珍香胶囊对裸鼠原位移植的人胃癌的抗癌作用

目的：了解珍香胶囊对裸鼠原位移植的人胃癌的疗效,为临床试验提供科学依据,方法：用珍香胶囊分别对人胃低分化腺癌SGC－7901以及人胃高分化腺癌MKN－28裸鼠原位移植模型进行治疗。实验分5组：珍香胶肮浓度组（4800mg/kg.bw),中浓度组（2400mg/kg.bw),低浓度组（1200mg/kg.bw)以及阳性对照组（丝裂霉素C1mg/kg.bw)和阴性且（生理盐水）,珍香胶囊灌胃给药,每天2次,连续给药40次,丝裂霉素C皮下注射给药,每2天1次,共给药10次,实验以荷人胃癌裸鼠的生命延长率,胃指数,血清唾液酸（SA）含量作为疗效评价指标,实验重复3次,:(1) 香胶囊高,中,低三剂量对荷人胃癌SGC－7901裸鼠生命延长率分别为57．78％－72．03％（P＜0．01）,42．22％－56．59％（P＜0．01）,28．13％－33．79％（P＜0．01）,阳性对照丝裂霉素C对荷人胃癌SGC－7901裸鼠生命延长率为52．58％－60．02％（P＜0．01）,（2）经珍香胶囊高,中剂量治疗后,荷人胃癌MKN－28裸鼠的胃指数,血清SA含量显著减少（P＜0．01或P＜0．05）,结论：在裸鼠可耐受的剂量下,珍香胶囊对裸鼠原位移植的人胃低分化腺癌SGC－7901以及人胃高分化腺癌MKN－28均有明显的抗癌作用,且随着剂量增加,其抗癌疗效增强。     

甲基苯丙氨酸氮芥(AT-1420)抗瘤作用的研究

AT-1420即甲基苯丙氨酸氮芥。实验表明对大鼠W-255有显著的抗瘤活性,用0.155～1mg/kg/d×7,有 81～100％抑瘤率,用0.25～1mg/kg/d×7,有50～100％肿瘤消散率,疗效与消瘤芥相似。 对小鼠S-180,肝癌、网细胞肉瘤(L_2)均有明显的抗瘤作用,用0.6～0.8mg/kg/d×7～8腹腔给药,抑瘤率分别为48～52％,28％、41～50％,对艾氏腹水癌(EAC)生命延长率为177％。作为比较,消瘤芥用量为2.5～3.5mg/kg/d,对S-37抑制率为64％。AT-1420对EAC和W-256疗效较好,但对S-37无效,其他肿瘤和消瘤芥的疗效相似。另口服和注射给药均有效。 AT-1420对~3H-TdR参入EAC细胞中有明显的抑制作用,抑制率为70％(±8.1)。 测得大鼠腹腔注射一次的LD50为5.4mg/kg,7次给药的LD50为1.25mg/kg/次。测得小鼠腹腔注射一次的LD50为8mg/kg,而7次给药的LD50为1.13mg/kg/次。 上述表明AT-1420有明显的抗动物肿瘤作用,抗瘤谱广,口服和注射给药有效。疗效与消瘤介相似,且用量较小,故AT-1420值得进一步研究,考虑提供临床试用。     

