CK7、TTF-1、p63在非小细胞肺癌患者体内表达变化的意义研究

目的 观察细胞角蛋白7(CK7)、甲状腺转录因子-1(TTF-1)、p63蛋白在非小细胞肺癌患者体内的表达情况,并分析其临床意义.方法 选取80例非小细胞肺癌患者的非小细胞肺癌组织作为非小细胞肺癌组,另选取其正常肺组织作为对照组.观察非小细胞肺癌组织中CK7、TTF-1、p63的阳性表达率,比较不同临床病理特征非小细胞肺癌患者CK7、TTF-1、p63阳性表达率的差异,分析影响非小细胞肺癌患者CK7、TTF-1、p63阳性表达率的因素.结果 非小细胞肺癌组织中的CK7、TTF-1、p63阳性表达率均明显高于正常肺组织(P﹤0.001);不同TNM分期、淋巴结转移、组织学分型和分化程度非小细胞肺癌患者CK7、TTF-1、p63的阳性表达率比较,差异均有统计学意义(P﹤0.05),不同年龄、性别非小细胞肺癌患者CK7、TTF-1、p63的阳性表达率比较,差异均无统计学意义(P﹥0.05);多因素Logistic回归分析结果显示,淋巴结转移和组织学分型是非小细胞肺癌患者CK7、TTF-1、p63阳性表达的影响因素(P﹤0.05).结论 CK7、TTF-1、p63在非小细胞肺癌患者体内高表达,且与患者的淋巴结转移情况和组织学分型密切相关.     

CD24在非小细胞肺癌中的表达及其临床意义

目的:探讨CD24在非小细胞肺癌中的表达及其预后意义.方法:采用免疫组织化学方法检测CD24在73例非小细胞肺癌和10例正常肺组织中的表达,分析CD24表达与非小细胞肺癌临床病理参数的关系及其对患者预后评估价值.结果:非小细胞肺癌患者和正常肺对照组中CD 24的阳性表达率分别为82.2%和30%,两者差异显著(p=0.001).CD24的表达在各个临床病理参数之间不存在显著差异(P>0.05).CD24高表达患者的死亡风险较低表达者明显升高(RR=2.20,95%CI=1.023-4.731,P=0.044),累积生存率显著降低(P=0.036),多因素预后分析显示CD24的表达是非小细胞肺癌的独立预后因素(P=0.015).结论:CD24在非小细胞肺癌中表达增高,其表达对判断非小细胞肺癌的发展及预后具有一定的临床意义,为靶向治疗提供了潜在靶点.     

CD24在非小细胞肺癌中的表达及其临床意义

目的：探讨CD24在非小细胞肺癌中的表达及其预后意义.方法：采用免疫组织化学方法检测CD24在73例非小细胞肺癌和10例正常肺组织中的表达,分析CD24表达与非小细胞肺癌临床病理参数的关系及其对患者预后评估价值.结果：非小细胞肺癌患者和正常肺对照组中CD 24的阳性表达率分别为82.2%和30%,两者差异显著（p=0.001）.CD24的表达在各个临床病理参数之间不存在显著差异（P〉0.05）.CD24高表达患者的死亡风险较低表达者明显升高（RR=2.20,95%CI=1.023-4.731,P=0.044）,累积生存率显著降低（P=0.036）,多因素预后分析显示CD24的表达是非小细胞肺癌的独立预后因素（P=0.015）.结论：CD24在非小细胞肺癌中表达增高,其表达对判断非小细胞肺癌的发展及预后具有一定的临床意义,为靶向治疗提供了潜在靶点.     

