中药安普生对人胃癌SGC—7901细胞裸鼠移植瘤的治疗研究

将已接种了人胃癌ＳＧＣ－７９０１细胞的裸鼠随机分为４组，分别局部注射生理盐水、安普生、５－Ｆｕ、华蟾素后进行肿瘤生长抑制率、光镜组织学及电镜超微结构观察。结果表明，安普生组的瘤体积呈动态小趋势，肿瘤细胞坏死明显，抑瘤效果明显优于其他组；且未见任何毒副作用。为临床治疗胃癌提供了理论依据。     

温郁金对人胃癌裸鼠移植瘤生长和环氧合酶-2表达的影响

背景：温郁金为常用传统中药材，研究发现其组分具有抗癌作用。目的：研究温郁金对人胃癌裸鼠移植瘤生长和环氧合酶-2（COX-2）表达的影响，探讨其抑制胃癌的作用机制。方法：将人胃癌细胞系SGC-7901种植于裸鼠皮下，建立胃癌移植瘤模型。待瘤体长至约2mm时，12只荷瘤裸鼠随机分为治疗组和对照组，分别予温郁金提取液0．3ml和等量0．9％NaCl溶液灌胃，每日2次，连续7周。每周测量一次瘤体大小，7周后处死裸鼠，测定肿瘤重量。以免疫组化Elivision^TM plus法检测肿瘤组织COX-2的表达。结果：治疗组裸鼠移植瘤体积和重量均显著低于对照组．抑瘤率为42．5％；肿瘤组织COX-2阳性染色强度和阳性细胞百分率亦显著低于对照组。结论：温郁金对人胃癌裸鼠移植瘤的生长具有明显抑制作用，抑制肿瘤组织中COX-2的表达可能是其作用机制。     

TNP-470对胃癌生长抑制作用的实验研究

目的研究TNP-470(血管生成抑制剂)对胃癌生长的抑制作用。方法采用裸鼠皮下种植人胃癌细胞株,成瘤后随机分为治疗组及对照组,皮下注射TNP-470 30mg/kg,隔日1次,连续8次后,处死动物,测定瘤重及肿瘤微血管密度。结果实验组瘤重明显低于对照组(P<0.05),肿瘤微血管密度明显低于对照组(P<0.05)。结论TNP-470可明显抑制胃癌细胞生长,治疗组肿瘤微血管密度明显低于对照组。     

SN50联合5-氟尿嘧啶通过调节NF-κB信号通路抑制人胃癌裸鼠移植瘤生长的研究

目的探讨NF-κB通路抑制剂SN50联合5-氟尿嘧啶(5-FU)对人胃癌裸鼠移植瘤生长的影响及机制。方法建立荧光素酶标记的人胃癌细胞株SGC7901,常规传代培养,采用对数生长期细胞建立人胃癌裸鼠皮下移植瘤模型。14 d后随机分为4组:对照组、5-FU干预组、SN50干预组、5-FU+SN50干预组。每组8只动物,共给药4周。观察并记录各组裸鼠皮下移植瘤的生长情况,游标卡尺测量瘤体长短径,于停药次日处死裸鼠,称取瘤重,计算肿瘤体积、肿瘤生长抑制率、绘制肿瘤生长曲线。通过体内可见光成像技术分别于第1、7、14、21、28天对裸鼠进行活体成像,记录移植瘤光子数,绘制皮下移植瘤光子数曲线图。免疫组化方法检测移植瘤中NF-κBp65表达情况。结果与其他三组相比,5-FU+SN50干预组肿瘤体积、抑瘤率及光子数差异均有统计学意义(P0.05);与对照组及SN50干预组比较,5-FU干预组肿瘤体积和光子数明显减少(P0.05),抑瘤率明显增加(P0.05);SN50干预组与对照组相比,肿瘤体积、抑瘤率及光子数差异无统计学意义(P0.05)。NF-κBp65阳性率依次为对照组47.4%、5-FU组57.1%、SN50组11.8%、5-FU+SN50组25.0%。结论 5-FU单药及5-FU+SN50均能抑制裸鼠胃癌皮下移植瘤的生长,而联合应用效果更明显;SN50可通过抑制NF-κB信号转导通路的活化,显著增强5-FU对裸鼠胃癌皮下移植瘤的抑制作用。     

