层粘蛋白和纤维连接蛋白的表达与肺癌转移和预后的关系

目的：探讨原发性肺癌ＬＮ和ＦＮ的表达与转移及预后的关系。方法：采用免疫组化ＬＳＡＢ法检测１７９例肺癌标本中ＬＮ和ＦＮ的表达。结果：中、高分化的肺鳞癌的ＬＮ的表达强度明显不同于低分化者（ｔ＊＝３．０７，２．６７，Ｐ均＜０．０１），ＬＮ的表达强度在有无淋巴结转移的两组鳞癌间，差异具有显著性意义（χ２＝１１．１３，Ｐ＜０．０５），ＬＮ和ＦＮ的表达强度在鳞癌５年以上生存组明显不同于半年内死亡组（ｔ△＝２．８５，２．４９，Ｐ△＜０．０１，＜０．０５），ＦＮ表达强度在３组不同生存期的肺腺癌间，差异具有显著性意义（Ｈｃ＝７．５３，Ｐ＜０．０５）。结论：ＬＮ和ＦＮ的表达可作为评估肺癌淋巴结转移及预后的有价值的指标。     

芳烃羟化酶及吸烟与肺癌的关系探讨

为研究芳烃羟化酶及吸烟与肺癌的关系，采用ＡＨＨ直接测定法检查了肺癌患者４０例，其它癌症患者３２例及健康人４５例血液淋巴细胞中ＡＨＨ的诱导力。根据吸烟状况和ＡＨＨ诱导力不同分析患肺癌的相对危险度：（１）肺癌组与对照组相比，不吸烟者中ＡＨＨ高诱导力型发生肺癌的相对危险性升高２倍，吸烟者相对危险性升高４－６倍。（２）肺鳞癌组与对照组相比，不吸烟者中ＡＨＨ高诱导力型的相对危险性升高４倍，吸烟者升高７倍。     

80例肺癌患者免疫球蛋白,补体及CEA分析

目的：研究肺肿瘤体液免疫指标的变化及其与ＣＥＡ的关系。方法：用自动生化分析仪和放免法定量测定８０例肺癌患者的血清球蛋白、ＩｇＧ、ＩｇＡ、ＩｇＭ及补体３（Ｃ３）、补体４（Ｃ４）的量，设肺炎和正常人两组为对照组，运用ＳＰＳＳ软件进行统计。结果：肺癌组的球蛋白、ＩｇＧ、ＩｇＡ比肺炎和正常人明显升高（Ｐ〈０．０５），Ｃ３则比正常人降低（Ｐ〈０．０５），ＩｇＭ、Ｃ４两组无差异（Ｐ〉０．０５），ＣＥＡ阳性和Ｃ     

食管鳞癌自发细胞凋亡和核增殖抗原p53关系的研究

目的通过对食管鳞癌组织中凋亡细胞的原位观察和核增殖抗原（ＰＣＮＡ）的表达状态的研究,探讨不同增殖情况的食管鳞癌组织细胞凋亡情况,同时研究ｐ５３基因的突变和ｐ５３蛋白的表达对食管鳞癌组织细胞凋亡的影响。方法３０例术前未经任何治疗的食管鳞癌手术标本,分别进行凋亡细胞的原位检测（ＴＵＮＥＬ）、ＰＣＮＡ、ｐ５３蛋白的免疫组化染色和ｐ５３基因５,６,７,８外显子ＰＣＲ－ＳＳＣＰ检测。结果不同增殖能力的癌组织中,细胞凋亡的程度差异有显著性（Ｐ＜０．０５）。ｐ５３基因突变组中,增殖程度高与增殖程度低者之间癌细胞凋亡的程度差异有显著性（Ｐ＜０．０５）。ｐ５３基因突变组与非突变组、ｐ５３蛋白表达阳性组与非阳性组癌细胞凋亡的程度差异无显著性（Ｐ＞０．０５）。结论食管鳞癌组织中,细胞增殖活跃则自发性凋亡也相应增多     

