斑蝥素诱导人胰腺癌细胞凋亡的实验研究

目的 探讨斑蝥素（Cantharidin）对人胰腺癌细胞凋亡的影响及其作用机制。方法采用MTT法观察斑蝥素对人胰腺癌细胞株SW1990细胞增殖的抑制作用。采用Hoechst33258染色、TUNNEL染色、流式细胞术检测细胞凋亡改变，并以RT—PCR和Westernblot检测凋亡调节基因p53和Bcl-2、Bax的表达。结果 5mol／L斑蝥素能明显抑制人胰腺癌SW1990细胞的生长，呈现凋亡特征。RT—PCR和Westernblot检测可见Bax、p53基因表达显著增加，而Bcl—2基因表达减少。结论 斑蝥素能诱导人胰腺癌细胞凋亡，其作用可能与上调p53、Bax基因和下调Bcl-2基因有关。     

斑蝥素诱导人胰腺癌细胞凋亡的实验研究

目的 探讨斑蝥素(Cantharidin)对人胰腺癌细胞凋亡的影响及其作用机制.方法 采用MTT法观察斑蝥素对人胰腺癌细胞株SW1990细胞增殖的抑制作用.采用Hoechst 33258染色、TUNNEL染色、流式细胞术检测细胞凋亡改变,并以RT-PCR和Western blot检测凋亡调节基因p53和Bcl-2、Bax的表达.结果 5μmol/L斑蝥素能明显抑制人胰腺癌SW1990细胞的生长,呈现凋亡特征.RT-PCR和Western blot检测可见Bax、p53基因表达显著增加,而Bc1-2基因表达减少.结论 斑蝥素能诱导人胰腺癌细胞凋亡,其作用可能与上调p53、Bax基因和下调Bcl-2基因有关.     

瑞香狼毒药效组分对裸鼠肝癌移植瘤的抑制及其机制

目的:评价瑞香狼毒药效组分抑制人肝癌细胞株BEL-7402裸鼠皮下移植瘤作用的强度,并探讨其机制.方法:建立人肝癌BEL-7402裸小鼠皮下移植瘤模型研究瑞香狼毒药效组分Zp1111抗肿瘤作用与对荷瘤裸鼠体质量与免疫器官的影响,免疫组织化学法检测用药前后BEL-7402皮下移植瘤组织Bcl-2与Bax阳性表达的变化.结果:Zp1111对裸小鼠皮下移植瘤BEL-7402具有较强的抑制作用,187.5mg/kg、250mg/kg(折合成生药量)剂量时对移植瘤的相对肿瘤增殖率T/C小于60%;该组分能显著上调BEL-7402移植瘤组织Bax基因的表达,但对Bcl-2的表达影响较弱.结论:瑞香狼毒药效组分在体内对人肝癌细胞BEL-7402裸鼠移植瘤具有较强的抑制作用并呈现一定的剂量依赖关系,该组分具有一定的诱导凋亡作用,可能与上调Bax有关.     

p53、Bcl-2及 Bax 在大肠腺癌中的表达及临床意义

目的：观察大肠腺癌中p53、Bcl-2及Bax阳性表达情况,并探讨其临床意义。方法采用免疫组织化学方法检测大肠腺癌、大肠腺瘤、正常大肠黏膜组织中p53、Bcl-2及Bax阳性表达情况,并分析其在大肠腺癌组织中的阳性表达与患者临床病理特征的关系。结果与正常大肠黏膜组织比较,大肠腺癌组织中p53、Bcl-2阳性表达明显升高、Bax阳性表达明显降低（P均＜0．01）。 p53、Bcl-2、Bax表达与大肠腺癌患者肿瘤细胞分化程度、浸润深度、淋巴结转移以及Dukes分期明显相关（ P均＜0．01）,与性别、年龄无关。 p53的表达与Bcl-2的表达呈正相关（P＜0．01）,与Bax的表达呈负相关（P＜0．01）,Bcl-2的表达与Bax的表达呈负相关（P＜0．01）。结论 p53、Bcl-2及Bax可相互作用,共同参与大肠腺癌的发生、发展过程。     

