APP和VPP联合方案治疗晚期食管癌30例分析

目的：探讨晚期食管ＡＰＰ方案治疗的疗效与毒副作用。方法：ＡＰＰ方案（ＡＤＭ＋ＰＹＭ＋ＰＤＤ）与ＶＰＰ方案（ＶＣＲ＋ＰＹＭ＋ＰＤＤ）对照。结果：ＡＰＰ方案治疗１５例，ＣＲ５例（３３．３３％），ＰＲ４例（２６．７％），Ｓ５例（３３．３％），Ｐ１例（６．７％），有效率（ＣＲ－ＰＲ）６０％。ＶＰＰ方案治疗１５例，ＰＲ８例（５３．３％），Ｓ５例（３３．３％），Ｐ２例＊（１３．４％），有效率（ＣＲ＋ＰＲ）５３     

DDP,5Fu／CF加干扰素治疗晚期鼻咽癌的初步报告

目的：评价ＤＤＰ＋５Ｆｕ／ＣＦ＋ＩＮ（干扰素）方案治疗晚期鼻咽癌的疗效和毒性反应。方法：本文采用ＤＤＰ＋５Ｆｕ／ＣＦ＝ＩＮＦ（ＤＤＰ２０ｍｇ／ｍ＾２×５，５Ｆｕ３００ｍｇ－４００ｍｇ／ｍ＾２×５，ＩＮＦ３×１０＾６Ｕ×３）方案共治疗晚期鼻咽癌２６例；结果：２５例可评价儿，总有效率（ＣＲ＋ＰＲ）８０％（２０／２５），ＣＲ率１２％，中位缓解期４．８月（２－１２月）。在放疗和／七化疗后复发转移的２１例中     

HCE方案治疗常规方案失效的非小细胞肺癌156例分析

目的：探讨羟基喜树碱（ＨＣＰＴ）、卡铂（ＣＢＰ）和足叶乙甙（ＶＰ－１６）联合治疗常规方案（ＭＶＰ）失效的晚期非小细胞肺癌的疗效。方法：１５６例晚期非小细胞肺癌患者接受常规方案２￣４周期治疗失效后改用ＨＣＰＴ＋ＣＢＴ＋ＶＰ－１６（ＨＣＥ）化疗：ＨＣＰＴ ６ｍｇ／ｍ＾２,ｉｖ,ｄｌ￣５;ＣＢＰ ３００ｍｇ／ｍ＾２,ｉｖ,ｄｌ;ＶＰ－１６ １００ｍｇ,ｉｖ,ｄｌ￣５。２８天为１周期,每例用药２周期。观察     

羟基喜树碱、依托泊苷、5-氟尿嘧啶联合治疗老年人晚期胃癌40例

目的：探讨羟基喜树碱（ＨＣＰＴ）、依托泊苷（ＶＰ１６）、５－氟尿嘧啶（５－ＦＵ）联合方案治疗老年人晚期胃癌的疗效和毒副作用。方法：比较ＦＣＰＴ＋ＶＰ１６＋ＣＦ＋５－ＦＵ（ＥＬＦＨ）方案与ＨＣＰＴ＋５－ＦＵ＋ＶＰ１６（ＥＦＨ）方案。结果：ＥＬＦＨ组４２例有效率为５２．４％。ＥＦＨ组４０例有效率为４２．５％,两组疗效比较差异无显著性。ＦＬＦＨ组毒副反应较ＥＦＨ组发生率高,主要为骨髓抑制、恶心呕吐、口腔     

超抗原活化Th1细胞介导的对肿瘤细胞杀伤效应的研究

目的：本文对超抗原葡萄球菌肠毒素Ｂ（ＳＥＢ）活化的Ｔｈ１细胞介导的对肿瘤细胞杀伤作用进行了研究。方法：人外周血淋巴细胞与ＳＥＢ共同培养,用流式细胞术测定增殖细胞亚群;用酶联双夹心法测定ＩＬ－２、ＩＬ－４水平,用Ｋ５６２,ＨＬ－６０肿瘤细胞和自身淋巴细胞作为靶细胞测定效应细胞和细胞因子的杀伤活性。结果：ＳＥＢ共同培养６ｄ的淋巴细胞,ＣＤ４＾＋Ｔ细胞由３７．５％增加到４８．５％;ＣＤ１６＾＋淋巴细胞由     