小鼠H22肝癌皮下移植瘤的生长与血硫氧还蛋白还原酶活性的相关性

背景与目的：研究表明硫氧还蛋白还原酶（thioredoxin reductase，TrxR）在肿瘤组织中的表达较正常组织中明显增多且活性升高．但关于肿瘤生长与血TrxR活性的关系报道却很少。本实验的目的是研究小鼠H22肝癌皮下移植瘤的生长与血TrxR活性的关系。方法：建立H22肝癌昆明小鼠皮下移植瘤动物模型，分为5组：空白组不接种肿瘤细胞，模型组接种肿瘤细胞，这两组小鼠均给予5％。羧甲基纤维素钠灌胃作为对照；乙烷硒啉低、中、高剂量组均接种肿瘤细胞，并分别灌胃给予36mg／kg、72mg／kg、216mg／kg乙烷硒啉。于肿瘤接种前、肿瘤生长至100mm，给药前、给药第1天、给药第4天及给药第10天5个时间点行眼眶取血，二硫代双硝基苯甲酸（dithio-bis-nitrobenzoic acid，DTNB）法测定血浆TrxR活性。处死小鼠剥离皮下肿瘤，DTNB法测定肿瘤组织TrxR活性。结果：给药结束时低、中、高剂量乙烷硒啉组小鼠的抑瘤率分别达到59．5％、74.3％、74．9％。空白组小鼠血TrxR活性稳定：接种肿瘤后小鼠血TrxR活性随肿瘤体积增大而增加，呈明显正相关；给药结束时，低、中、高剂量乙烷硒啉组小鼠血TrxR活性抑制率分别为59．2％、68．4％、68．9％，而肿瘤组织中TrxR活性抑制率分别为15．3％、25．8％、29．8％。结论：H22肝癌小鼠血TrxR活性与其肿瘤生长呈正相关；不同剂量的TrxR抑制剂乙烷硒啉干预后,血TrxR活性能够被不同程度地抑制，与肿瘤生长的抑制呈一致性．     

以磺胺嘧啶为载体的氟尿嘧啶靶向药物抗鼠H22肝癌实验研究

[目的]在动物体内评价以磺胺嘧啶（SF）为载体的氟尿嘧啶（5-Fu）靶向药物（SFPEG5-Fu）的抗肿瘤疗效及急性毒性。[方法]40只荷肝癌H22小鼠按体重随机分为4组：0．9％NaCl组、SFPEG5-Fu组、5-Fu组、SFPEG＋5-Fu（30：1，m／m）组，每组10只小鼠。生理盐水组作为阴性对照组，其他3组分别以相应5-Fu剂量为20mg／kg的SFPEG5-Fu、5-Fu、SFPEG＋5-Fu（30：1，m／m）尾静脉给药，每天1次，连续给药5d。给药后7d计算肿瘤抑制率。并观察给药组荷瘤小鼠的生存期。SFPEG5-Fu以最大给药剂量、最大给药体积尾静脉一次给药20只健康昆明小鼠，给药第14d处死小鼠。对小鼠进行尸体解剖检查，取肝、脾、肾、肺、胰腺、心脏、胃、肠、胸骨进行常规病理检查了解SFPEG5-Fu的急性毒性。[结果]与生理盐水组相比，SFPEG5-Fu，5-Fu，SFPEG＋5-Fu（30：1，m／m）3组肿瘤生长明显受到抑制（P〈0．01），给药后SFPEG5-Fu组小鼠皮下瘤体积小于其他3组（P〈0．01）．5-Fu组和SFPEG＋5-Fu组间小鼠皮下瘤体积无明显差异（P〉0．05）。SFPEG5-Fu组小鼠生存期长于5-Fu组、SFPEG＋5-Fu组小鼠生存期（P〈0．05）及生理盐水组小鼠生存期（P〈0．01）。SFPEG5-Fu的最大耐受量为4g／kg，可以认为LD50〉4g／kg。组织学检查发现肝细胞出现广泛的气球样变性的改变，有点状坏死，胸骨造血功能有轻到中度抑制。[结论]SFPEG5-Fu对荷肝癌H22小鼠有明显的抑制肿瘤作用及较低的毒性，并可延长荷瘤小鼠的中位生存期。     

人参皂甙Rg3对小鼠肝癌H22腹水瘤的治疗研究

目的：研究人参皂甙Rg3治疗小鼠恶性腹腔积液的疗效。方法：100只雌、雄各半昆明种小鼠随机分为5组：Ⅰ组生理盐水组（0．9％NS）;Ⅱ组顺铂组（DDP0．5mg／kg）;Ⅲ组低剂量人参皂甙Rg3组（LPD0．3mg／kg）;Ⅳ组中剂量人参皂甙Rg3组（MPD1．0mg／kg）;Ⅴ组高剂量人参皂甙Rg3组（HPD3．0mg／kg）。所有小鼠肝癌H22腹水瘤模型建立后24小时开始分别腹腔注射0．2ml／只治疗,每日1次,共14天,同时观察小鼠的生活状态和体重。治疗结束后24小时,处死各组半数小鼠测各项指标,剩余小鼠停止治疗并观察生存时间。结果：各用药组较生理盐水组在腹水量（P〈0．05）、腹水中瘤细胞数和瘤细胞存活率方面都下降（P〈0．05）;随着人参皂甙Rg3给药浓度的增加,腹水中瘤细胞数及瘤细胞存活率下降（P〈0．05）;人参皂甙Rg3高剂量组腹水中瘤细胞数及瘤细胞存活率低于DDP组（P〈0．05）。各实验用药组较生理盐水组小鼠寿命延长,其中中剂量人参皂甙Rg3组延长最明显（P〈0．05）。结论：人参皂甙Rg3对小鼠恶性腹腔积液的形成具有抑制作用,这为临床应用提供了实验依据。     