Northern印迹杂交分析nm23基因在人肺癌中的表达研究

目的探讨ｎｍ２３基因表达在人肺癌中的作用。方法通过Ｎｏｒｔｈｅｒｎ印迹杂交,检测４０例人肺癌组织和１９例非癌肺组织的ｎｍ２３Ｈ１和ｎｍ２３Ｈ２ｍＲＮＡ表达,采用地高辛标记和检测系统显示杂交信号,并分析ｍＲＮＡ表达与肺癌临床特征的关系。结果低分化鳞癌的ｎｍ２３Ｈ２ｍＲＮＡ表达较中高分化鳞癌显著降低（Ｐ＜０．０１）,小细胞肺癌的ｎｍ２３Ｈ１和ｎｍ２３Ｈ２ｍＲＮＡ表达较肺鳞癌明显降低。但在有或无淋巴结转移的原发癌灶组织间,以及肺癌的临床分期间,ｎｍ２３基因ｍＲＮＡ表达差异无显著性（Ｐ＞０．０５）。结论ｎｍ２３基因ｍＲＮＡ表达与肺癌的组织分化有关,未发现其在肺癌中的癌转移抑制作用。     

血浆心钠素含量变化与肺癌关系的研究

用放射免疫法测定５５例肺癌中尉得及３０例健康成年人，３０例慢性支撖这炎（慢支炎）病人血压血浆心钠素含量。慢支炎组ＡＮＰ含量高于健康成人组，但统计学处理无显著性差异，Ｐ〉０．０５。肺癌组ＡＮＰ含量比健康人组和慢支炎组均增高明显，Ｐ〈０．０１。其中小非细胞肺癌４０例，阳性率分别为８０％和６０％，二者之间无显著性差异，Ｐ〉０．０５。肺癌患者血浆ＡＮＰ含量，Ｉ期最低，Ⅳ期最高，Ⅰ、Ⅱ期之间比较Ｐ〉０．０５     

血浆心钠素测定与肺癌关系的初步研究

作者测定了６４例原发性肺癌、３２例肺良性疾病患者和３２名健康人血浆心钠素（ａｔｒｉａｌｎａｔｒｉｕｒｅｔｅｃｐｏｌｙｐｅｐ－ｔｉｄｅ，ＡＮＰ）含量，并比较了１５例肺癌患者治疗前后血浆ＡＮＰ含量变化。结果表明肺癌组血浆ＡＮＰ显著高于肺良性疾病组和健康对照组（Ｐ＜０．０１）；小细胞肺癌（ＳＣＬＣ）显著高于鳞癌和腺癌（Ｐ＜０．０１）；晚期肺癌高于早期肺癌（ｐ＜０．０５）；ＡＮＰ对肺癌诊断的敏感性为４３．７５％，特异性为８５．９３％，诊断符合率为６４．８４％；治疗后ＡＮＰ显著低于治疗前（Ｐ＜０．００１）。所以血浆ＡＮＰ的测定有助于肺癌的诊断和组织学分类，也是判断病情和疗效的一项较有效指标。     

nm23基因在人肺癌中的表达及其与肺癌淋巴结转移的关系

应用ＬＳＡＢ免疫组织化学染色方法，研究转移抑制基因ｎｍ２３表达产物二磷酸核苷激酶（ＮＤＰＫ）在人肺癌中的表达及其意义。结果表明：ＮＤＰＫ／ｎｍ２３在人肺癌中有较高的表达，阳性率为５４．５％（４８／８８），其中鳞癌４３．５％（２０／４６），腺癌的６６．７％（２８／４２），在腺癌中的表达较鳞癌高（Ｐ＜０．０５）。在鳞癌中，无肺门或纵隔淋巴结转移者其阳性率为５９．３％（１６／２７），伴有肺门或纵隔淋巴结转移者阳性率为２１．１％（４／１９），差异有显著意义（Ｐ＜０．０５）；ＮＤＰＫ／ｎｍ２３表达与肺腺癌有无肺门或纵隔淋巴结转移无显著相关（Ｐ＞０．０５）；与肺癌分化程度和临床病理分期无显著相关。本组结果表明：ｎｍ２３基因可能在肺鳞癌和腺癌形成及转移过程中起不同的调节作用，其表达程度与肺鳞癌淋巴结转移呈负相关，与肺腺癌有无淋巴结转移无关。     