TTF-1在小细胞肺癌和肺腺癌中的表达及其临床意义

目的:探讨甲状腺转录因子-1（TTF-1）在小细胞肺癌(SCLC)和肺腺癌中的表达及其临床意义。方法:采用免疫组化SP法检测79例SCLC组织和270例肺腺癌组织中TTF-1的表达情况,统计患者的临床资料,分析TTF-1表达与临床特征的相关性,采用Kaplan-Meier曲线对随访数据进行预后分析。结果:SCLC（P＜0.001）和肺腺癌（P＜0.001）组织中TTF-1的表达率均显著高于癌旁肺组织,SCLC组织中TTF-1的阳性表达率明显高于肺腺癌组织（P=0.007）。SCLC组织中TTF-1的阳性表达水平与术前血清神经元特异性烯醇化酶（NSE）水平呈正相关（P=0.007）,TTF-1表达阴性的患者,中位生存期明显短于表达阳性的患者（19.639个月 vs 38.754个月,P=0.043）。肺腺癌组织中TTF-1的阳性表达水平与区域淋巴结转移程度（P=0.046）、术前血清癌胚抗原（CEA）水平（P=0.016）呈正相关,TTF-1的表达水平与中位生存期无关（P=0.167）。 SCLC预后独立危险因素有术前血清NSE升高和TTF-1阴性表达;肺腺癌预后独立危险因素是区域淋巴结转移。 结论:TTF-1可作为SCLC和肺腺癌鉴别诊断的分子标志物,可能对SCLC患者的预后有一定的指导意义。     

70岁以上晚期非小细胞肺癌的预后研究及中医药治疗疗效

目的 探讨影响晚期70岁以上非小细胞肺癌患者预后的相关因素,评价中药干预70岁以上晚期NSCLC的临床疗效。方法 采用回顾性分析,复习210例70岁以上晚期非小细胞肺癌的病历资料,统计分析影响预后的相关因素,评价中医药疗效。 结果 210例70岁以上晚期NSCLC的中位生存期为17.7个月;1年、2年、3年生存率分别为60.0%、42.2%、25.8%。单因素分析显示,年龄（是否大于75岁）、吸烟指数、组织学类型、ECOG评分、既往是否接受手术治疗、是否放疗、全身系统治疗（化疗、靶向治疗）及中医综合治疗周期与生存期均显著相关（P＜0.05）。而性别、临床分期、首诊中医证型（P＞0.05）与生存期并无显著相关性。多因素分析结果显示,吸烟（P=0.041,95%CI：1.017～1.415）、ECOG评分（P=0.044,95% CI：1.007～1.664）是预后的独立危险因素;既往手术史(P=0.002,95%CI：0.348～0.796)、全身治疗(P=0.038,95%CI:0.638～0.987)、中医综合治疗(P=0.001,95%CI:0.609～0.885)是预后的独立保护因素。结论 吸烟、ECOG评分高的老年肺癌患者预后的独立危险因素。既往手术治疗、系统全身治疗（包括化疗、靶向治疗）及中医综合治疗周期越长是70岁以上晚期NSCLC预后的独立保护因素。长期中药辨证治疗能有效延长老年晚期NSCLC生存期。对于老年晚期肺癌无法耐受其他治疗的情况下,中医药治疗可作为首选方案。     

基于Oncomine和Kaplan-Meier Plotter数据库分析GPX2在非小细胞肺癌组织中的表达和临床意义

目的:探讨谷胱甘肽过氧化物酶2（glutathione peroxidase 2,GPX2）在非小细胞肺癌组织中的表达及预后意义。方法:基于Oncomine和Kaplan-Meier Plotter数据库,收集关于GPX2表达的相关数据集,深入挖掘GPX2在非小细胞肺癌组织与正常组织中的差异表达情况。采用Kaplan-Meier法进行预后分析,并绘制生存曲线。此外,通过单/多因素COX回归进一步评估GPX2在不同临床特征中的预后评估价值。结果:与正常组织相比,GPX2在非小细胞肺癌组织中高表达（P＜0.001）。 GPX2高表达非小细胞肺癌患者的总体生存率（HR=1.42,95%CI:1.25~1.61,P=5.6E-08）和肺腺癌患者的总体生存率（HR=1.35,95%CI:1.07~1.71,P=0.011）均差于低表达组。但GPX2表达水平对鳞癌患者预后无显著影响（HR=1.06,95%CI:0.84~1.35,P=0.61）。此外,本研究也发现GPX2的表达对同一临床特征（如男性、临床分期、吸烟/不吸烟、经化疗方式治疗）的患者的预后有预测评估价值。多因素分析结果显示临床分期和GPX2的表达是非小细胞肺癌患者预后的独立影响因素。结论:检测非小细胞肺癌组织中GPX2的表达有助于患者预后评估。     