CD44V6表达与胰腺癌增殖,转移及预后关系的研究

目的：探讨ＣＤ４４Ｖ６表达与胰腺癌增殖活性、淋巴结转移以及预后的关系。方法：应用免疫组ＬＳＡＢ法检测４７例胰腺癌组织中ＣＤ４４Ｖ６和ＰＣＮＡ的表达。结果：予性率为５７．４％（２７／４７）,与胰吕组织学类型及分级无关,伴淋巴结转移者ＣＤ４４Ｖ６阳性率（８１．０％,１７／２１）,明显高于无淋巴结转移者（３８．５％,１０／２６）,两者间有极显著性差性差异（Ｘ＾２＝８．５８,Ｐ〈０．０１）,ＣＤ４４Ｖ６阴     

国产澳沙利铂治疗大肠癌Ⅱ期临床研究

目的：评价国产注射用奥沙利铂单药及与５－氟尿嘧啶（５－Ｆｕ）－四氢叶酸（ＣＦ）联合用于治疗大肠癌的疗效及毒副反应。方法：收治带瘤大肠癌患４９例,按随机方法,分别入单药组１１例（单用奥沙利铂）,联合组２０例（奥沙利铂＋５－Ｆｕ＋ＣＦ）,和对照组１８例（５－Ｆｕ＋ＣＦ）。结果：单药组有效率２７．３％,联合组３０．０％,对照组５．６％,单药组和联合组疗效高于对照组,且奥沙利铂对大肠癌常见转移部位如肝脏     

羟基喜树碱,醛氢叶酸加氟苷联合方案治疗大肠癌54例报告

目的 观察ＨＣＰＴ＋ＣＦ＋ＦＵＤＲ方案对大肠癌的临床疗效。方法 ５４例Ｄｕｋｅｓ’Ｄ期大肠癌患者，ＣＦ每天１００ｍｇ，第１～５天静滴：ＴＵＤＲ每天３００～４００ｍｇ／ｍ＾２，第１～５天继ＣＦ后静滴；ＨＣＰＴ每天６～８ｍｇ／ｍ＾２，第１～１０天静滴。每２８天重复为１周期，所有患者都接受４～６个周期化疗。结果 ＣＲ６例（１１．１％），ＲＰ２３例（４２．６％），ＣＲ＋ＰＲ５３．７％（２９／５４）。其主要     

急性髓细胞白血病细胞CD34抗原表达的临床及生物学意义

为研究ＣＤ３４在急性髓细胞白血病（ＡＭＬ）中的临床及生物学意义，用流式细胞术检测了１０７例ＡＭＬＣＤ３４表达。结果显示４８．５％的患者ＣＤ３４阳性表达，Ｍ３（１５．８％）低于其他亚型（ｐ〈０．０５）。ＣＤ３４＾＋者肝脾肿大常见。ＣＤ３４表达在ｔ（８；２１）、正常核型及ｔ（１５；１７）组分别为７２．０％、４０?７％及１７．６％。ＣＤ３４＾＋者的完全缓解率（４１．９％）明显低于ＣＤ３４＾－者的５９．６     

HCV、HBV与肝硬变及原发性肝癌关系的初步探讨

作者对８０例肝硬变（ＬＣ）、１１２例原发性肝癌（ＰＨＣ）的血清抗ＨＣＶ及ＨＢＶ检测发现：（１）ＰＨＣ、ＬＣ的抗ＨＣＶ阳性率分别为２８．６％和１８．８％，ＨＢＶ阳性率分别为６４．３％和６７．５％；（２）有无用血液及血液制品者间的抗ＨＣＶ及ＨＢＶ阳性率差异显著；（３）ＬＣ、ＰＨＣ患者的抗ＨＣＶ阳性率在ＨＢＶ阴性（１５．４％和２５％）与ＨＢＶ阳性（２０．４％和３０．６％）间无明显差异；（４）在抗ＨＣＶ阴、阳性ＰＨｃ中，抗ＨＢｅ、抗ＨＢｃ单阳性率，抗ＨＢｓ与抗ＨＢＣ及抗ＨＢｃ与抗ＨＢｅ双阳性率，差异非常显著。结果表明，ＨＢＶ感染仍为ＬＣ及ＰＨＣ的主要致病因素，但ＨＣＶ与ＨＢＶ存在着重叠感染，亦可能起着共同作用。     