凋亡抑制蛋白XIAP在胰腺癌组织中的表达及意义

目的 通过检测XIAP在胰腺癌中的表达，探讨其对胰腺癌发生、发展的可能作用及临床意义。方法 应用免疫组化SP法检测10例正常胰腺组织、14例胰腺良性病变和42例胰腺癌组织中XIAP的表达，并分析其与胰腺癌临床病理参数的关系。结果 XIAP在正常胰腺组织、胰腺良性病变及胰腺癌中均有表达。正常胰腺组织中，高表达占20％，良性病变中占21．4％，而胰腺癌中，高表达占59．5％，较前二者均有显著性差异（P〈0．05）。42例胰腺癌组织中，XIAP表达强度与性别、年龄、肿瘤部位、肿瘤大小、分化程度、临床分期及淋巴结转移均无显著相关。结论 XIAP在正常胰腺组织，胰腺的良性病变及胰腺癌中均有表达，但在胰腺癌中呈高表达，表明XIAP在胰腺癌的发生中起到一定作用；XIAP的表达与胰腺癌各项临床病理参数无相关性。     

胃癌组织中Bcl-2、p53蛋白表达及分析

采用免疫组化法检测Bcl-2和p53蛋白在胃癌组织中的表达.发现:Bcl-2和p53蛋白在正常胃黏膜组织不表达;Bcl-2在高分化腺癌和重度不典型增生的阳性表达率明显高于中、低度分化腺癌和中、轻度不典型增生组织,p53在重度不典型增生及低分化腺癌阳性表达率均明显高于中、轻度不典型增生和中重度分化腺癌.胃癌淋巴结转移组Bcl-2阳性率明显低于无淋巴结转移组,p53阳性率明显高于无淋巴结转移组.二者的表达呈显著负相关.认为Bcl-2和p53通过细胞凋亡参与肿瘤的发生、发展的不同价段,对判断胃癌的预后有一定的参考价值.     

斑蝥素对胰腺癌细胞系PANC1、CFPAC-1的凋亡诱导作用及机制研究

目的 研究斑蝥素对胰腺癌细胞系PANC1、CFPAC-1的凋亡诱导作用及机制。方法 用斑蝥素处理PANC1、CFPAC-1细胞。四甲基偶氮唑蓝(MTT)法检测细胞增殖;流式细胞术检测细胞凋亡;酶化学法检测caspase活性;RT-PCR及蛋白质印迹法检测凋亡相关基因的表达。结果 斑蝥素呈剂量依赖性明显抑制胰腺癌细胞系PANC1、CFPAC-1增殖及诱导细胞凋亡。10μmol/L斑蝥素处理细胞72 h,PANC1、CFPAC-1细胞的增殖抑制率最高,分别达(52.95 +6.34)％和(71.21 +6.30)％。处理24h,PANC1细胞的早期和晚期凋亡细胞分别从7.35％增加到24.89％、6.36％增加到17.73％;CFPAC-1细胞从6.39％增加到24.70％、9.21％增加到12.58％(P值均＜0.01)。PANC1细胞的caspase 8和caspase9活性分别为对照组的(155.8±11.5)％和(194.6±14.7)％;CFPAC-1细胞分别为对照组的(182.5±24.3)％和(215.8±12.2)％(P值均＜0.01)。促凋亡基因TNF-α、TRAILR1、TRAILR2、Bad、Bak和Bid表达增加,抗凋亡基因Bcl-2表达减少。结论 斑蝥素通过激活Caspase、上调促凋亡基因及下调抗凋亡基因的表达从而诱导胰腺癌细胞凋亡。     

凋亡抑制基因Survivin在胰腺癌中的表达及临床意义

应用免疫组化S-P法检测凋亡抑制基因Survivin在27例胰腺癌组织、11例癌旁正常组织中的表达。结果胰腺癌组织Survivin蛋白表达率显著高于正常胰腺组织（P〈0．05）;且随临床、病理分期增加、淋巴结转移,Survivin蛋白阳性表达率逐渐升高（P〈0．05）。提示Survivin的异常表达与胰腺癌的发生、发展密切相关,可能是影响胰腺癌预后的重要分子指标。     