非小细胞肺癌p53、FHIT、K-RAS基因突变与吸烟相关性Meta分析

目的:从循证医学的角度对非小细胞肺癌患者p53、FHIT、K-RAS基因突变异常表达与吸烟相关性进行Meta分析。方法:检索中国学术期刊网全文数据库(CNKI)、中国科技期刊数据库(维普资讯网)、美国国立图书馆PubMed数据库,美国临床肿瘤学会(ASCO)论文集,辅以手工检索;检索时间段为1990年-2010年。检索出p53、FHIT、K-RAS基因突变与吸烟关系研究的文献197篇,最终符合纳入标准的文献26篇。对纳入文献进行方法学质量评价,采用Meta分析专用软件Review Manager 5.0进行统计分析。结果:共纳入26个研究,分别对有相同统计内容且可以合并统计的p53、FHIT、K-RAS基因突变与吸烟关系合并OR值并计算95%CI。分别为:吸烟人群p53基因突变率较高,表现为低表达,[OR=3.50,95%CI(2.45-5.00),总体效应检验Z=6.88,P<0.0001];吸烟人群K-RAS基因突变率明显偏高,表现为高表达,[OR=4.50,95%CI(3.00-6.75),总体效应检验Z=7.26,P<0.0001];吸烟人群FHIT基因突变率较高,表现为低表达,[OR=2.99,95%CI(1.01-8.88),总体效应检验Z=1.98,P=0.005]。结论:吸烟与p53、FHIT、K-RAS基因突变率呈正相关,其中p53、FHIT基因高表达为保护性因素,K-RAS基因高表达为危险因素。     

CD47在非小细胞肺癌中的表达及意义

摘 要： ［目的］ 通过检测CD47在非小细胞肺癌中的表达,了解CD47在非小细胞肺癌表达的意义及其与预后的相关性。［方法］ 采用免疫组化EnvisionTMplus法检测52例非小细胞肺癌患者癌及癌旁组织中CD47的表达,分析CD47与非小细胞肺癌患者临床病理参数及预后的关系。［结果］ CD47在非小细胞肺癌及癌旁组织中表达阳性率分别为80.8%(42/52),34.6%(18/52),癌组织CD47阳性率明显高于癌旁组织(P＜0.05)。CD47与非小细胞肺癌患者的临床分期、淋巴结转移相关(P＜0.05)。CD47阳性患者术后3年总体生存率低于阴性患者(χ2=4.314,P=0.038)。［结论］ CD47与非小细胞肺癌侵袭、转移和预后密切相关,有可能成为非小细胞肺癌的参考指标。     

非小细胞肺癌中FHIT蛋白表达与暴露因素的关系

目的探讨非小细胞肺癌中FHIT蛋白表达与暴露因素的关系.方法采用S-P免疫组化法检测77例非小细胞肺癌组织和25例非恶性肿瘤肺组织中FHIT蛋白的表达.采用相同的调查表对病例和对照的既往暴露史进行直接询问调查.结果吸烟肺癌患者FHIT蛋白表达阴性的危险性比不吸烟肺癌患者增加3.83倍(95%CI=2.55-9.15,P=0.014);与不食用奶制品者相比,十年前食用奶制品者FHIT蛋白表达阴性的危险性减少40.00%(95%CI=0.50-0.74,P=0.018).结论吸烟、食用奶制品可能与FHIT蛋白异常表达有关.     