胃康宁冲剂抑制胃癌生长与转移的实验研究

[目的]研究胃康宁含药血清在体内对胃癌细胞生长和转移的影响。[方法]将人胃癌MGC-803细胞注入祼小鼠腋前皮下,待生长成瘤后取出,将瘤块植入裸鼠胃壁内,建立胃癌原位移植瘤模型。设对照组、胃康宁高剂量组、胃康宁低剂量组,灌胃4周。检测各组原位肿瘤抑瘤率、肝及淋巴结转移情况。[结果]胃康宁高剂量组可明显抑制原位肿瘤的生长,对胃周淋巴结转移有明显抑制作用,对肝脏转移无明显抑制作用。[结论]胃康宁冲剂对胃癌的生长和转移有一定的抑制作用。     

木霉菌醇对胃癌大鼠肿瘤抑制作用及对MrP4、胃肠道功能的影响

目的 探讨木霉菌醇对胃癌大鼠肿瘤的抑制作用及对MrP4、胃肠道功能的影响。方法 将40只健康大鼠随机分为健康组、胃癌组、木霉菌醇组(给予木霉菌醇40 mg/kg灌胃)、白藜芦醇组(给予白藜芦醇50 mg/kg灌胃),每组10只，采用生存状态积分评定各组大鼠生存状态；酶联免疫法检测各组大鼠胃泌素、胃动素水平；检测各组大鼠肿瘤体积及肿瘤生长抑制率；HE染色检测大鼠胃癌组织形态；TUNEL法检测大鼠胃癌组织细胞凋亡情况；免疫组化检测MrP4表达。结果 与健康组大鼠相比，在药物干预5 d、10 d、15 d及21 d各个时间点胃癌组大鼠生存状态分数、血清中胃动素和胃泌素的水平均降低，胃癌组织中MrP4的阳性表达率明显上升(P<0.05);与胃癌组相比，在药物干预后各时间点木霉菌醇组和白藜芦组大鼠生存状态分数、血清中胃动素、胃泌素的水平及胃癌组织的细胞凋亡率均显著升高，大鼠瘤体体积及胃癌组织中MrP4的阳性表达率降低(P<0.05);白藜芦组大鼠生存状态分数、血清中胃动素、胃泌素的水平及胃癌组织的细胞凋亡率均高于木霉菌醇组，大鼠瘤体体积及胃癌组织中MrP4的阳性表达率低于木霉菌醇组(...     

胃癌能谱CT表现与肿瘤标志物CEA、CYFRA21-1浓度的相关性

目的探讨胃癌能谱电子计算机断层扫描(能谱CT)表现与肿瘤标志物癌胚抗原(CEA)、细胞角蛋白19片段(CYFRA21-1)浓度的相关性。方法选择胃癌患者60例为研究对象纳入胃癌组,胃上皮内瘤变患者50例纳入胃上皮内瘤变组,并选择同期健康体检的健康受试者50例为对照组。对3组进行能谱CT扫描,并对3组受试者进行肿瘤标志浓度检查测定。比较3组能谱CT值水平、肿瘤标志物CEA、CYFRA21-1水平,并采用Pearson相关性检验对患者能谱CT值大小与肿瘤标志物CEA、CYFRA21-1浓度间进行相关性分析。结果 3组在40 keV时动脉期、门静脉期CT值、碘浓度、水浓度值比较差异有统计学意义(P0.05),胃癌组各项指标水平值显著均低于胃上皮内瘤变组及对照组(P0.05)。3组CEA、CYFRA21-1水平值比较差异有统计学意义(P0.05),胃癌组各项指标显著高于胃上皮内瘤变组及对照组(P0.05)。胃癌患者的动脉期、门静脉期CT值、碘浓度、水浓度值与肿瘤标志物CEA、CYFRA21-1呈明显的负相关性(P0.05)。结论能谱CT诊断可以为胃癌患者的临床诊断提供准确的定量诊断信息和高分辨率的图像信息,在早期胃癌的诊断、病情评估中有重要临床应用价值。     