肺癌患者血清超氧化物歧化酶同工酶活力测定及其意义

对肺癌患者、肺部良性疾患者及健康人血清超氧化物歧化酶（Ｔ—ＳＯＤ）总活性及其铜锌超氧化物歧化酶（ＣｕＺｎ—ＳＯＤ）和锰超氧化物歧化酶（Ｍｎ—ＳＯＤ）同工酶活性进行测定。结果表明；随癌变发生，宿主血清总ＳＯＤ活力逐渐下降，健康组（１４．６３±２．１７Ｎｕ／ｍｌ）与肺部良性疾患组（１４．３７±２．２３Ｎｕ／ｍｌ）相比，后者呈下降趋势，但两组间差异无显著性（Ｐ＞０．０５）；二者与肺癌组（１２．８５±２．９６Ｎｕ／ｍｌ）相比，差异均有显著性（Ｐ＜０．０５）。健康组血清ＣｕＺｎ—ＳＯＤ活性（７．４２±１．７Ｎｕ／ｍｌ）与肺部良性组ＣｕＺｎ—ＳＯＤ活性（７．０９±１．４３Ｎｕ／ｍｌ）相比，后者下降，但二者差异无显著性（Ｐ＞０．０５）；而肺癌组ＣｕＺｎ—ＳＯＤ活性（６．０１±１．４６Ｎｕ／ｍｌ）与健康组和肺部良性组差异均有极显著性（Ｐ＜０．０１）。Ｍｎ—ＳＯＤ活性在各组间差异无显著性（Ｐ＞０．０５）。检测人血清ＳＯＤ及其同工酶活性，将有助于肺癌的诊断及治疗。     

CAC和CAP方案治疗晚期非小细胞肺癌的疗效比较

１９９２年９月至１９９４年６月我科采用环磷酰胺，阿霉素和卡铂或顺铂组成ＣＡＣ和ＣＡＰ方案分别治疗非小细胞肺癌３２例和３０例，有效率ＣＡＣ组为４０．６％，ＣＡＰ组３２．６％，两组无显著性差异（Ｐ〉０．０５）。ＣＡＰ组的胃肠道毒性比ＣＡＣ组严重（Ｐ〈０．０５），ＣＡＣ组的骨髓抑制ＣＡＰ组严重（Ｐ〈０．０５）。     

Aryl hydrocarbon hydroxylase inducibility and lymphoblast formation in lung cancer patients.

Aryl hydrocarbon hydroxylase (AHH) inducibility and lymphoblast formation were studied in lymphocytes from healthy control subjects and from lung cancer patients undergoing radiotherapy. The relationship between AHH inducibility and percentage lymphoblasts was statistically significant only for the pre-treatment patients (r = 0.598; p less than 0.05). In the control group and in patients undergoing radiotherapy the correlation between AHH inducibility and lymphoblast formation was positive but statistically it was not significant. Our data do not suggest a linear relationship between AHH inducibility and lymphoblast formation.     

Aryl hydrocarbon hydroxylase inducibility in lung cancer patients undergoing radiotherapy

Aryl hydrocarbon hydroxylase (AHH) inducibility was studied in cultured lymphocytes from 21 healthy control subjects and from 15 lung cancer patients selected for radiation therapy. AHH inducibility of the patients was measured prior to, during and at the end of radiation therapy. Four of 15 patients had values comparable to the healthy controls. Cellular DNA and protein measurements of cultured lymphocytes were the same for patients and healthy controls. There was no significant difference in the percentage of lymphoblast formation and percentage of cell survival between the two groups. Radiation therapy reduces the number of lymphocytes in vivo and the amount of lymphoblast formation in vitro. AHH inducibulity is signifcantly lowered by radiation in the patients who had very high inducibility at pre-treatment level. DNA and protein contents of cultured lymphocytes did not change during radiation therapy.     

Aryl hydrocarbon hydroxylase in lymphocytes and lung tissue from lung cancer patients and controls

The inducibility of aryl hydrocarbon hydroxylase (AHH) activity in peripheral mitogen-treated lymphocytes, and of AHH and other monoxygenase activities in lung samples, was studied in 41 patients--34 with pulmonary carcinoma, 4 with a benign lung tumour and 3 with chronic obstructive pulmonary disease. Lymphocyte AHH induction alone was studied in 43 non-smoking and 37 smoking surgical patients. Absolute induced and non-induced AHH activities were at about the same level in the lymphocytes from the lung cancer patients as in those from the non-smoking controls, whereas the activities in smoking controls were about 100% higher. The mean inducibility ratios were very similar in all groups, ranging from 4.4 in the benign tumour patients to 5.4 in both control groups. Thymidine incorporation was on average about 40% lower in the lymphocytes from the lung cancer patients. AHH activity was detectable in all the peripheral lung samples, both normal or tumorous tissue, and its inter-individual variation was more than 67-fold. ECDE activity was also detectable in all the samples studied and its correlation with AHH activity was statistically significant (r = 0.888), suggesting that the same enzyme metabolizes both substrates. ERDE was detectable only in the samples with the highest AHH and ECDE activities. There was no correlation between basal or induced lymphocyte AHH activities and lung tissue AHH activity, but there were statistically significant correlations between lung AHH activity and the inducibility ratio with (r = 0.618) or without correction by thymidine incorporation (r = 0.442). These correlations suggest that there are common regulatory factors for AHH inducibility in different tissues. No significant difference in any drug metabolism parameter measured was observed between the lung cancer patients and the controls.     