中国非吸烟人群被动吸烟与肺癌关系的meta分析

背景与目的 本研究旨在探讨中国非吸烟人群被动吸烟与肺癌的关系.方法 通过计算机检索Medline、PubMed、CENTRAL(theCochrane central register of controlled trials)、中国生物医学文献数据库系统(CBM)、中国期刊全文数据库(CNKI)、中文科技期刊全文数据库(VIP)等收集国内外1987年-2007年间公开发表的关于中国非吸烟人群被动吸烟与肺癌的研究文献,应用统计软件Stata 11.0进行数据分析,计算其合并优势比(odds ratio,OR)和95%置信区间(confidence interval,CI).采用Begg和Eggr法对发表偏倚进行量化检测.结果 纳入分析的文章共有16篇,合并分析结果表明:中国非吸烟人群被动吸烟与肺癌的关系有统计学意义(OR=1.13,95%CI:1.05-1.21,P=0.001).每日被动吸烟≥20支、成年时期被动吸烟、非吸烟女性被动吸烟、被动吸烟暴露于工作环境等与肺癌的发生关系具有统计学意义,P值、OR值及95%CI分别为:P=0.000 3、OR=1.78、95%CI: 1.30-2.43,P=0.000 1、OR=1.50、95%CI:1.23-1.83,P=0.000 7、OR=1.50、95%CI: 1.19-1.90,P＜0.000 1、OR=1.41、95%CI:1.19-1.66.结论 中国非吸烟人群中,被动吸烟是肺癌发生的一个重要危险因素,尤其是暴露量≥20支/日、成年时期被动吸烟、女性、工作环境的被动吸烟与肺癌的发生关系密切.     

SULT1A1 Arg213His polymorphism and lung cancer risk: a meta-analysis

Background: The SULT1A1 Arg213His polymorphism is reported to be associated with lung cancer risk. However, this relationship remains controversial. For better understanding a meta-analysis was therefore performed. Methods: An extensive search was performed to identify all case-control studies investigating association between SULT1A1 Arg213His polymorphism and lung cancer risk. The strength was assessed by odds ratio (OR) with the corresponding 95% confidence interval (95%CI). Results: A total of five publications covering 1,669 cases and 1,890 controls were included in this meta-analysis. No significant association between SULT1A1 Arg213His polymorphism and lung cancer risk was observed in overall comparisons in all genetic models (dominant model: OR=1.33, 95%CI=1.00-1.76, P=0.05; additive model: OR=1.30, 95%CI=0.93-1.81, P=0.12; recessive model: OR=1.21, 95%CI=0.89-1.66, P=0.23). However, on subgroup analysis, an elevated risk in mixed populations with variant His allele was revealed in the dominant model (OR=1.66, 95% CI=1.06-2.62, P=0.03). Furthermore, the SULT1A1 Arg213His polymorphism was associated with an increased risk of lung cancer in both females and males in the dominant model (females: OR=1.72, 95%CI=1.29-2.27, P=0.00; males: OR=1.46, 95%CI=1.19-1.78, P=0.00). No significant association between this polymorphism and different smoking status (smokers and non-smokers) and the other ethnicities (Asians and Caucasians) was shown. Conclusions: The results of this meta-analysis indicate that the SULT1A1 Arg213His polymorphism is not associated with lung cancer risk in Asians and Caucasians, but possible elevation for genotype (GA/AA) in mixed populations and males and females needs further investigation.     

Has lung cancer in the elderly different characteristics at presentation?

Lung cancer is the first cause of cancer death for males aged > or =35 years, and the second for females aged between 35 and 70 years. Elderly patients seem to have the worst performance status (PS) and earlier stage of disease at diagnosis. We analyzed data concerning 1,035 patients with lung cancer referred to the National Cancer Institute of Naples. The variables considered in the analysis were: gender; type of cancer [small cell lung cancer (SCLC), non-small cell lung cancer (NSCLC)]; ECOG (Eastern Cooperative Oncology Group) PS, the stage of disease at diagnosis, the histological type, age at diagnosis. In order to better assess the relevance of age at diagnosis in lung cancer patients we categorized the age into two groups (young < or =70; old >70 years). The statistical analyses were performed using chi2 trend test with corresponding p-value and odds ratios (OR) for the examined variables, with a corresponding 95% confidence interval. These were derived using multiple logistic regression, fitted by the maximum likelihood method. For all the 1035 patients the risk between the age at diagnosis and the performance status was not statistically significant (OR=1.1, 95%CI 0.8-1.5). We repeated the same risk distinguishing the histological type and we analyzed the performance status for the SCLC (OR=1.0, 95%CI 0.4-2.5) and the stage at diagnosis (OR=1.0, 95%CI 0.4-3.0), without any significant difference. Our study showed that elderly patients with lung cancer do not seem to have different characteristics at presentation, particularly related to stage of disease, PS and histology, as compared to their younger counterpart. Other characteristics such as type and number of co-morbidities and organ function differ in the two groups of populations.     