TNP-470抑制小鼠恶性腹腔积液形成的实验研究

目的 :研究血管生成抑制剂TNP 4 70对小鼠恶性腹腔积液形成的抑制作用。方法 :将小鼠肝癌腹水型细胞系Hca F2 5接种于小鼠腹腔 (2× 10 5/鼠 )。将 10 0只小鼠随机分成对照组 (0 9%NS) ,化疗组 (DDP 1mg/kg) ,TNP 4 70低、中、高剂量组 (30mg/kg、6 0mg/kg、90mg/kg)。自第 2天起分别腹腔内给药 (0 2ml/鼠 ) ,隔日给药 ,共 7次。第 15天处死部分小鼠测各项指标 ,余小鼠观察生存期。结果 :化疗组 ,TNP 4 70低、中、高剂量组的腹水抑制率分别为 74 77% ,5 2 33%、80 11%和 92 89% ;腹膜瘤结节的形成率分别为 10 0 % ,70 %、80 %、5 0 %和 30 %。在生存时间上 ,各治疗组较对照组明显延长生存期 (P <0 0 5 )。结论 :TNP 4 70具有抑制小鼠恶性腹腔积液的形成和延长小鼠生存时间的作用。     

NJY冻干粉对生理机能的影响及其免疫调节和抗肿瘤作用

目的：研究NJY冻干粉对机体体能的影响及其免疫调节作用和抗肿瘤作用。方法：分别按NJY冻干粉16、32、64mg/kg剂量给ICR种小鼠灌胃给药,进行负重游泳实验、耐缺氧实验、迟发超敏反应实验和巨噬细胞吞噬功能实验,观察NJY冻干粉对小鼠生理机能及免疫功能的影响。用NJY冻干粉给S180荷瘤昆明小鼠灌胃,观察对肉瘤生长的影响。另用NJY冻干粉给S180荷瘤昆明小鼠灌胃,并给小鼠腹腔一次性注射环磷酰胺,观察NJY冻干粉对环磷酰胺化疗作用的影响,以及NJY冻干粉对移植性S180腹水瘤小鼠存活时间的影响。结果：NJY冻干粉16mg/kg和64mg/kg组小鼠抗疲劳能力较对照组明显提高（P〈0.05）;32mg/kg和64mg/kg组小鼠耐缺氧能力较对照组明显提高（P〈0.05）;NJY冻干粉32mg/kg和64mg/kg组小鼠耳肿胀率较对照组明显增加（P〈0.05）;NJY冻干粉给药组巨噬细胞吞噬指数与对照组比较差异无统计学意义（P〉0.05）。NJY冻干粉给药组小鼠S180型肉瘤抑瘤率与对照组比较差异无统计学意义（P〉0.05）;NJY冻干粉给药组腹水瘤小鼠生命延长率与对照组比较差异无统计学意义（P〉0.05）;环磷酰胺60mg/kg与NJY冻干粉合用后,抑瘤率较环磷酰胺对照组显著提高（P〈0.05）。结论：NJY冻干粉具有免疫增强作用,可以提高小鼠的抗疲劳能力和耐缺氧能力,能增强环磷酰胺的抗肿瘤作用。     