The Relationship between Aryl Hydrocarbon Hydroxylase and Polymorphisms of the CYP1A1 Gene

We examined the relationship between aryl hydrocarbon hydroxylase (AHH) and the frequency of a Msp I mutation in the 3'-flanking region of cytochrome P450 (CYP) 1A1 (Mspl polymorphism) and another mutation in exon 7 (Ile-Val polymorphism) in 84 healthy male subjects in Fukuoka, Japan. AHH inducibility (3-methylcholanthrene (MC)-induced AHH activity/non-induced AHH activity) was correlated with the MspI polymorphism (P<0.0001) and age class (P=0.015), whereas no correlation was found for the Ile-Val polymorphism (P=0.509). Age-adjusted AHH inducibility (mean±SE) of the predominant homozygote (genotype A), the heterozygote (genotype B) and a homozygote rare allele (genotype C) genotypes was 4.89±0.36, 4.82±0.29 and 13.61±1.44, respectively. The genotype C showed much higher AHH inducibility than genotypes A and B (P<0.001), while no significant difference was observed between genotypes A and B. Non-induced AHH activity was also correlated with these polymorphisms. The AHH activity of a homozygous mutant Val/Val genotype (0.076±0.010 pmol/min/10⁶ cells) was significantly higher (P<0.05) than that of the wild-type homozygous Ile/Ile (0.044±0.004 pmol/min/10⁶ cells) and heterozygous Ile/Val (0.047±0.007 pmol/min/10⁶ cells) genotypes. Our study suggests that the genotypes C and Val/Val, which are more frequent in smoking-related lung cancer, are closely related with high AHH inducibility and high non-induced AHH activity, respectively. Thus, the positive relationship between AHH inducibility and lung cancer is supported by our study. If our results are confirmed and the assessment of genotype becomes feasible on a population basis, identification of smokers who have genetically high susceptibility to lung cancer (genotype C or Val/Val) may become important for the prevention of lung cancer.     

Aryl hydrocarbon hydroxylase in persons with lung or laryngeal cancer.

To test whether the distribution of AHH inducibility is shifted toward the high end of the range in patients who had lung and laryngeal cancer, we measured this trait in 59 patients (32 lung and 27 laryngeal) who had resectable tumors and had been disease-free for a period of time. The advantage of selecting patients who were free of clinical disease was that measurement of their AHH inducibility should not have been affected by the disease state. Patient and control populations showed no difference in basal and induced AHH activity of AHH inducibility. The mean AHH inducibility in patients who had lung cancer was 3.20 +/- 0.20; in patients who had laryngeal cancer 2.96 +/- 0.18, and for all controls 3.29 +/- 0.04 (no significant difference at p = 0 05). Further analysis of the distribution of AHH inducibility in the patient group compared to controls showed no suggestion of a shift toward the higher end of the range in patients who had lung and laryngeal cancer.     

Aryl hydrocarbon hydroxylase inducibility is not altered in bladder cancer patients or their progeny.

We investigated the possible influence of aryl hydrocarbon hydroxylase (AHH) on susceptibility to bladder cancer in humans. AHH inducibility was measured in the cultured lymphocytes of 16 patients who were being followed after successful treatment for bladder cancer, in 53 progeny of bladder cancer patients, and in matched controls. In both the progeny and patient populations, no evidence was found for a difference between the distribution of AHH inducibility or induced AHH activity compared to the distribution among control individuals. Thus, AHH acitivity or inducibility does not appear to be a major determinant of bladder cancer risk in humans.     