Differences between small-cell lung cancer and non-small-cell lung cancer among tobacco smokers

It is known that smoking increases the risk for all histological subtypes of lung cancer. To date, the factors that determine why some patients develop small-cell lung cancer (SCLC) while others develop non-small-cell lung cancer (NSCLC) remain unknown. We compared the characteristics of 774 smokers with SCLC and NSCLC diagnosed during the period January 1999 till December 2002. Multivariate logistic regression was used to estimate the odds ratio (OR) with 95% CI. Testing of linear trend across categories of pack-years was also conducted. Six hundred and sixty-five NSCLC were compared to 109 SCLC. Among SCLC, there were significantly more females (20.2% versus 12.8%), current-smokers (81.7% versus 71.9%) as well as smokers who had smoked more than 40 pack-years (75.6% versus 50.3%). Comparing SCLC with NSCLC among the men only, having smoked more than 40 pack-years was associated with a significantly elevated odds ratio (OR) of 3.71 of developing SCLC (95% CI, 1.05-13.1; p=0.041). There was a decreasing trend in OR with increasing smoking cessation period. When comparing SCLC with adenocarcinoma, the women had a higher OR of 2.37 of developing SCLC (95% CI, 1.05-5.31; p=0.037) compared to the men. Our findings suggest that cumulative smoking exposure in terms of pack-years smoked is an important determining factor for the preferred development of SCLC among smokers.     

Association between polymorphisms in UDP-glucuronosyltransferase 1A6 and 1A7 and colorectal cancer risk

Genetic polymorphisms of uridine diphosphate-glucuronosyltransferases 1A6 (UGT1A6) and 1A7 (UGT1A7) may lead to genetic instability and colorectal cancer carcinogenesis. Our objective was to measure the interaction between polymorphisms of these repair genes and tobacco smoking in colorectal cancer (CRC). A total of 68 individuals with CRC and 112 non-cancer controls were divided into non-smoker and smoker groups according to pack-years of smoking. Genetic polymorphisms of UGT1A6 and UGT1A7 were examined using polymerase chain reaction-restriction fragment length polymorphism (PCR-RFLP). We found a weak association of UGT1A6 polymorphisms with CRC risk (crude odds ratio [OR], 1.65; 95% confidence interval [95%CI], 0.9-3.1, P=0.107; adjusted OR 1.95, 95%CI 1.0-3.8, P=0.051). The ORs for the UGT1A7 polymorphisms were statistically significant (crude OR: 26.40, 95%CI: 3.5-198.4, P=0.001; adjusted OR: 21.52, 95%CI: 2.8-164.1, P=0.003). The joint effect of tobacco exposure and UGT1A6 polymorphisms was significantly associated with colorectal cancer risk in non-smokers (crude OR, 2.11; 95%CI, 0.9-5.0, P=0.092; adjusted OR 2.63, 95%CI 1.0-6.7, P=0.042). In conclusion, our findings suggest that UGT1A6 and UGT1A7 gene polymorphisms are associated with CRC risk in the Japanese population. In particular, UGT1A6 polymorphisms may strongly increase CRC risk through the formation of carcinogens not associated with smoking.     

Tobacco smoking and chewing, alcohol drinking and lung cancer risk among men in southern India

