肺癌的家族危险性分析

目的：判断肺癌的家族危险性，探讨遗传因素对肺癌发病的影响。方法：利用遗传流行病学的理论与方法，选择并确定了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：肺癌先证者的亲属（父母、兄弟姐妹）患肺癌的危险性是配偶家系亲属（父母、兄弟姐妹）的1．85倍（P＜0．01）；先证家系的双亲患肺癌和女性亲属患肺癌的危险性分别是配偶家系双亲和女性亲属的2．66倍和2．64倍（P＜0．01）；女性肺癌先证者的双亲患肺癌的危险性是女性对照双亲患肺癌的2．27倍（P＜0．01）。各种家系分析的结果基本一致。结论：肺癌先证者的亲属对肺癌的易感性比配偶的亲属高，遗传因素是肺癌的危险因素之一。     

男性肺癌的遗传流行病学有研究

安徽医科大学环境卫生学的金永堂等对194例男性肺癌先证者核心家系，及176例男性对照组核心家系的资料进行了分析。结果表明，肺癌先证者亲属患肺癌的危险性叭足大于对照组亲属，其中以上一代即父母亲患肺癌的危险性差异有显著性，但在兄弟姐妹中患肺癌的危险性无显著差异。对不同性别亲屈进行的分析结果表明，女性金属患肺癌的厄险性在男性肺癌先证者组是对照组的2．43倍，而男性亲属患肺癌的危险性两组间无显著性差异。作者认为，遗传因素是肺癌发生的危险因素，且女性的易患性可能比男性高；从遗传学角度看，在男性肺癌发生过程中虽然女…     

宣威女性肺癌患者肺组织中PAHS-DNA加合物的表达

背景与目的宣威地区燃煤污染被认为是当地女性肺癌高发的主要原因。本研究旨在通过检测PAH-DNA加合物在宣威女性肺癌患者肺组织中的表达,探讨宣威地区燃煤污染产生的大量多环芳烃类物质与当地女性肺癌的关系。方法收集2007年7月-2008年11月云南省肿瘤医院经手术切除的宣威地区女性肺癌患者20例、宣威地区男性肺癌患者20例、非宣威地区女性肺癌患者20例、宣威地区女性肺良性病变患者10例、非宣威地区女性肺良性病变患者10例,肺癌患者取癌组织、癌旁组织、正常肺组织,肺良性病变患者取正常肺组织,总计患者80例,组织200份。采用免疫荧光法检测组织中PAH-DNA加合物的表达,IPP6.0软件进行图像分析及半定量测定,SPSS13.0统计软件进行统计学处理。结果PAH-DNA加合物在宣威女性肺癌患者癌组织、癌旁组织和正常肺组织中的表达阳性率(90%、80%、65%)高于宣威男性肺癌患者(35%、30%、30%)及非宣威女性肺癌患者(20%、15%、10%)(P0.01);在宣威女性肺良性病变患者(阳性率70%)肺组织中的表达也高于非宣威女性肺良性病变患者(阳性率10%);在癌组织、癌旁组织、正常肺组织中的表达有逐渐降低的趋势,但差别无统计学意义(P0.05)。结论PAH-DNA加合物在宣威女性肺组织中的表达较高,而在宣威男性、非宣威女性中表达较低。     

宣威地区女性肺癌与8-羟基脱氧鸟苷的关系

目的研究8-羟基脱氧鸟苷(8-hydroxy-2-deoxyguanosine,8-OHdG)与宣威地区女性肺癌的关系。方法利用ELISA方法测定尿液中8-OHdG含量。采用饱和苦味酸法测定尿液中肌酐含量。最终数值采用尿肌酐(creafine,Cr)值较正,单位为ng/mg。结果（1）8-OHdG在所有患者的尿液中均有表达,在肺癌患者尿液中含量高于肺良性病变患者(P＜0.01);（2）宣威地区女性肺癌患者尿液中8-OHdG含量高于宣威地区男性肺癌患者和非宣威地区女性肺癌患者(P＜0.01);（3）宣威地区女性肺良性病变患者尿液中8-OHdG含量高于宣威地区男性肺良性病变患者和非宣威地区女性肺良性病变患者(P＜0.01)。结论DNA氧化损伤产生的8-OHdG可能在肺癌的发生、发展中起着重要作用。宣威地区女性受到的氧化损伤高于宣威地区男性和非宣威地区女性,这可能是宣威地区女性肺癌高发的因素之一。     