凋亡抑制蛋白XIAP在胰腺癌组织中的表达及意义

目的 通过检测XIAP在胰腺癌中的表达,探讨其对胰腺癌发生、发展的可能作用及临床意义.方法 应用免疫组化SP法检测10例正常胰腺组织、14例胰腺良性病变和42例胰腺癌组织中XIAP的表达,并分析其与胰腺癌临床病理参数的关系.结果 XIAP在正常胰腺组织、胰腺良性病变及胰腺癌中均有表达.正常胰腺组织中,高表达占20%,良性病变中占21.4%,而胰腺癌中,高表达占59.5%,较前二者均有显著性差异(P ＜ 0.05).42例胰腺癌组织中,XIAP表达强度与性别、年龄、肿瘤部位、肿瘤大小、分化程度、临床分期及淋巴结转移均无显著相关.结论 XIAP在正常胰腺组织、胰腺的良性病变及胰腺癌中均有表达,但在胰腺癌中呈高表达,表明XIAP在胰腺癌的发生中起到一定作用;XIAP的表达与胰腺癌各项临床病理参数无相关性.     

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。     

Tiam1基因沉默对胰腺癌细胞裸鼠移植瘤生长的影响

目的研究沉默T淋巴瘤侵袭转移诱导因子(Tiam)1基因对胰腺癌细胞裸鼠移植瘤生长的影响,并探讨其可能的分子机制。方法通过RNA干扰(RNAi)技术沉默胰腺癌BxPC-3细胞中Tiam1的表达,Western印迹实验检测其沉默效果;将转染处理过的胰腺癌细胞接种于裸鼠皮下,建立胰腺癌皮下移植瘤模型;观察肿瘤生长情况并绘制肿瘤生长曲线,裸鼠处死后,取瘤称重;苏木素-伊红(HE)染色法观察移植瘤组织病理学结构;免疫组织化学染色法(IHC)检测移植瘤组织增殖相关蛋白Ki-67,转移相关蛋白E-钙黏蛋白(cadherin)、波形蛋白(Vimentin)、Slug的表达。结果 RNAi技术可有效沉默胰腺癌BxPC细胞中Tiam1的表达,并成功构建胰腺癌裸鼠移植瘤模型;与对照组比较,si-Tiam1组裸鼠肿瘤体积与质量均明显降低(P<0.05);HE染色结果显示,与对照组比较,si-Tiam1组中肿瘤组织出现细胞皱缩、片状坏死等病理性改变;IHC结果显示,与对照组相比,si-Tiam1组移植瘤组织中Ki-67、Vimentin、Slug的表达明显降低,而E-cadherin的表达明显升高。结论沉默Tiam1能有效抑制胰腺癌裸鼠移植瘤的生长,其机制可能与Ki-67、Vimentin、Slug表达的降低及E-cadherin的表达增强有关,提示Tiam1有可能成为胰腺癌基因治疗的新靶标。     

STAT3基因沉默对人胰腺癌SW1990细胞的裸鼠移植瘤生长的影响

目的 观察信号转导与转录激活因子3（STAT3）基因表达沉默后对人胰腺癌SW1990细胞的裸鼠移植瘤生长的影响,探讨其机制.方法 构建靶向STAT3短发卡RNA（shRNA）表达载体,稳定转染胰腺癌SW1990细胞（SW1990-RNAi组）,以转染阴性对照shRNA表达载体细胞（SW1990-Con组）及亲本SW1990细胞（SW1990组）作为对照.应用蛋白质印迹法检测各组细胞STAT3、血管内皮生长因子（VEGF）、基质金属蛋白酶2（MMP-2）蛋白的表达.建立各组细胞的裸鼠皮下移植瘤模型,观察移植瘤的生长,应用免疫组化法检测移植瘤的CD34表达,计算肿瘤的微血管密度（MVD）.结果 SW1990组、SW1990-Con组、SW1990-RNAi组细胞的STAT3蛋白表达量分别为84.69±9.31、82.00±7.76、7.93±1.24,VEGF蛋白表达量分别为82.94±8.97、80.86±10.28、39.04±6.23,MMP-2蛋白表达量分别为40.88±5.09、38.26±5.71、12.54±2.15,SW1990-RNAi组均显著低于其他两组（P值均＜0.05）,而SW1990-Con组与SW1990组细胞的3种蛋白表达量差异均无统计学意义.SW1990组、SW1990-Con组、SW1990-RNAi组裸鼠移植瘤的重量分别为（2.2±0.4）、（2.2±0.3）、（0.5±0.3）g,瘤组织的MVD分别为每高倍视野（20.35±2.41）、（18.79±1.94）、（9.62±1.06）个,SW1990-RNAi组均显著低于其他两组（P值＜0.05或＜0.01）,而SW1990组与SW1990-Con组间的差异均无统计学意义.结论 STAT3基因表达被抑制后SW1990细胞的裸鼠移植瘤生长减缓,其机制可能是通过下调VEGF及MMP-2的表达、抑制肿瘤血管形成所致.     