全反式维甲酸对阿糖胞苷诱导HL-60细胞凋亡的影响

目的 :探讨 HL- 6 0细胞经全反式维甲酸 (ATRA)作用后对化疗药物阿糖胞苷 (Ara- C)诱导凋亡敏感性的变化。方法 :应用光镜检查凋亡细胞形态 ,DNA电泳检查梯状条带及流式细胞仪检测细胞周期分布、凋亡细胞率和 bcl- 2蛋白表达的阳性细胞率和相对荧光强度 (MFI)。结果 :ATRA0 .3mg/ L 作用 HL- 6 0细胞 72 h后 ,S期细胞显著减少至 32 .9% (P<0 .0 5 ) ,G0 / G1 期细胞明显增加达 5 8.5 % (P<0 .0 5 ) ,bcl- 2阳性细胞率和 MFI分别下降至 18%和 0 .6 3(P<0 .0 5 ) ;Ara- C1.5 m g/ L 作用 HL- 6 0细胞 4h,凋亡细胞率为 5 5 .1% ,DNA电泳见明显的梯状条带。当 HL- 6 0细胞经 ATRA0 .3m g/ L 作用 72 h后再加 Ara- C1.5 m g/ L 继续培养 4h,细胞凋亡率明显减少至 34 .4% (P<0 .0 5 ) ,DNA电泳见梯状条带亮度减弱。结论 :ATRA降低 HL- 6 0细胞对 Ara- C诱导凋亡敏感性 ,其机制可能与 ATRA阻滞 G0 / G1 期细胞进入 S期有关     

麦草粉与绿茶对亚硝化鱼露致微核率增高的抑制作用

应用小鼠骨髓嗜多染经细胞（ＰＣＥ）微核试验方法，研究麦草粉与绿茶对胃癌高发区鱼露径亚硝化后致突变的抑制作用，结果表明：２０％麦草粉，１０％绿茶可降低亚硝化鱼露所致的小鼠微核率增高的作用（Ｐ〈０．０１），将按成分换算后相当于０．０２％ＶＣ的２０％麦草粉干预组和０．００２％ＶＣ的１０％绿茶干预组与０．１％ＶＣ干预对照组比较，微核出现率没有显著差异（Ｐ〉０．０５）。提示麦草粉，绿茶的抑制作用尚与ＶＣ外的     

STUDY ON THE ANTIMUTAGENICTTY OF ORIDONIN

目的 :探讨冬凌草甲素的抗突变作用。方法 :采用Ames试验及小鼠骨髓嗜多染红细胞 (PCE)微核试验。结果 :冬凌草甲素在未加S9条件下 ,对TA98及TA10 0回复突变具有明显的抑制作用 ,其最高抑制率分别达 89 1%及 80 2 % ;对由环磷酰胺(CP)诱导的小鼠骨髓PCE微核发生率也有显著的拮抗作用 (P <0 .0 1)。结论 :冬凌草甲素在本实验条件下具有抗突变活性     

褪黑激素抗胶质瘤作用的体内试验

目的探讨ＭＬＴ体内抗胶质瘤作用。方法观察荷Ｃ６鼠胶质瘤大鼠接受ＭＬＴ治疗后肿瘤大小,生存期,病理组织学及细胞凋亡的变化。结果ＭＬＴ治疗后Ｃ６胶质瘤生长延缓,荷瘤大鼠生存期延长,诱发肿瘤细胞凋亡。结论ＭＬＴ有一定抑瘤作用,值得进一步临床实验。     