泰兴市食管癌、胃癌和肝癌遗传流行病学调查

目的：研究遗传因素在食管癌，胃癌和肝癌发生中的作用。方法：通过遗传流行病学病例对照研究，对泰兴市489个家系（食管癌先征家系132个，胃癌先证家系79个，肝癌先证家系80个，对照家系198个），应用Li-Mantel和Falconer方法进行分离比及遗传度的估算。结果：泰兴市食管癌，胃癌和肝癌的分离比分别为0.0839,0.1206和0.1271,明显低于0．25，遗传度分别为18．84％（男性22．6％，女性14．69％），21．42％（男性18．23％，女性31．53％）和35．74％（男性30．56％，女性54．90％）。结论：遗传因素在泰兴市食管癌，胃癌和肝癌的发病中有一定的作用，但并非泰兴市癌症高发的主要危险因素。     

宣威地区室内污染物与肺癌发病关系的研究

宣威地区是女性肺癌高发病地区之一。大量研究显示宣威地区 C1烟煤燃烧后释放的室内污染物与宣威肺癌的发病关系密切,本文从该地区的地理位置、肺癌发病死亡特点、室内多环芳烃类化合物及二氧化硅与肺癌发病关系概括当前的研究进展。     

1200例不同病理类型肺癌电子支气管镜下特点与临床分析

目的对1200例确诊的肺癌患者病理类型、镜下表现及临床特点进行分析,探讨肺癌病理分型与年龄、性别、镜下表现及临床特点的关系,同时通过对重复癌的研究进一步揭示电子支气管镜检查的必要性。方法采用常规支气管镜直视活检、CT定位肺活检和刷检的方法,确定诊断和病理类型。结果1200例肺癌中男性845例（70．4％）,女性355例（29．6％）;鳞癌507例（42．3％）,腺癌278例（23．2％）,小细胞癌356例（29．7％）,大细胞癌1例（0．1％）,未分型癌58例（4．7％）;同时双原发肺癌24例（2．0％）,异时性双原发肺癌4例（0．3％）。结论鳞癌、腺癌、小细胞癌等均以50岁-69岁为高发年龄段。男性鳞癌发病较多,女性腺癌及小细胞癌发病较多。鳞癌、腺癌以右肺上叶最多见,小细胞癌以左肺上叶最多见。鳞癌、小细胞癌镜下以增殖型为主,腺癌以浸润型为主。重视术前支气管镜检查,可显著减少误诊率,为临床治疗提供依据。     

胃癌双Y核心家系的遗传流行病学系列研究(Ⅱ)--分离比和遗传度的研究

目的 探讨遗传因素造成扬中市胃癌家族肾聚集性的作用方式与强度。方法 利用全新设计的双Ｙ核心家系调查方法,对扬中市４４８个胃癌核心家系和４３７个对照家系,共５２４２人进行了分离比和遗传度研究。结果 祛除先证者后,扬中市胃癌家系的调整分离比为０．０１４３,表明同胞中胃癌发病率远低于单基因遗传病的０．２５,符合多基因遗传方式;一级亲属中胃癌的调整遗传度为２３．８％,男性（２７．８％）明显高于女性（１７．     