膜型基质金属蛋白酶1在胃癌及癌周组织中的表达及临床意义

目的探讨膜型基质金属蛋白酶1(MT1-MMP)在胃癌及其周围组织中的表达和临床意义。方法收集胃癌病例110例,利用免疫组化染色、RT-PCR分析MT1-MMP在手术切除肿瘤组织及瘤旁组织中表达的差异,以及与患者临床特点及预后的关系。结果 110例肿瘤标本根据染色结果评定,高表达组(>4分)74例,低表达组(≤4分)36例,而瘤旁组织仅有5例呈低表达,其余均未见明显表达。RT-PCR显示Ⅰ、Ⅱ期胃癌与Ⅲ、Ⅳ期胃癌之间表达也具有统计学差异(P<0.05),不同组织类型的胃癌之间表达无明显差异。患者肿瘤早期转移、2年复发率及生存率与MT1-MMP表达具有一定的相关性。结论 MT1-MMP在胃癌组织中表达明显高于癌旁肿瘤组织,与胃癌的病理类型无关,而与胃癌的分期有关。MT1-MMP高表达的胃癌患者,其预后往往差于低表达患者。MT1-MMP有可能作为胃癌治疗的一个新的靶向基因位点。     

SLP-2 siRNA对裸鼠胃癌移植瘤细胞增殖及凋亡的影响

目的:探讨SLP-2siRNA对裸鼠胃癌移植瘤细胞增殖及凋亡的影响.方法:设计合成化学修饰的SLP-2siRNA,将胃癌细胞SGC-7901接种于裸鼠皮下建立裸鼠胃癌移植瘤模型,随机分为转染SLP-2siRNA组、阴性对照组和空白对照组,于肿瘤局部分别多点多次注射化学修饰SLP-2siRNA、阴性对照siRNA及生理盐水.检测3组移植瘤细胞增殖及凋亡状况,RT-PCR及免疫组织化学技术检测移植瘤细胞内SLP-2mRNA及蛋白的表达.结果:与两对照组相比,注射化学修饰的SLP-2siRNA后,裸鼠胃癌移植瘤细胞生长速度减慢、移植瘤体积减小(P=0.009,P=0.003).抑制瘤率分别为26.74%和30.15%,细胞凋亡无明显变化(P>0.05),肿瘤细胞内SLP-2mRNA及蛋白的表达量降低.结论:SLP-2siRNA可抑制人胃癌裸鼠移植瘤的生长,但对细胞凋亡无影响,提示SLP-2基因参与促进胃癌细胞增殖.     

rmhTNF对人胃癌细胞株裸鼠移植瘤模型的治疗作用

背景:重组改构人肿瘤坏死因子(rmhTNF)是原型TNF-α的改构体,前期实验显示其对体外培养的人胃癌细胞株具有抑制增殖和诱导凋亡作用。目的:初步研究rmhTNF对人胃癌细胞株裸鼠移植瘤模型的治疗作用。方法:雄性BALB/c裸鼠皮下接种人胃癌细胞株BGC-823构建移植瘤模型,随机予rmhTNF、TNF-α,5-氟尿嘧啶(阳性对照)和0.9%NaCl溶液(阴性对照)进行干预,观察各组裸鼠一般情况、移植瘤生长情况及其组织病理学改变。结果:建模裸鼠成瘤率为100%。各药物干预组移植瘤生长均明显减慢,其中rmhTNF组生长抑制最为明显,生长曲线较阴性对照组明显下移,抑瘤率显著高于TNF-α组和阳性对照组(83.1%对59.8%和50.1%,P0.01),一般情况与接种前相比无明显改变,移植瘤组织中可见较多凋亡和坏死细胞。结论:BGC-823细胞在BALB/c裸鼠皮下有良好的成瘤性。rmhTNF在体内能直接诱导胃癌细胞凋亡和坏死,对人胃癌细胞株裸鼠移植瘤模型具有治疗作用。     

矿物中药硇砂提取液抑制肝癌的实验研究

制备一种能够替代无水乙醇的,毒性低、弥散性好、可使肿瘤坏死更完全的中药提取液。制备硇砂提取液,用于大鼠肝癌细胞系CBRH-7919和体内肝癌大鼠模型的实验性治疗。硇砂提取液有较好的体外杀伤癌细胞和体内抑瘤作用。体外条件下与无水乙醇比较,作用优于或相当于前者,并且表现出明显的药物量-效关系;体内实验表明:该提取液局部注射可使肿瘤体积显著缩小,甚至坏死,组间对照有显著性差异。初步毒性试验提示该提取液毒性较小,与无水乙醇相近,但局部刺激等毒副作用较小。该中药提取液整体抑制肿瘤效果优于后者,且弥散性好、作用相对彻底,有可能替代无水乙醇用于肝癌等恶性实体瘤的局部治疗。     