脑瘤消胶囊对艾氏腹水癌小鼠的抗肿瘤作用

目的 观察脑瘤消胶囊对艾氏腹水癌小鼠的抗肿瘤作用，探讨该药治疗颅内肿瘤的作用机制。方法随机将小鼠分为6组：正常对照组、荷艾氏腹水癌模型组、模型 环已亚硝脲40mg/kg组、模型 脑瘤消0．5、1．0和2．0g/kg剂量组。小鼠腹腔接种艾氏腹水癌后连续8天灌胃给药，每天1次，同时记录动物死亡时间。实验共重复3次。结果与模型组比较，脑瘤消胶囊各剂量组荷瘤小鼠的生存时间明显延长。结论灌胃给药0．5～2．0g/kg的脑瘤消胶囊对艾氏腹水癌具有明显抗肿瘤作用。     

雷舒宁(黏质沙雷菌苗)抗肿瘤转移的实验研究

目的　探讨雷舒宁 (黏质沙雷菌苗 )抑制脾脏接种的小鼠肝癌HCA肝转移的作用及其分子机制。方法　腹腔注射雷舒宁 ( 6mg/kg、4mg/kg、2mg/kg 3个剂量组 ) ,连续隔日给药 6次 ,计算小鼠生命延长率。采用定量逆转录 -聚合酶链反应技术(RT -PCR )检测实验组和对照组nm 2 3基因、Tiam -1基因的表达。结果　雷舒宁可明显延长肝癌小鼠的生存期 ,3个剂量组的延长率分别为 5 5 .8%± 1.3% ,49.2 %± 1.6%、43.2 %± 1.7% ,具有明显的剂量 -效应关系 (P <0 .0 5 )。肿瘤原发灶nm 2 3-1、Tiam -1基因的表达水平明显高于癌旁正常组织 ,雷舒宁能明显抑制侵袭诱导基因Tiam -1和nm 2 3-1的表达。对肿瘤原发灶和转移灶nm 2 3-1基因抑制率分别为 5 5 .6%、5 7.8%。对肿瘤原发灶和转移灶Tiam -1基因抑制率分别为 34 .8%、36.7%。结论腹腔注射黏质沙雷氏菌苗可明显抑制小鼠肝癌HCA肿瘤转移相关基因nm 2 3-1和Tiam -1的表达     

左金丸对小鼠S180肿瘤细胞获得性多药耐药P—gp的表达及血清肿瘤标志物的影响

目的：研究左金丸、黄连和吴茱萸对小鼠获得性多药耐药S180腹水肿瘤细胞生长的抑制作用,以及对肿瘤细胞P—gP的表达和血清4种肿瘤标志物：（TM）酸性磷酸酶（ACP）、碱性磷酸酶（AKP）、醛缩酶（ALD）和乳酸脱氢酶（LDH）活力的影响。方法：PFC方案建立S180多药耐药细胞模型,将耐药后S180细胞悬液以每只小鼠0．2ml接种于腹腔,黄连、吴茱萸及左金丸灌胃给药7d,观察小鼠体重、脾指数、肝指数、生命延长率（ILS）,流式细胞仪测定P-糖蛋白（P—gp）的表达率,试剂盒检测血清中肿瘤标志物的活力。结果：左金丸给药组对小鼠S180多药耐药细胞增长有明显的抑制作用,能有效降低肝指数,提高脾指数,提高生命延长率（ILS）（60．26％）的作用明高于黄连（21．85％）和吴茱萸单独给药（20．53％）（P〈0．01）。同时,左金丸给药组能有效逆转$180肿瘤细胞中P—gp的表达（2．69％）至接近S180细胞对照组水平（1．65％）,显著低于模型组（16．07％）,也强于黄连（5．69％）及吴茱萸（9．15％）单独给药时的逆转效果。并且左金丸可有效降低血清中ALD（75．944-12．47U·L^-1）和LDH（1632．924-494．48u·L^-1）的活力,提高血清中ACP（103．284-10．36U·100ml^-1）和AKP（34．564-4．91U·100ml^-1）的活力,与黄连、吴茱萸给药组比较有显著性差异（P〈0．01）。结论：黄连和吴茱萸合用能产生明显的配伍协同抗肿瘤作用,对P—gp的表达和血清中肿瘤标志物的影响可能是其抗肿瘤和逆转多药耐药的潜在机制。     