非小细胞肺癌和肺结核中血清BCAR1水平的临床意义

探讨血清BCAR1水平在非小细胞肺癌和肺结核中的临床意义。方法:采用酶联免疫试剂方法（ELISA）检测2009年3月至2010年5月期间65例非小细胞肺癌（NSCLC）,26例肺良性肿瘤（炎性假瘤15例、错构瘤7例、纤维瘤4例）,30例肺结核患者（结核瘤17例,空洞型肺结核13例）,40例正常人血清BCAR1水平。结果:NSCLC组血清BCAR1水平高于肺良性肿瘤组和正常对照组（P<0.001）,而与肺结核组无显著差异（P>0.05）;血清BCAR1水平与性别、年龄和淋巴结转移无关（P>0.05）;与鳞癌和腺癌病理类型无关（P>0.05）,支气管肺泡癌BCAR1血清水平低于其它类型NSCLC（P=0.02）;BCAR1血清水平随着临床分期增加有逐渐递增的趋势;BCAR1血清水平在切除肿瘤后其血清水平降低;肺结核组BCAR1血清水平高于正常对照组和肺良性肿瘤组（P<0.001）,与结核病变的直径呈正相关（rs=0.92,P<0.001）,切除结核病变后其血清水平下降,空洞型肺结核血清中BCAR1水平高于结核瘤（P<0.001）;肺良性肿瘤组和正常对照组血清BCAR1水平无显著性差异（P>0.05）。结论:血清BCAR1可以作为NSCLC和肺结核诊断、了解病情进展和判断治疗效果新指标。      

Determination of benzopyrene-hydroxylase (cytochrome P-450) activity in patients with lung cancer

The study was concerned with comparison of inducibility index (ii) for benzopyrene-hydroxylase in mitogen-activated lymphocytes in patients with primary cancer of the lung, other cancers (breast, stomach, lower lip, rectum, skin and thyroid gland) and in lymphocytes of blood donors. The highest ii values were registered in bronchogenic carcinoma patients. Smokers, both lung cancer patients and healthy donors, revealed high values (80.0 and 83.3%, respectively). A modified "lymphocytic test" to assess the risk factor for primary lung cancer is suggested.     

中国人食管癌及肺癌发病风险与p53基因多态性

目的　比较中国北方人对食管癌及肺癌的易感性与p5 3基因第 72密码子多态性的关系。方法　应用序列特异性引物 ,以PCR方法检测 173例食管鳞状上皮癌、98例非小细胞肺癌患者及 136例健康对照者的p5 3基因第 72密码子的基因型。结果　食管癌与肺癌组p5 3等位基因及基因型分布无明显差异。食管癌和肺癌组的Pro等位基因频率明显高于对照组 (P值分别为 0 .0 2 4及0 .0 2 7)。Pro/Arg及Arg/Arg基因型频率在两肿瘤组及对照组差异无显著性 (P >0 .0 5 ) ,而食管癌和肺癌组的Pro/Pro基因型频率明显高于对照组 (P值分别为 0 .0 4 1及 0 .0 2 6 )。Pro纯合子患食管癌与肺癌的风险较Arg纯合子高 2倍左右 [校正比值比分别为 2 .12 (95 %CI=1.13～ 4 .0 1)和 2 .30 (95 %CI =1.13～ 4 .93) ],且与吸烟无协同作用。结论　Pro/Pro基因型为中国北方人患食管癌及肺癌的独立易感因素 ,两种肿瘤的发病可能有共同的遗传基础。     

Genetic control of interindividual variations in the inducibility of aryl hydrocarbon hydroxylase in cultured human lymphocytes.

Interindividual and intraindividual variations in aryl hydrocarbon hydroxylase (AHH) induction by 3-methylcholanthrene were studied in cultured lymphocytes from normal adult volunteers. Using eight pairs of monozygotic and eight pairs of dizygotic twins, we examined to what extent these variations are controlled by heritable factors and whether AHH inducibility correlations in an individual with the plasma half-lives of three drugs. Substantial overestimation of the induction ratio (fold inducibility) may occur if the nonlinearity of the assay standard curve is not considered. Fold inducibility remains relatively constant for an individual, but large intraindividual variations occur in absolute "control" and "induced" AHH activities. Fetal calf serum may contain inducers of AHH activity that vary with the particular lot of serum, thereby rendering the apparent induction ratio an imprecise indicator of genetic susceptibility to induction by 3-methylcholanthrene. The index of heritability for AHH fold inducibility in twins studied with different lots of fetal calf serum (0.80) or with a single lot of fetal calf serum (0.77) suggests nonetheless that genetic rather than environmental factors are mainly responsible for interindividual variations in AHH inducibility by 3-methylcholanthrene in human lymphocytes. In these twins a significant but poor correlation (r=-0.551; 0.03 less than p less than 0.05) occurs between AHH inducibility in culture and the plasma antipyring half-life, but not between AHH inducibility and phenylbutazone or bishdroxycoumarin half-lives.