479例肝细胞癌先证者家族聚集性分析

目的通过肝细胞癌（HCC）先证者一级亲属发病调查情况,探讨HCC病例分布的家族聚集性的特点。方法应用临床流行病学横断面研究方法,对2004～2008年广西医科大学附属肿瘤医院HCC先证者家系中一级亲属HCC发病情况进行调查,回顾性采用Poisson（泊松）分布模型拟合,并用频数分布拟合优度的x。检验进行验证。对有家族史的HCC分布用二项分布（p＋q）n模型拟合。HCC分离比采用Li—Mantel—Gart法估算。结果HCC先证者479例,占住院人数16．91％（479／2832）。该家族中实际病例数分布超越了二项分布的概率范围（P=0．028）。HCC的分离比为0．04,分离比方差为0．00001509,标准误为0．003885,95％可信限区间：0．033784～0．046216。结论HCC发病具有家族聚集现象,主要集中在一级亲属,HCC的遗传方式为多基因遗传,HCC先证者家系是HCC发病的危险因素之一。     

肺癌主要危险因素的研究进展

国内外有大量文献和统计研究确定了肺癌相关危险因素。其中最肯定的危险因素为吸烟,但引起肺癌的其他危险因素研究结果却很不一致,如雌激素、饮食、慢性呼吸系统疾病等。全文结合国际癌症研究所有关人类致癌物评估的结果,对近年来肺癌危险因素的研究进展,尤其是我国人群的肺癌研究进行阐述。我国云南锡矿工职业暴露和筛查队列、云南宣威肺癌高发现场、上海女性健康队列等揭示了吸烟、室内燃煤污染、职业性氡暴露、非吸烟女性雌激素与肺癌的关系。     

Familial aggregation of lung cancer in a high incidence area in China

To investigate whether lung cancer clusters in families in a high incidence county of China, an analysis was conducted using data on domestic fuel history and tobacco use for family members of 740 deceased lung cancer probands and 740 controls (probands' spouses). Lung cancer prevalence was compared among first-degree relatives of probands and of controls, taking into account various factors using logistic regression and generalised estimating equations. First-degree relatives of probands, compared with those of controls, showed an excess risk of lung cancer (odds ratio (OR)=2.05, 95% confidence interval (CI): 1.68-2.53). Overall, female relatives of probands had a greater risk than did their male counterparts, and the risk was 2.90-fold for parents of probands as compared with parents of spouses. Female relatives of probands had 2.67-fold greater risk than female controls. Lung cancer risk was particularly marked among mothers (OR=3.78, 95% CI: 2.03-7.12). Having two or more affected relatives was associated with a 2.69-5.40-fold risk increase. The risk elevation was also found for other cancers overall. Results confirm previous findings of a genetic predisposition to lung cancer, and also imply that lung cancer may share a genetic background with other cancers.     

Cancer aggregation and complex segregation analysis of families with female non-smoking lung cancer probands in Taiwan

Previous studies have found that having a first-degree blood relative with lung cancer was a possible predictor of lung cancer risk, but some studies have indicated that the association is non-significant or only significant for a subset of the studied population. To determine the familial aggregation and whether there is any evidence for a gene controlling the susceptibility to developing lung cancer in female non-smokers, multiple logistic regression methods for estimating covariate effects and maximum likelihood segregation analyses were performed using data from 216 female non-smoking lung cancer probands (2328 individuals) in a population-based case-control study. Having a family history of lung cancer was found to be a significant predictor of lung cancer for non-smoking females (Adjusted Odds Ratio (OR)=5.7, 95% Confidence Interval (CI)=1.9-16.9). Having a female relative with lung cancer (adjusted OR=14.4, 95% CI=2.7-75.5) was more strongly associated with the lung cancer risk than was having a male relative with lung cancer. This association was stronger for probands aged less than 60 years at onset (adjusted OR=11.2, 95% CI=2.2-56.9). All of the Mendelian models fitted the data significantly better than the sporadic (no major type) model or the environmental model (P<0.00l). The Mendelian codominant models provided the best fit of the data for the early onset probands and showed a stronger effect for a major susceptibility locus for non-smoking lung cancer probands. The results of this study provide evidence that a rare autosomal codominant gene may influence the risk lung cancer in non-smoker and is responsible for the familial aggregation observed in non-smoking lung cancer patients.     