反义miRNA-21/rAV-Tumstatin腺病毒载体对膀胱癌细胞生长的抑制作用

目的探讨反义miRNA-21/rAV-Tumstatin腺病毒载体双靶向治疗对裸鼠原位膀胱移植瘤生长的抑制作用。方法应用携带反义miRNA-21/rAV-Tumstatin的载体经尿道膀胱灌注治疗移植癌,采用二苯基溴化四氮唑蓝(MTT)法测定瘤细胞的增殖,原位末端标记(TUNEL)法检测瘤细胞的凋亡。结果 MTT法检测结果显示,反义miRNA-21,rAV-Tumstatin和联合应用组细胞的增殖率分别为48.7%±6.2%、35.8%±9.4%和27.8%±3.7%,均明显低于对照组(92.8%±7.4%,P<0.01)。TUNEL法检测结果提示,四组的瘤细胞凋亡率依次是:联合用药组(79.3%±4.1%),反义miRNA-21组(51.2%±7.5%),rAV-Tumstatin组(57.8%±6.9%),对照组(8.3%±2.6%),组间比较差异均有统计学意义(P<0.01)。用载体分别治疗的三组成瘤裸鼠的肿瘤生长均受到不同程度的抑制,但是联合应用组肿瘤生长更缓慢,与另外两组比较,差异具有统计学意义(P<0.05),而且自28 d始其肿瘤生长几乎处于停滞状态。结论反义miRNA-21和rAV-Tumstatin单独应用虽也能不同程度地通过抑制肿瘤细胞增殖、诱导其凋亡,从而遏制膀胱癌细胞生长,但针对致癌基因和抑癌基因的双位靶向用药,疗效显著优于单一用药,也更接近理想治疗。     

shRNA干扰技术沉默VEGF表达治疗血管内皮瘤的实验研究

目的构建血管内皮生长因子（VEGF）短发夹RNA真核表达质粒（shVEGF）,观察其对血管内皮瘤细胞系（EOMA）细胞体外增殖及动物实验的影响。方法构建真核表达质粒pGenesil-3-shVEGF并转染EOMA细胞,采用CCK-8法检测shVEGF对EOMA细胞增殖能力的影响。建立EOMA细胞裸鼠皮下移植瘤模型,分为对照组和shVEGF组,肿瘤出现后,隔日测量瘤体体积,并观察体积变化。结果转染48h后EOMA细胞增殖受到抑制。体内实验显示经shVEGF治疗后,裸鼠皮下移植瘤体生长缓慢,体积明显缩小。结论RNA干扰技术实现VEGF基因沉默,能明显抑制EOMA细胞增殖及体内肿瘤生长,提示shVEGF在血管内皮瘤、血管瘤等血管瘤样病变的生物治疗中可能有较好的应用前景。     

In vivo anti-tumor effect of hybrid vaccine of dendritic cells and esophageal carcinoma cells on esophageal carcinoma cell line 109 in mice with severe combined immune deficiency

AIM： To develop a fusion vaccine of esophageal carcinoma cells and dendritic cells （DC） and observe its protective and therapeutic effect against esophageal carcinoma cell line 109 （EC109）.
METHODS： The fusion vaccine was produced by fusing traditional polyethyleneglycol （PEG）, inducing cytokine, sorting CD34＋ magnetic microbead marker and magnetic cell system （MACS）. The liver, spleen and lung were pathologically tested after injection of the fusion vaccine. To study the therapeutic and protective effect of the fusion vaccine against tumor EC109, mice were divided immune group and therapeutic group. The immune group was divided into P, E, D and ED subgroups, immunized by phosphate buffered solution （PBS）, inactivated EC109, DC and the fusion vaccine respectively, and attacked by EC109 cells. The tumor size, weight, latent period and mouse survival period were recorded and statistically analyzed. The therapeutic group was divided into four subgroups： P, inactivated EC109, D and ED subgroups, which were attacked by EC109 and then treated with PBS, inactivated EC109, DC, and EC109-DC respectively. Pathology and flow cytometry were also used to study the therapeutic effect of the fusion vaccine against EC109 cells.
RESULTS： Flow cytometry showed that the expression of folate receptor （FR）, EC109 （C）, Des （D） in human nasopharyngeal carcinoma cell line （HNE1） （B） was 78.21%, 89.50%, and 0.18%, respectively. The fusion cells （C） were highly expressed. No tumor was found in the spleen, lung and liver after injection of the fusion vaccine. Human IgG was tested in peripheral blood lymphocytes （PBL）. In the immune group, the latent period was longer in EC109-DC subgroup than in other subgroups, while the tumor size and weight were also smaller than those in ED subgroup. In the therapeutic group, the tumor size and weight were smaller in ED subgroup than in P, inactivated EC109 and DC subgroups.
CONCLUSION： Fusion cells are highly expressed not only in FR but     