In India, lung cancer is one of the most common and lethal cancers, and tobacco smoking remains its most important etiologic factors. The objective of our study is to examine the effects of different tobacco consumption forms, including smoking and chewing, on lung cancer risk of men in southern India, especially to compare the effects of bidi smoking to cigarette smoking on lung carcinogenesis. We also evaluated the possible role of Indian alcohol beverages and non-Indian alcohol beverages on lung carcinogenesis. We conducted a case-control study in Chennai and Trivandrum. In total, 778 lung cancer cases and 3,430 controls, including 1,503 cancer controls and 1,927 healthy controls, were recruited. The effects of cigarette, bidi smoking, chewing and alcohol drinking on the risk of lung cancer were estimated from unconditional multivariate logistic regression. We also applied the generalized additive model (GAM) with locally-weighted running-line smoothers (loess) to find the most plausible curve for the dose-response relationship. The results from GAM suggest a plateau after 35 years of smoking or 10 cigarette-equivalent pack-years for both cigarette and bidi. The OR is 4.54 (95%CI=2.96-6.95) and 6.45 (95%CI=4.38-9.50) for more than 30 years of cigarette-only and bidi-only smoking, respectively, and 6.87 (95%CI=4.62-10.2) and 10.7 (95%CI=5.82-19.6) for more than 12 weighted cumulative cigarette-only and bidi-only consumption, respectively. The lung cancer risk of former cigarette smokers drops down more quickly after quitting smoking compared to former bidi smokers. There is no evidence for the effect of chewing and lung cancer risk nor clear evidence of an effect of overall alcohol drinking among never-smokers, although Indian alcohol drinking seemed to remain associated with lung cancer risk under limited power (OR=2.67, 95%CI=1.02-7.02). Bidi smoking seems to have a stronger carcinogenic effect than cigarette smoking: this difference holds no matter which aspect of smoking was considered.     

GSTM1 and NAT2 polymorphisms in operable and non-operable lung cancer patients

We have genotyped 657 Norwegian men, including 282 lung cancer patients (147 non-operable and 135 operable) and 375 healthy referents (210 smokers and 165 non-smokers), to study the possibility that glutathione S-transferase M1 (GSTM1)-null and/or N-acetyl transferase 2 (NAT2)-slow genotypes confer susceptibility towards lung cancer in smokers. Compared with smoking referents, there was a significant over-representation of the GSTM1-null genotype among patients with squamous cell carcinoma (SQ) [odds ratio (OR) = 1.7, 95% confidence interval (95%CI) = 1.1-2.7], and the NAT2-slow genotype among patients with large cell carcinoma or mixed histological diagnosis (LM) (OR = 2.5, 95%CI = 1.0-6.1). In contrast to operable patients, non-operable patients showed a clear over-representation of slow genotypes if they were younger (相似文献   

CHRNA5 rs16969968 Polymorphism Association with Risk of Lung Cancer - Evidence from 17,962 Lung Cancer Cases and 77,216 Control Subjects

Background: Genetic studies have shown a possible relationship between the rs16969968 polymorphism inCHRNA5 and the risk of lung cancer. However, the results have been conflicting. Thus we rigorously conducteda meta-analysis to clarify any association. Materials and Methods: A total of 10 case-control studies involving17,962 lung cancer cases and 77,216 control subjects were analysed. Odds ratios (ORs) with 95% confidenceintervals (CIs) were used to measure the strength of the association. Results: We found the CHRNA5 rs16969968polymorphism to be associated with the risk of lung cancer (AA vs GG: OR=1.60, 95%CI=1.51-1.71). On stratifiedanalysis by smoking status, a statistically significant increased risk was observed in the smoking group (AA vsGG: OR=1.80, 95%CI=1.61-2.01). However, this polymorphism was not associated with lung cancer risk inAsians (AA vs GG: OR=0.95, 95%CI=0.35-2.59), whereas it was linked to increased risk of lung cancer amongCaucasians (AA vs GG: OR=1.65, 95%CI=1.55-1.76). Conclusions: Our meta-analysis provided statisticalevidence for a strong association between rs16969968 polymorphism and the risk of lung cancer, especially insmokers and Caucasians. Application of this relationship may contribute to identification of individuals at highrisk of lung cancer and indicate a chemoprevention target.     

