposures and lung cancer among Chinese nonsmoking women

The high incidence of lung cancer among Chinese females, despite a low smoking prevalence, remains poorly explained. Cooking fume exposure during frying could be an important risk factor. We carried out a population-based case-control study in Hong Kong. Cases were Chinese female nonsmokers with newly diagnosed primary lung cancer. Controls were female nonsmokers randomly sampled from the community, frequency matched by age groups. Face-to-face interviews were conducted using a standardized questionnaire. The "total cooking dish-years," categorized by increments of 50, was used as a surrogate of cooking fumes exposure. Multiple unconditional logistic regression was used to estimate the odds ratios (OR) for different levels of exposure after adjusting for various potential confounding factors. We interviewed 200 cases and 285 controls. The ORs of lung cancer across increasing levels of cooking dish-years were 1, 1.17, 1.92, 2.26, and 6.15. After adjusting for age and other potential confounding factors, the increasing trend of ORs with increasing exposure categories became clearer, being 1, 1.31, 4.12, 4.68, and 34. The OR of lung cancer was highest for deep-frying (2.56 per 10 dish-years) followed by that of frying (1.47), and stir-frying had the lowest OR (1.12) among the three methods. Cumulative exposure to cooking by means of any form of frying could increase the risk of lung cancer in Hong Kong nonsmoking women. Practical means to reduce exposures to cooking fumes should be given top priority in future research.     

Attributable risk of lung cancer in lifetime nonsmokers and long-term ex-smokers (Missouri,United States)

A population-based, case-control study of incident lung cancer among women in Missouri (United States) who were lifetime nonsmokers and long-term ex-smokers was conducted between 1986 and 1992. The study included 618 lung cancer cases and 1,402 population-based, age matched controls. Information on lung-cancer risk factors was obtained by interviewing cases, next-of-kin of cases (36 percent and 64 percent of the cases, respectively) and controls. Year-long radon measurements also were sought in every dwelling occupied for the previous five to 30 years. Population attributable risks (PAR) for specific risk factors were computed for all subjects, for lifetime nonsmokers, for long-term ex-smokers, by histologic cell type (i.e., adenocarcinoma cf nonadenocarcinoma) and for direct interviews with case (for living cases) and for next-of-kin interviews (for dead cases or cases too ill to complete an interview). The mean age at lung cancer diagnosis was 71 years, and nearly 50 percent of the lung cancers were histologically confirmed adenocarcinomas. Almost 40 percent of all lung cancers among lifetime nonsmokers and almost 50 percent of lung cancers among all subjects could be explained by the risk factors under study. Dietary intake of saturated fat and nonmalignant lung disease were the two leading identified risk factors for lung cancer among the lifetime nonsmokers, followed by environmental tobacco smoke, and occupational exposures to known carcinogens. A small nonsignificant risk was found for study subjects exposed to median domestic radon concentration of 4 pCi/l (25-year time-weight average). Since only a small fraction of the population is exposed at this level, it is estimated that the PAR for domestic radon was less than two percent in Missouri. The risk for saturated fat intake was similar for lifetime nonsmokers, ex-somkers, adenocarcinoma cases, and nonadenocarcinoma cases; however, the increased risk was much more pronounced for next-of-kin interviews (PAR=31 percent) than for interviews with the study subjects (PAR = nine percent). A similar pattern of PAR was identified among ex-smokers but, in this group, the lingering effect of a history of smoking was also very important. Along with saturated fat intake (PAR=20 percent), the combined effect of previous active and passive smoking even after 15 years of cessation of active smoking was responsible for more lung cancer than any other risk factor under study (PAR=59 percent).Drs Alavanja, Benicbou, Swanson, and Boice are with the Epidemiology and Biostatistics Program, National Cancer Institute, Bethesda, MD, USA. Dr Brownson is with the Department of Community Health, Saint Louis University School of Public Health, St Louis, MO, USA. Address correspondence to Dr Alavanja, Epidemiology and Biostatistics Program, National Cancer Institute, EPN/543, 6130 Executive Blvd, Bethesda, MD 20892, USA.