Antiangiogenic therapy for human pancreatic carcinoma xenografts in nude mice

AIM: To investigate the anti-tumor effects of antiangiogenic therapy (a combination of TNP-470, an antiangiogenic compound, with gemcitabine, an antimetabolite) on human pancreatic carcinoma xenografts and its mechanism. METHODS: A surgical orthotopic implantation (SOI) model was established by suturing small pieces of SW1990 pancreatic carcinoma into the tail of pancreas in nude male mice. Mice then received either single therapy (n = 24) or combined therapy (n = 32). Mice receiving single therapy were randomly divided into control group, G100 group receiving 100 mg/kg gemcitabine IP on d O, 3, 6 and 9 after transplantation, and T30 group receiving 30 mg/kg TNP-470 s.c on alternate days for 8 wk. Mice receiving combined therapy were randomly divided into control group, T15 group, G50 group and combination group (TNP-470 30 mg/kg and gemcitabine 50 mg/kg). Animals were killed 8 wk after transplantation. Transplanted tumors, liver, lymph node and peritoneum were removed. Weight of transplanted tumors, the T/C rate (the rate of mean treated tumor weight to mean control tumor weight), change of body weight, metastasis rate, and 9-wk survival rate were investigated. Tumor samples were taken from the control group, T30 group, G100 group and combination group. PCNA index (PI) and microvessel density (MVD) were investigated by immunohistochemical staining for PCNA and factor VIII, respectively. RESULTS: There was a significant inhibitory effect on primary tumor growth of pancreatic carcinoma in G100 group, compared to T30 group, whereas tumor metastasis was significantly inhibited in T30 group compared to G100 group. There was no significant improvement in survival rate in these two groups. No significant inhibitory effect on tumor growth and metastasis in T15 group and G50 group. However, significant anti-tumor and anti-metastatic effects were observed in the combination group with a significant improvement in survival rate. The inhibitory effect on tumor growth in combination group enhanced 2 times in comparison with G50 group and 5 times in comparison with T15 group. Moreover, 25% of the animals hearing tumors were cured by the combination therapy. The levels of MVD and PI were 14.50±5.93 and 0.41±0.02,12.38±1.60 and 0.30±0.07, 7.13±2.99 and 0.37±0.03, and 5.21±1.23 and 0.23±0.02 respectively in the control group, G100 group, T30 group and combination group. A significant inhibitory effect on PI level and MVD level was observed in G100 group and T30 group respectively whereas both MVD and PI levels were significantly inhibited in the combination group (P<0.05). CONCLUSION: Antiangiogenic therapy shows significant anti-tumor and anti-metastatic effects, and is helpful to reduce the dosage of cytotoxic drugs and the side effects. These effects are related to the antiangiogenic effect of TNP-470 and cytotoxic effect of gemcitabine.     

Effect of antidepressants on body weight, ethology and tumor growth of human pancreatic carcinoma xenografts in nude mice