广州地区肺癌的病例-对照研究

目的探讨广州地区人群发生肺癌的危险因素.方法将1998-2001年新诊断的原发性肺癌病例445例按性别、年龄1∶1配对选取445例健康者进行对照研究、问卷调查、建立数据库、单因素分析和多因素条件Logistic回归分析,筛选肺癌的主要危险因素.结果单因素分析发现32个暴露因素与肺癌发生有关;多因素分析发现肺癌有9个主要危险因素和1个保护因素,他们是1)吸烟OR及95%CI为3.19(2.18～4.67);2)被动吸烟来源于父亲OR为2.43(1.51～3.90);3)被动吸烟来源于配偶OR为2.33(1.26～4.30);4)肺结核病史OR为2.36(1.13～4.94);5)家庭用煤为燃料OR为3.44(1.38～8.57);6)常食用腌、酸菜OR为3.83(2.34～6.27);7)常食用咸鱼OR为4.49(2.86～7.06);8)经常下厨用猛火炒菜OR为4.45(3.03～6.56);9)职业接触金属类毒物OR为8.76(2.28～33.64).10)经常体育锻炼OR为0.59(0.33～1.06),可能是一个候选的保护因素.结论肺癌的发生与多种暴露因素有关,从其病因学来看,肺癌是可以预防与控制的.     

Susceptibility of Lung Cancer with Polymorphisms of CYP1A1, GSTM1, GSTM3, GSTT1 and GSTP1 Genotypes in the Population of Inner Mongolia Region

Background: To study the relationship of susceptibility to lung cancer with the gene polymorphisms of CYP1A1, GSTM1, GSTM3, GSTT1, GSTP1 and smoking status in Han and Mongolian populations of Inner Mongolia, an autonomous region of China. Materials and Methods: PCR-RFLP, allele-specific and multiplexPCR were employed to identify the genotypes of CYP1A1, GSTM1, GSTM3, GSTT1 and GSTP1 in a case-control study of 322 lung cancer patients diagnosed by bronchoscopy and 456 controls free of malignancy. Results: There is a significant difference in genotypic frequency of GSTT1 of healthy Mongolian and Han subjects. A statistically prominent association was found between CYP1A1 Msp1 (vt/vt) (OR=4.055, 95%CI:2.107-7.578, p=0.000), GSTM1 (-) (OR=2.290, 95%CI:1.467-3.573, p=0.000) and lung cancer in Mongolians. Similarly, in the Han population, CYP1A1 Msp1 (vt/vt) (OR=3.194, 95%CI:1.893-5.390, p=0.000) and GSTM1 (-) (OR=1.884, 95%CI:1.284-2.762, p=0.001) carriers also had an elevated risk of lung cancer. The smokers were more susceptibleto lung cancer 2.144 fold and 1.631 fold than non-smokers in Mongolian and Han populations, respectively. The mokers who carried with CYP1A1 Msp1 (wt/vt+vt/vt), exon7 (Val/Val+Ile /Val), GSTM1 (-), GSTM3 (AB+BB),and GSTT1 (-) respectively were found all to have a high risk of lung cancer. Conclusions: CYP1A1 Msp1 (vt/vt) and GSTM1 (-) are risk factors of lung cancer in Han and Mongolian population in the Inner Mongolia egion. The smokers with CYP1A1 Msp1 (wt/vt+vt/vt), CYP1A1 exon7 (Val/Val+Ile /Val), GSTM1 (-), GSTM3(AB+BB), and GSTT1 (-) genotypes, respectively, are at elevated risk of lung cancer.     

化疗相关性白细胞减少等因素对小细胞肺癌生存期的影响

目的 探讨影响小细胞肺癌（small cell lung cancer,SCLC）患者生存期的因素。方法 回顾性研究123例SCLC患者的临床资料,利用SPSS15.0统计软件Cox回归模型分析性别、年龄、吸烟、合并症、临床分期、ECOG评分、治疗方法、CEA、化疗相关性白细胞减少（chemotherapy induced leucopenia,CIL ）9个预后因素对生存期的影响。结果随访1～52月,死亡103例。6月、1年、2年、3年、4年存活率分别为70.7%、34.1%、8.94%、2.4%、0.8%,中位生存期11月[95%CI(9.328, 12.627)]。Cox回归多因素分析显示,影响预后的独立因素是：ECOG评分（P=0.000）、化疗联合放疗（P=0.000）、临床分期（P=0.024）、CIL(P=0.013)。结论临床分期早、ECOG评分低、接受化疗联合放疗且出现CIL的SCLC患者生存期长、预后好。