缩氨基硫脲过渡金属配合物抗癌活性研究

［目的］研究3－硝基苯乙酮缩氨基硫脲（HL）过渡金属配合物的抗癌活性。［方法］测试了配体和6个配合物对S180腹水癌细胞的体外抗癌活性及配合物Cu（L）2、Zn（L）2对S180腹水癌小鼠的生命延长作用和对S180实体瘤的抑制作用。［结果］配合物Cu（L）Cl、Cu（L）2、Zn（HL）2Cl2、Zn（L）2对S180腹水癌细胞有强的杀伤作用。配合物Cu（L）2、Zn（L）2剂量为10mg/kg时,对S180荷瘤小鼠的存活时间延长率分别为132．4％和55．2％,对S180实体瘤的抑癌率分别为81.59％和62.11％。［结论］配合物Cu（L）2是一种抗癌活性较好的物质。     

Ability of sera from mice treated with Ge-132, an organo-germanium compound, to inhibit experimental murine ascites tumors

Serum specimens from mice treated orally with Ge-132 (100 mg/kg) exhibited antitumor activity against Ehrlich (allogeneic) and RL 1 (syngeneic) ascites tumors in BALB/c mice. Sera obtained from mice 24 hours after Ge-132 administration displayed the highest antitumor effect and the antitumor activity was dose-dependent. Sera prepared from mice 12, 36 or 48 hours after Ge-132 treatment had no protective effect. Circulating interferon (IFN) was induced at 24 hours after administration. The antiviral activity of serum from Ge-132-treated mice was inactivated by treatment with trypsin, low pH, and anti-IFN-gamma antiserum. The inactivated preparations of serum IFN induced by Ge-132 did not show antitumor activity when administered to mice bearing Ehrlich ascites tumors. These results suggest that the antitumor activity in the sera of Ge-132-treated mice may have been expressed through IFN-gamma which was induced by Ge-132.     

Antitumor and Cytotoxic Activities of Methanol Extract of Indigofera linnaei Ali.

Methanol extract of Indigofera linnaei (MEIL) was investigated for antitumor, cytotoxic and antioxidantactivities against transplantable tumors and human cancer cell lines. In vitro cytotoxicity was evaluated in HeLa,Hep-2, HepG-2, MCF-7, HT-29, Vero and NIH 3T3 cells by MTT assay and in vivo antitumor activity with Ehrlichascites carcinoma (EAC) and Dalton’s ascites lymphoma (DLA) tumor-bearing mice. Activity was measuredby monitoring the mean survival time, effect on hematological parameters, antioxidant enzyme levels and solidtumor volume. The extract exhibited strong in vitro cytotoxicity against all the tested cancer cell lines, but itwas found to be safe with normal cells. MEIL at the dose of 200 and 400 mg/kg, significantly increase the meansurvival time (P<0.001), exerted a protective effect on the hemopoietic system, demonstrated in vivo antioxidantactivity and significantly reduce solid tumor volume (P<0.01). These results show a significant antitumor andcytotoxic effect of MEIL against EAC, DLA and human cancer cell lines and support the ethnomedical use ofIndigofera linnaei.     

Antitumor activity of 7-ethyl-10-[4-(1-piperidino)-1-piperidino]carbonyloxy-camptothec in, a novel water-soluble derivative of camptothecin, against murine tumors

The search for new water-soluble analogues of camptothecin (CPT) with higher activity and less toxicity has led to the development of a novel compound, 7-ethyl-10-[4-(1-piperidino)-1-piperidino]carbonyloxy-camptothecin (CPT-11), which showed significant antitumor activity against a broad spectrum of experimental tumor models by i.p., i.v., or oral administration. When its activity against L1210 was compared with that of CPT and known derivatives, CPT-11 was most effective, giving the highest maximum increase in life span (ILS) and showing good activity over a wide dose range. The antitumor activity of CPT-11 was shown against tumors not only in the ascites form but also in the solid form. Included among the more susceptible murine tumors are S180, Meth A fibrosarcoma, Lewis lung carcinoma, Ehrlich carcinoma, MH134 hepatoma, mammary carcinoma of C3H/HeN mice, L1210, and P388 leukemia. Probable cures of these tumors were induced frequently by CPT-11. The antitumor activity of CPT-11 against i.p.-implanted L1210 was superior to that of Adriamycin in maximum ILS, the number of cured mice, and the therapeutic ratio. CPT-11 at a dose of 100 mg/kg produced an ILS in excess of 300% with five of six mice surviving tumor free, and effected 100% tumor regression at 200 mg/kg, whereas the optimum dose of Adriamycin, 12.5-25 mg/kg, brought about 114-129% ILS with one of six mice surviving. The acute toxicity of CPT-11 was extremely low, particularly in the case of oral administration. CPT-11 is expected to be clinically useful.     