AIM： To investigate the effects of mirtazapine and fluoxetine, representatives of the noradrenergic and specific serotonergic antidepressant （NaSSA） and se- lective serotonin reuptake inhibitor （SSRI） antidepres- sant respectively, on body weight, ingestive behavior, locomotor activity and tumor growth of human pancre- atic carcinoma xenografts in nude mice. METHODS： A subcutaneous xenograft model of hu- man pancreatic cancer cell line SW1990 was estab- lished in nude mice. The tumor-bearing mice were ran- domly divided into mirtazapine group [10 mg/（kg·d）], fluoxetine group [10 mg/（kg·d）] and control group （an equivalent normal saline solution） （7 mice in each group）. Doses of all drugs were administered orally, once a day for 42 d. Tumor volume and body weight were measured biweekly. Food intake was recorded once a week. Locomotor activity was detected weekly using an open field test （OFT）. RESULTS： Compared to the fluoxetine, mirtazapine significantly increased food intake from d 14 to 42 and attenuated the rate of weight loss from d 28 to 42 （t = 4.38, P 〈 0.05）. Compared to the control group, food intake was significantly suppressed from d 21 to 42 and weight loss was promoted from d 35 to 42 in the fluoxetine group （t = 2.52, P 〈 0.05）. There was a significant difference in body weight of the mice after removal of tumors among the three groups. The body weight of mice was the heaviest （13.66 ± 1.55 g） in the mirtazapine group and the lightest （11.39 ± 1.45 g） in the fluoxetine group （F（2,12） = 11.43, P 〈 0.01）. The behavioral test on d 7 showed that the horizontal and vertical activities were significantly increased in the mirtazapine group compared with the fluoxetine and control groups （F（2,18） = 10.89, P 〈 0.01）. These effects disappeared in the mirtazapine and fluoxetine groups during 2-6 wk. The grooming activity was higher in the mirtazapine group than in the fluoxetine group （10.1 ± 2.1 vs 7.1 ± 1.9 ） （t = 2.40, P ?     

CIK细胞对裸鼠人胃癌移植瘤生长的抑制作用

目的: 探讨CIK细胞对裸鼠人胃癌移植瘤生长的抑制作用.方法: 用淋巴细胞分离液分离外周血单个核细胞, 给予多种细胞因子(rhIFN-γ、CD3mcAb、rhlL-2、rhlL-1), 诱导生成CIK细胞.培养人胃癌细胞株SGC-7901, 接种至40只裸鼠右腋皮下, 10 d后随机分2组, 每组20只, 分别为CIK组和对照组. 连续5 d在接种肿瘤细胞部位处给予CIK细胞和生理盐水注射治疗, 观察CIK细胞对胃癌移植瘤模型的抗肿瘤疗效.结果: CIK组胃癌肿块质量和生存期与对照组相比, 均具有显著性差异(1.21±0.34 g vs2.73±0.45 g, 65.8±6.2 d vs 44.3±4.8 d, 均P<0.01). 裸鼠体内实验表明, CIK细胞能够显著抑制胃癌细胞的生长, 其抑瘤率可达47.6%,明显高于对照组( P<0.01).结论: CIK细胞在裸鼠体内对人胃癌移植瘤有特异性抑瘤作用, 并可以延长裸鼠生存时间.     

Effect of somatostatin and tamoxifen on the growth of human pancreatic cancers in nude mice

We studied the effects of SMS 201-995 (SMS), a somatostatin analog, and tamoxifen, an antagonist of estrogenic actions, on the growth of human pancreatic cancers (SKI and PGER) in vivo. Male nude mice were inoculated with either SKI or PGER by passage of tumor chunks (3 mm2) to the scapular region. Mice from each tumor group were randomly allocated to one of four treatment groups: group 1, control group; group 2, SMS (100 micrograms/kg t.i.d.); group 3, tamoxifen (10 mg/kg three times a week); and group 4, SMS (100 micrograms/kg t.i.d.) + tamoxifen (10 mg/kg three times a week). The somatostatin analog, SMS, given alone or as a combined regimen with tamoxifen, significantly reduced (a) the rate of growth of SKI, and (b) DNA, RNA, and protein content of the tumors. On the other hand, in the case of PGER tumors, none of the treatment regimens significantly influenced the growth of PGER in vivo. Despite showing no significant effects during the study, PGER tumors in mice receiving tamoxifen alone had significantly lower total DNA, RNA, and protein contents compared to control tumors; this was reversed on combined treatment with SMS. None of the growth parameters of PGER was effected by SMS alone. We conclude that, in the case of SKI, SMS with or without tamoxifen was effective as a growth inhibitory agent, whereas in the case of PGER, tamoxifen alone was effective. This finding suggests that independent pathways mediate the growth-inhibitory effects of tamoxifen and SMS, and that different pancreatic cancers may respond to the two agents differently, some with inhibition, some not.     