Role of valence state and solubility of chromium compounds on induction of cytotoxicity, mutagenesis, and anchorage independence in diploid human fibroblasts

We previously showed that carcinogenic nickel, arsenic, and chromium(VI) compounds induced anchorage independence (AI) in diploid human fibroblastic cells (HFC) derived from foreskins (K. A. Biedermann and J. R. Landolph, Cancer Res., 47: 3815-3823, 1987). To elucidate the role of the valence state of chromium and solubility of chromium compounds in inducing AI, we studied the ability of soluble and insoluble hexavalent [chromium(VI)] and trivalent [chromium(III)] chromium compounds to induce mutation and AI in HFC. Chromium(VI) compounds (PbCrO4, CaCrO4, Na2CrO4, and CrO3) were 1000-fold more cytotoxic to HFC (average 50% lethal dose 0.5 microM) than chromium(III) compounds (CrCl3, Cr2O3, Cr2S3; average 50% lethal dose 500 microM). However, equal concentrations (0.1-10.0 microM) of soluble or insoluble chromium compounds in either +6 or +3 valence states induced similar increases in frequencies of AI in HFC (100-200/10(5]. Chromium(VI)- and chromium(III)-induced AI was a stable phenotype. All soluble chromium(VI) and insoluble chromium(III) compounds studied induced mutation to 6-thioguanine resistance at cytotoxic concentrations in HFC. Insoluble PbCr(VI)O4 and a soluble form of Cr(III)Cl3 were inactive in this assay. Mutation induction by chromium(III) compounds only occurred at cytotoxic concentrations (100-1000 microM) 1000-fold greater than those concentrations of chromium(VI) compounds (0.25-1 microM) which were cytotoxic, mutagenic, and induced AI. Soluble hexavalent Na2(51)CrO4 was taken up facilely by cells at concentrations that induced cytotoxicity, mutation, and AI. At concentrations of 0.25-1.0 microM, which induced AI but were not cytotoxic or mutagenic, or concentrations of 1-1000 microM, which were cytotoxic and mutagenic, soluble trivalent 51CrCl3 was not taken up by cells. An insoluble form of CrCl3 was not taken up intracellularly but did avidly associate with cells over the concentration range 1 to 100 microM which induced AI, cytotoxicity, and mutagenicity. Therefore, both chromium(VI) and chromium(III) compounds induced genotoxic effects in human fibroblasts. Cellular uptake, cytotoxicity, mutagenicity, and AI induced by soluble chromium(VI) compounds all occurred at the low concentrations of 0.2 to 1.0 microM; hence mutagenicity and induction of AI may be coupled for soluble chromium(VI) compounds but not for insoluble PbCrO4, which induced AI but was not mutagenic. Cytotoxicity and mutagenicity of insoluble chromium(III) occurred at concentrations of 10-100 microM, but induction of AI occurred at concentrations of 0.1-10 microM, indicating that inductions of mutagenicity and AI were not coupled for chromium(III) compounds.(ABSTRACT TRUNCATED AT 400 WORDS)     

BALB/C小鼠免疫耐受模型建立及移植人体肺癌初步研究

目的：获得一种能移植人体肿瘤并存活的动物模型。方法：将郑氏植物蛋白（ZPP）0.1ml皮下注射BALB／C小鼠，诱导其免疫耐受性移植人体肺肿瘤组织。结果：移植肺肿瘤在模型动物体内存活，成功率可达65％（26／40），而对照组小鼠体内移植瘤全部被排斥，不能存活。结论：ZPP可引起小鼠对人体肺肿瘤细胞免疫耐受，使移植瘤成活。     

8-Br-cAMP诱导人食管癌细胞凋亡的研究

目的 :本文主要研究人食管癌 10 9细胞株经 8 Br cAMP诱导后细胞凋亡的发生。方法 :用TUNEL法观察诱导后细胞凋亡情况。结果 :人食管癌 10 9例细胞株自发凋亡率为 10 3% ;经 8 Br cAMP诱导后凋亡倾向细胞增加。结论 :8 Br cAMP具有促进人食管癌细胞凋亡倾向的效应。     