Increased familial risk for lung cancer

For the determination of whether lung cancer clusters in families, an analysis was conducted on demographic and morbidity-mortality data, occupational and industrial experiences, and tobacco use practices for family members of 336 deceased lung cancer probands and 307 controls (probands' spouses). First-degree relatives of probands, compared with first-degree relatives of controls, showed a strong excess risk for lung cancer. Overall, male relatives of probands had a greater risk for lung cancer than did their female counterparts, and the risk was fourfold for parents of probands as compared with parents of spouses. Female relatives of probands over 40 years old were at nine times higher risk than similarly aged female controls, even among those who were non-smokers and who had not reported excessive exposure to hazardous occupations; the risk was fourfold to sixfold for heavy smokers. After control for the confounding effects of age, sex, cigarette smoking, and occupational and industrial exposures, relationship to proband remained a significant determinant of lung cancer, with a 2.4-fold greater risk among relatives of probands.     

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。     

Familial relative risk of colorectal cancer: a population-based study

This study aimed to assess the familial relative risk for colorectal cancer (CRC) and its variation according to age and gender. A population-based family study was carried out in France, from 1993 to 1998, including 761 families. Familial CRC risks were estimated from a cohort analysis of the relatives. No obvious decrease in CRC risk was found with increasing age, except when either the proband, or the relative, were in the youngest age class. The effect of the relatives' and probands' ages on the CRC risk differed according to their gender. The cumulative risk of CRC increased at an earlier age in male relatives of probands younger than 60 years of age, than in female relatives. This result suggests that mechanisms specific to females, possibly interacting with genetic factors, explain the difference in the cumulative risks between families with male and female probands.     

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。     

泰兴市食管癌、胃癌和肝癌遗传流行病学调查

目的　研究遗传因素在食管癌、胃癌和肝癌发生中的作用。方法　通过遗传流行病学病例对照研究 ,对泰兴市 489个家系(食管癌先证家系 13 2个 ,胃癌先证家系 79个 ,肝癌先证家系 80个 ,对照家系 198个 ) ,应用Li-Mantel和Falconer方法进行分离比及遗传度的估算。结果　泰兴市食管癌、胃癌和肝癌的分离比分别为 0 0 83 9、0 12 0 6和 0 12 71,明显低于 0 2 5 ;遗传度分别为 18 84%(男性 2 2 6% ,女性 14 69% )、2 1 42 % (男性 18 2 3 % ,女性 3 1 5 3 % )和 3 5 74% (男性 3 0 5 6% ,女性 5 4 90 % )。结论　遗传因素在泰兴市食管癌、胃癌和肝癌的发病中有一定的作用 ,但并非泰兴市癌症高发的主要危险因素     

DNA repair capacity and lung cancer risk in never smokers.

Besides secondhand smoke exposure, few other risk factors for lung cancer in lifetime never smokers have been identified. We present the estimates of lung cancer risk associated with suboptimal DNA repair capacity (DRC) measured by the host-cell reactivation assay in lifetime never smokers using data from 219 cases and 309 matched controls enrolled in a case-control study. Suboptimal DRC level (below the control median) conferred a significantly increased lung cancer risk in never smokers [odds ratio, 1.92; 95% confidence interval (95% CI), 1.3-2.9; P = 0.0024]. There was a 3.38-fold risk for individuals with DRC below the first quartile (95% CI, 1.8-6.3) compared with individuals with DRC above the third quartile. Secondhand smoke exposure in individuals with DRC below the control median was associated with a 3.81-fold risk of lung cancer (95% CI, 2.3-6.4). A 2.49-fold (95% CI, 1.1-5.6) risk was noted for the joint effects of lung cancer family history in first-degree relatives and suboptimal DRC. Relatives of probands (cases and controls) with lowest DRC (below the first quartile) were significantly more likely to be diagnosed with lung cancer (odds ratio, 2.69; 95% CI, 1.1-6.7) compared with relatives of probands with the most proficient DRC (above the third quartile). Relatives of probands with suboptimal (below the control median) versus proficient DRC also had an earlier age at diagnosis with lung cancer, although the only statistically significant difference was in female relatives (55.4 versus 67.7 years; P = 0.03).