Correlation between epidermal growth factor receptor concentration and the growth of human gastric cancer xenografts in nude mice.

Seven human gastric cancer xenografts with different concentrations of EGF receptor were established in nude mice. The expression of EGF receptor in the tumors was demonstrated by Western blotting with anti-EGF receptor antibody, binding assay with 125I-EGF and immunohistochemistry with anti-EGF receptor antibody. Western blotting revealed EGF receptor doublet bands at molecular masses of 150 KDa and 170 KDa in all of the samples. The concentration of 125I-EGF binding activity in the tumors ranged from 36.0 to 11,000 fmol/mg protein, with a mean of 345 fmol/mg protein. EGF receptor was also demonstrated immunohistochemically on the apical border of the glands and the cell membrane of the tumor cells. There seemed to be a close correlation between the concentration of 125I-EGF binding activity and the doubling time of these tumors in nude mice (gamma = -0.68). However, no definite correlation was observed between EGF ligand binding and histological features of intestinal type or diffuse type. The expression of EGF receptor appears to facilitate the growth of human gastric cancer xenografts in nude mice.     

抗抑郁药米氮平对吉西他滨治疗胰腺癌模型的辅助作用

目的探讨抗抑郁药米氮平对吉西他滨治疗的胰腺癌移植瘤裸鼠进食量、体重和肿瘤生长的影响。方法24只胰腺癌裸鼠皮下移植瘤模型随机分为对照组、吉西他滨组（术后第1、4、7、10天腹腔注射吉西他滨100mg/kg体重）和联用组（吉西他滨组＋米氮平10mg·kg^-1·d^-1灌胃,持续21d）,每组8只。术后21d处死裸鼠,比较3组动物体重、进食量、肿瘤体积的变化。结果吉西他滨组具有显著的抗肿瘤生长作用,但存在显著的胃纳减少和体重降低等不良反应。术后第21天,联用组和吉西他滨组胰腺癌移植瘤体积无明显差异,抑瘤率分别为69．13％和71．60％（P〉0．05）;联用组进食量（3．12±0．11）g、体重（14．68±0．42）g,稍高于吉西他滨组的（2．96±0．14）g和（14．38±0．61）g（P值均〉0．05）,但显著低于对照组的（4．65±0．13）g和（17．46±0．52）g（P值均〈0．05）。结论吉西他滨化疗具有显著的抗胰腺癌作用,米氮平虽无显著增效作用,但可在一定程度上减轻大剂量吉西他滨化疔的不良反应。     

Bombesin inhibits growth of human pancreatic adenocarcinoma in nude mice

Bombesin, a 14-amino acid peptide, exhibits direct and indirect effects on the gastrointestinal tract, including release of hormones, stimulation of pancreatic, gastric, and intestinal secretion and intestinal motility. Cholecystokinin (CCK) and gastrin, two of the hormones released by bombesin, have been shown to play a role in maintaining the growth of normal gastrointestinal mucosa as well as in eliciting trophic responses in normal and neoplastic tissue. We studied the effects of chronic bombesin treatment on the growth of a human ductal pancreatic adenocarcinoma (SKI) xenografted into nude mice, and on the growth of the normal nude mouse pancreas. Thirteen nude mice were implanted with SKI tumor and divided into two groups. Mice received 0.1 ml intraperitoneal injections of either bombesin (20 micrograms/kg) or the vehicle alone three times per day. Tumor areas were measured twice weekly until death (week 8), at which time the tumors and the host pancreas were excised, weighed, and assayed for protein, RNA, and DNA content. Significant inhibition of tumor growth was found in the bombesin-treated group at weeks 4, 5, 6, 7, and 8. Tumor area and weight at death (day 57) were significantly less in the bombesin-treated group (48 and 46%) as compared with control. We observed similar inhibition of tumor DNA (39%), RNA (38%), and protein (43%) content compared with controls. In contrast, bombesin significantly increased the weight (64%), protein (81%), and DNA (73%) content of the mouse pancreas compared with controls. We conclude that bombesin acts concurrently as both a trophic agent for normal host pancreas and a growth inhibitory agent in xenografted pancreatic cancer tissue.