树突状细胞融合瘤苗的体内抗肝癌效应

目的：观察小鼠脾树突状细胞（DC）与肝癌H22细胞融合瘤苗体内诱导抗肿瘤免疫反应。方法：采用细胞因子诱导、CD11c磁珠标记、MACS分选等技术与传统的聚乙二醇（PEG）法相结合制备DC与H22细胞融合瘤苗，进行致瘤性和诱导CTL活性检测。体内抗肿瘤实验分免疫保护组和免疫治疗组两大组，观察融合瘤苗对肿瘤保护和治疗作用。结果：1、融合瘤苗接种于小鼠体内未见肿瘤形成，脾、肺和肝等器官未出现肿瘤病变。2、接种活融合疫苗的免疫小鼠针对H22细胞细胞的脾CTL活性明显高于对照组小鼠（P＜0．01）。3、在免疫保护组，经融合瘤苗免疫的小鼠，肿瘤潜伏期较对照组明显延长（P＜0．05）。结论：1、DC与H22细胞的融合瘤苗无体内致瘤性，已失去其亲本H22细胞的恶性生长特征，完全可靠。2、融合细胞能明显激活小鼠脾特异性的CTL，提示已获得亲本DC提呈抗原的功能。3、融合瘤苗对H22细胞的攻击有明显的抵抗作用。4、融合瘤苗治疗荷瘤小鼠有一定的抑瘤效应，而以抵抗肿瘤攻击的免疫保护作用较为显著。     

选择性COX-2抑制剂尼美舒利对肺癌放射治疗增敏作用及其机制研究

目的 观察选择性环氧化酶抑制剂与放射治疗联合应用对人肺腺癌A549裸鼠移植瘤生长的影响并进一步探讨其放疗增敏机制.方法 首先构建人肺腺癌A549裸鼠移植瘤模型,待裸鼠移植瘤长至最长径6.0 mm时随机分为4组:对照组、尼美舒利组、放疗组、尼美舒利联合放疗组.尼美舒利溶于0.5％羟甲基纤维素钠中,采用灌胃方式给药,剂量为60 mg·kg1·d-1,共28 d.移植瘤最大径长至6.0 mm时予以局部单次大剂量放疗10 Gy.观察各组移植瘤最长径由6 mm长至12 mm所需时间,以移植瘤体积绘制生长曲线,计算抑瘤率,用免疫组化方法检测增殖细胞核抗原(PCNA)、前凋亡蛋白Bax、凋亡抑制蛋白Bcl-2在组织中表达情况,应用流式细胞技术测定细胞周期分布及凋亡率.结果 尼美舒利联合放疗对肺腺癌裸鼠移植瘤生长有明显抑制作用.对照组移植瘤最长径由6 mm增长至12 mm所需时间为(7.12±0.72)d,放疗组为(8.34±0.71)d,尼美舒利组为(11.29±0.78)d,尼美舒利联合放疗组为(14.62±0.19)d.放疗组抑瘤率为21.2％,尼美舒利组为18.3％,尼美舒利联合放疗组为41.7％.应用免疫组化方法检测移植瘤中PCNA和Bcl-2表达的阳性面积百分比及灰度值:尼美舒利联合放疗组、放疗组、尼美舒利组均低于对照组(P值均＜0.05),且尼美舒利联合放疗组低于放疗组及尼美舒利组(P值均＜0.05);Bax表达阳性面积百分比及灰度值:尼美舒利联合放疗组、放疗组、尼美舒利组均高于对照组(P值均＜0.05),且尼美舒利联合放疗组高于放疗组及尼美舒利组(P值均＜0.05).流式细胞仪检测细胞凋亡率及细胞周期分布:尼美舒利联合放疗组、放疗组、尼美舒利组凋亡率均高于对照组(P值均＜0.05),且尼美舒利联合放疗组高于放疗组及尼美舒利组(P值均＜0.05);G0/G1期各组差异无统计学意义(F＝2.731,P＞0.05);S期尼美舒利联合放疗组、放疗组、尼美舒利组均低于对照组(P值均＜0.05),且尼美舒利联合放疗组低于放疗组及尼美舒利组(P值均＜0.05);G2/M期尼美舒利联合放疗组同其他各组相比增多(P值均＜0.05),对照组、放疗组、尼美舒利组差异无统计学意义(P＞0.05).结论 尼美舒利可抑制人肺腺癌A549裸鼠移植瘤的生长,尼美舒利增强人肺腺癌A549裸鼠移植瘤对放射治疗的敏感性.其机制可能同抑制PCNA表达,从而抑制肿瘤细胞的生长,并通过抑制Bcl-2表达、增强Bax表达,而诱导A549细胞凋亡有关;还可能与细胞周期分布中对放疗不敏感的S期细胞数减少而对放疗敏感的G2/M期细胞数增加有关.     