Antitumor activity of Ge-132, a new organogermanium compound, in mice is expressed through the functions of macrophages and T lymphocytes

The antitumor activity of Ge-132 against a variety of allogeneic and syngeneic murine ascites tumors was first evaluated. The antitumor effects of Ge-132 were observed when mice inoculated with Ehrlich carcinoma (allogeneic) or RL male 1 leukemia (syngeneic) cells were treated orally. However, Ge-132 had no activity on a T-cell lymphoma (EL 4, syngeneic) or a methylcholanthrene-induced fibrosarcoma (Meth-A, syngeneic). The antitumor effect of Ge-132 in mice was related to the dose administered as well as the administration schedule. The antitumor activity of Ge-132 was next studied in mice pretreated with some blockers against immunocompetent cells. The antitumor efficacy of Ge-132 was not observed when tumor-bearing mice were treated with trypan blue and carrageenan or monoclonal anti-Thy 1.2 antibody. However, when natural killer cells were eliminated from mice bearing RL male 1 or Ehrlich ascites tumors by treatment with anti-asialo GM 1 antiserum, the antitumor efficacy of the compound was unchanged. These results suggest that Ge-132 is effective against certain ascites tumors regardless of whether the tumor is syngeneic or allogeneic. Further, its effect might be expressed through host defense mechanisms, including macrophages and/or T lymphocytes.     

Importance of T-cells and macrophages in the antitumor activity of carboxyethylgermanium sesquioxide (Ge-132)

The purpose of this study was to investigate the effective mechanisms of Ge-132, an organogermanium compound with immunomodulatory activity, on experimental murine ascites tumors. The antitumor effects of Ge-132 were observed when mice inoculated with Ehrlich carcinoma (allogeneic) or RL male 1 leukemia (syngeneic) cells were treated orally. However, Ge-132 had no activity on EL-4 lymphoma (syngeneic) or Meth A fibrosarcoma (syngeneic). The antitumor activity of Ge-132 was not observed when tumor-bearing mice were treated with trypan blue, carrageenan, or monoclonal anti-Thy 1.2 antibody. However, when natural killer (NK) cells were eliminated from mice bearing RL male 1 or Ehrlich ascites tumors by treatment with anti-asialo GM1 antiserum, the antitumor activity of the compound was unchanged. This suggests that Ge-132 was effective against certain ascites tumors regardless of whether the tumor was syngeneic or allogeneic. Furthermore, its effect might be expressed through host defense mechanisms, including macrophages and/or T-cells.     

Inhibitory effect of meloxicam, a selective cyclooxygenase-2 inhibitor, and ciglitazone, a peroxisome proliferator-activated receptor gamma ligand, on the growth of human ovarian cancers

BACKGROUND: It was recently reported that high expression of peroxisome proliferator-activated receptor gamma (PPARgamma) and low expression of cyclooxygenase-2 (COX-2) might be involved in the inhibition of ovarian tumor progression and confirmed that PPARgamma activation could suppress COX-2 expression via the nuclear factor-kappaB pathway in ovarian cancer cells. METHODS: The current study investigated whether meloxicam, a selective COX-2 inhibitor, and ciglitazone, a ligand for PPARgamma, inhibit the growth of human ovarian cancer cell lines and aimed to elucidate the molecular mechanism of their antitumor effect. Tumor growth and survival were examined in female nu/nu mice xenografted with subcutaneous OVCAR-3 tumors or with intraperitoneal DISS tumors and treated with meloxicam (162 ppm in diet, every day) or ciglitazone (15 mg/kg intraperitoneally once a week). RESULTS: Both meloxicam and ciglitazone treatments significantly suppressed the growth of OVCAR-3 tumors xenotransplanted subcutaneously and significantly prolonged the survival of mice with malignant ascites derived from DISS cells as compared with controls. Meloxicam treatment decreased COX-2 expression in tumors by 2.5-fold compared with that observed in untreated tumors. Although ciglitazone treatment did not alter COX-2 expression in tumors, it reduced the expression of microsomal prostaglandin (PG) E synthase, which converts COX-derived PGH(2) to PGE(2). Both meloxicam and ciglitazone decreased PGE(2) levels in serum as well as in ascites. Reduced microvessel density and induced apoptosis were found in solid OVCAR-3 tumors treated with either meloxicam or ciglitazone. CONCLUSIONS: These results indicate that both meloxicam and ciglitazone produce antitumor effects against ovarian cancer in conjunction with reduced angiogenesis and induction of apoptosis.     