甘蓝汁的抗诱变作用及其机理研究

本文通过微核试验和肝组织中谷胱甘肽－Ｓ－转移酶（ＧＳＴ）活性、还原型谷胱甘肽９ＧＳＨ）含量及细胞色素Ｐ４５０含量测定，在哺乳动物整体水平，从遗传学和生化毒理角学角度研究了甘蓝汁的抗诱变作用及其机理。结果发现，甘蓝汁对环磷酰胺（ＣＰ）诱发的小鼠骨髓多染红细胞（ＰＣＥ）微核细胞率有显著抑制作用，抑制率达４７．２％。Ｗｉｓｔａｒ大鼠饮甘蓝汁１０ｄ后，肝脏ＧＳＴ活性增加２５．０％，ＧＳＨ含量提高４７．８％     

微核形态用于区分非整倍体毒剂和染色体断裂剂的研究

目的 :通过比较非整倍体毒剂和染色体断裂剂诱导的各种微核形态类别的差异 ,探讨以微核形态指标区分两类诱变剂的可能性。方法 :对 6种标准诱变剂 (非整倍体毒剂 :秋水仙碱 ,长春新碱 ;染色体断裂剂 :环磷酰胺 ,丝裂霉素C ,乙基磺酸甲酯 ,γ射线 )诱导的小鼠骨髓红细胞微核 ,进行形态学分类分析。结果 :①非整倍体毒剂诱导的环形微核率显著高于染色体断裂剂 (分别为 33 8± 2 8,17 4± 8 3;P =0 .0 0 3) ,而圆形微核率显著低于后者 (分别为 5 1 6± 6 5 ,72 3± 9 1;P <0 .0 0 0 1) ,肾形微核率有高于染色体断裂剂诱导的微核的趋势 ,但差别无显著性 (分别为 14 6± 6 7,10 2± 6 3,P =0 .0 7) ;两类诱变剂诱导的 3种类别的微核 95 %可信区间差异很大 ,其中圆形微核率和环形微核率完全分离 ;②得到通过微核形态区分两类诱变剂的判别方程。结论 :微核的圆形、环形和肾形的发生率可用于区分非整倍体毒剂与染色体断裂剂的参考     

Occupational exposure to metal compounds and lung cancer. Results from a multi-center case�Ccontrol study in Central/Eastern Europe and UK

Purpose

To study the association between occupational exposure to metals including chromium, cadmium, nickel, and arsenic compounds, within a population-based study design, while adjusting for confounding factors.

Methods

A population-based lung cancer case?Ccontrol study in Central/Eastern Europe and UK was conducted in 1998?C2003, including 2,853 cases and 3,104 controls. Exposure to 70 occupational agents was assessed by local expert-teams for all subjects. Odds ratios (OR) for exposure to dust and fumes/mist of chromium, nickel, cadmium, arsenic, as well as inorganic pigment dust and inorganic acid mist, were adjusting for smoking, age, center, sex, and exposure to other occupational agents including the metals under study.

Results

Exposure to arsenic (prevalence = 1.4%) was associated with an increased lung cancer risk ((OR) 1.65, 95% confidence interval (95% CI):1.05?C2.58). For chromium dust (prevalence = 4.8%, OR: 1.25, 95% CI: 0.95?C1.65), a linear upward trend for duration and cumulative exposure was observed. A weak association was observed for exposure to cadmium fumes (prevalence = 1.8%, OR: 1.19, 95% CI: 0.77?C1.82), which was strongest for the highest category of cumulative exposure (OR: 2.04, 95% CI: 1.07?C3.90). No increased risk was observed for inorganic acid mist, inorganic pigment dust, or nickel, after adjustment for other metals. An independent effect of nickel cannot be excluded, due to its collinearity with chromium exposure.

Conclusions

Occupational exposure to metals is an important risk factor for lung cancer. Although the strongest risk was observed for arsenic, exposure to chromium dust was most important in terms of attributable risk due to its high prevalence.