Gonadotropin-releasing hormone signaling pathways in an experimental ovarian tumor

Previous results showed that GnRH signaling is altered in cells from rat luteinized ovarian tumors (tumor group) because it did not activate the phospholipase C pathway, in contrast to control ovarian cells from superovulated prepubertal rats (SPO). In the present work, alternate GnRH-induced second messengers such as phospholipase A(2) and phospholipase D activation, cAMP production, ERK1/2 phosphorylation, and the presence of G proteins were evaluated to determine GnRH mechanism of action in tumor cells. G proteins examined were present in both cell types. Buserelin, a GnRH agonist, (1, 10, and 100 ng/ml) increased phosphatidylethanol in SPO, indicating phospholipase D activation. Only 100 ng/ml buserelin induced a significant response in the tumor group. Buserelin (100 ng/ml) increased (3)H-arachidonic acid in culture media in SPO, indicating phospholipase A(2) activation; no effect was observed in the tumor group. Buserelin (100 and 1000 ng/ml) induced pertussis toxin-insensitive cAMP increases in both cell types, with similar potencies. In the tumor group, buserelin (100 ng/ml) inhibited human chorionic gonadotropin-induced cAMP and progesterone; this effect was protein kinase C (PKC) dependent (inhibited by GF109203X, a PKC inhibitor). Buserelin (100 and 1000 ng/ml) induced ERK1/2 phosphorylation in both cell kinds. Buserelin-induced ERK1/2 activation was G(i/0) independent and PKC dependent. Only in the tumor group, buserelin-induced ERK1/2 activation was cAMP dependent (abolished by SQ 22536, the adenylyl cyclase inhibitor). Furthermore, dibutyryl cAMP-induced ERK1/2 activation in the tumor group was PKC dependent (inhibited by GF109203X). In conclusion, activation of phospholipases in tumor cells does not seem to mediate GnRH effects. GnRH signaling seems to involve adenylyl cyclase activation, PKC stimulation, and ERK1/2 phosphorylation.     

TK gene combined with mIL-2 and mGM-CSF genes in treatment of gastric cancer

AIM: Cancer gene therapy has received more and more attentions in the recent decade. Various systems of gene therapy for cancer have been developed. One of the most promising choices is the suicide gene. The product of thymidine kinase (TK) gene can convert ganciclovir (GCV) to phosphorylated GCV, which inhibits the synthesis of cell DNA, and then induces the cells to death. Cytokines play an important role in anti-tumor immunity. This experiment was designed to combine the TK gene and mIL-2/mGM-CSF genes to treat gastric cancer, and was expected to produce a marked anti-tumor effect. METHODS: TK gene was constructed into the retroviral vector pLxSN, and the mIL-2 and mGM-CSF genes were inserted into the eukaryotic expressing vector pIRES. The gastric cancer cells were transfected by retroviral serum that was harvested from the package cells. In vitro study, the transfected gastric cancer cells were maintained in the GCV- contained medium, to assay the cell killing effect and bystander effect. In vivo experiment, retroviral serum and cytokines plasmid were transfected into tumor-bearing mice, to observe the changes of tumor volumes and survival of the mice. RESULTS: In vitro experiment, 20 % TK gene transduced cells could cause 70-80 % of total cells to death. In vivo results showed that there was no treatment effect in control group and TK/GCV could inhibit the tumor growth. The strongest anti-tumor effect was shown in TK+mIL-2+mGM-CSF group. The pathologic examination showed necrosis of the cancer in the treated groups. CONCLUSION: TK/GCV can kill tumor cells and inhibit the tumor growth in vivo. IL-2 and GM-CSF strongly enhance the anti-tumor effect. Through the retrovirus and liposome methods, the suicide gene and cytokine genes are all expressed in the tissues.