Antitumor activity of polysaccharide fractions from pine cone extract of Pinus parviflora Sieb. et Zucc

Hot water extract of pine cone (PCE) of Pinus parviflora Sieb. et Zucc. dose-dependently suppressed both solid and ascites tumor cells transplanted into various mice. Acidic polysaccharides of PCE significantly increased the survival time of mice bearing ascites tumor cells, and activity increased with acidity. One of the four polysaccharide fractions obtained by NaOH extraction showed the most potent antitumor activity. This fraction significantly suppressed the growth of solid tumor cells, with occasional tumor regression and necrosis, and with little or no cytocidal effect on cultured tumor cells. All acidic polysaccharides were able to activate mouse macrophage-like cell line J774.1. There did not appear to be any correlation between the antitumor activity of these polysaccharides and their content of arabinose (or fucose), mannose, galactose, glucose, or uronic acid.     

Antitumor activity of the aromatase inhibitor FCE 24928 on DMBA-induced mammary tumors in ovariectomized rats treated with testosterone

Summary The antitumor activity of the irreversible aromatase inhibitor FCE 24928 (4-aminoandrosta-1,4,6-triene-3,17-dione) was studied in ovariectomized and testosterone propionate (TP)-treated rats bearing 7,12-dimethylbenzanthracene (DMBA)-induced mammary tumors. This experimental condition was used as a model of postmenopausal breast cancer. TP was given s.c. three times per week for 4 weeks at a dose of 20 mg/kg per day, a treatment that is effective in maintaining tumor growth in ovariectomized rats (89% growing tumors). FCE 24928 given s.c. twice daily 6 days/week for 4 weeks at doses of 10 and 30 mg/kg per day inhibited the tumor growth-promoting effect of TP as shown by 81% and 80% tumor-regression rates. When FCE 24928 was given at various dose levels either s.c. (3, 10, and 30 mg/kg daily) or orally (10, 30, and 100 mg/kg per day), tumor regression were observed at all doses, amounting to 63%–93% and 63%–72%, respectively. In addition, FCE 24928 given alone (30 mg/kg daily s.c.) to ovariectomized rats did not affect ovariectomy-induced tumor regression. In conclusion, following both s.c. and oral administration, FCE 24928 was effective against DMBA-induced mammary tumors in ovariectomized TP-treated rats, a postmenopausal mammary tumor model.     

Splenectomy abolishes antitumor effect of immunotherapy with streptococcal preparation, OK-432, on mouse liver tumors

In the present study, we investigated the therapeutic effects of oral and subcutaneous administration of OK-432 prior to or following the transplantation of murine liver tumors. In addition, the effect of splenectomy on the antitumor activity of OK-432 was investigated. Mice which received OK-432 orally prior to tumor transplantation exhibited significantly lower tumor weight and significantly improved survival, when compared to the control mice. Prior subcutaneous injection of OK-432 did not show any antitumor activity. On the other hand, both oral and subcutaneous administration of OK-432, subsequent to tumor transplantation, led to a significant improvement of survival and a decrease in the number of lung metastases, although tumor weight was not affected. The anti-tumor effect of OK-432 required the presence of the spleen, since the survival of the mice with liver tumors was not improved by OK-432 if splenectomy and tumor transplantation were performed simultaneously. These results suggest that immunotherapy with OK-432 may beneficial in the treatment of liver tumors and that these effects are dependent on the presence of the spleen.