Granulocyte-Macrophage Colony-stimulating Factor Augments Lymphokine-activated Killer Activity from Pleural Cavity Mononuclear Cells of Lung Cancer Patients without Malignant Effusion

The role of recombinant granulocyte-macrophage colony-stimulating factor (GM-CSF) in augmentation of lymphokine-activated killer (LAK) cell induction by interleukin-2 (IL-2) from pleural cavity mononuclear cells (PCMNCs) was examined in sixteen patients with resectable primary lung cancer not associated with malignant effusion. None of the patients had received any anticancer therapy prior to this study. Incubation of PCMNCs of patients without malignant effusion with GM-CSF for 4 days in the presence of IL-2 resulted in a significant increase in LAK activity against natural killer-resistant Daudi cells. This result was obtained by using the 4 h ⁵¹Cr-release assay. PCMNCs and blood mononuclear cells (BMNCs) were harvested simultaneously from pleural cavity lavage fluid and peripheral blood in lung cancer patients. The LAK activity developed from PCMNCs and BMNCs following incubation with IL-2 for 4 days, but the LAK activity from PCMNCs was significantly lower than that from BMNCs ( P < 0.05). Incubation of PCMNCs with GM-CSF augmented the LAK activity from PCMNCs to a level as high as that from BMNCs. These results suggest that the combined use of GM-CSF with IL-2 may result in augmentation of LAK activity developed from PCMNCs of lung cancer patients without malignant effusion.     

常规化疗药物诱导卵巢癌OVCAR-3细胞凋亡特点的分析

目的：观察抗卵巢癌药物顺铂、紫杉醇和阿霉素对卵巢癌细胞系ＯＶＣＡＲ－３体外生长和生存的影响并分析由它们所致的细胞死亡性质。方法：采用细胞形态学观察、细胞动力学检测及ＤＮＡ片段化分析等细胞和分子生物学方法,研究化疗药物对卵巢癌细胞的凋亡诱导作用。结果：上述药物在抑制ＯＶＣＡＲ－３细胞生长的同时可不同程度地诱导细胞凋亡。其中,紫杉醇诱导细胞凋亡的能力最强;较低剂量紫杉醇（１０＾－８Ｍ）和顺铂（２μｇ／     

Binding Properties and Proliferative Effects of Human Recombinant Granulocyte-Macrophage Colony-stimulating Factor in Primary Leukemia and Lymphoma

Binding of radiolabeled human granulocyte-macrophage colony-stimulating factor (GM-CSF) was studied with blast cells front eight patients with acute myeloblastic leukemia (AML), and neoplastic lymphoid cells from one patient with acute lymphoblastic leukemia (ALL), two patients with chronic lymphocytic leukemia (CLL) and one patient with undiagnosed B cell neoplasia. In all AML cases studied, Scatchard graphs of the direct binding data were curvilinear, and were best fitted by curves derived from a two-binding-site model; one site with high affinity ( K d₁= 12–71 p M ; 174–602 sites/cell) and the other with low affinity ( K d₂= 0.5–2,7 n M ; 1137–6020 sites/cell). A cross-linking study on blast cells from one AML patient demonstrated specific bands which were similar to those reported for peripheral blood neutrophils. Furthermore, blast colony assays for the same preparations showed remarkable proliferative response to GM-CSF in the concentration range from 0.3 n M to 7.0 n M (ED₅₀ >0.7 n M ). This concentration range is approximately one order of magnitude higher than that which is effective for colony formation from normal bone marrow progenitors (ED₅₀= 0.l n M ). No significant correlation could be observed between the responsiveness of blast progenitors to GM-CSF, and the numbers or affinities of GM-CSF binding sites demonstrated on blast cells. In studies with neoplastic lymphoid cells from four patients, ¹²⁵I-GM-CSF also specifically bound in two cases, while response to GM-CSF was not observed in these cases. These results indicate that the expression of GM-CSF receptor is not restricted to the GM-CSF-responsive AML blast cells, but can be observed in other AML blast cells and even in neoplastic lymphoid cells.     

Isolation of a cDNA for a Growth Factor of Vascular Endothelial Cells from Human Lung Cancer Cells: Its Identity with Insulin-like Growth Factor II

We have found growth-promoting activity for vascular endothelial cells in the conditioned medium of a human lung cancer cell line, T3M-11. Purification and characterization of the growth-promoting activity have been carried out using ammonium sulfate precipitation and gel-exclusion chromatography. The activity migrated as a single peak just after ribonuclease. It did not bind to a heparin affinity column. These results suggest that the activity is not a heparin-binding growth factor (including fibroblast growth factors) or a vascular endothelial growth factor. To identify the molecule exhibiting the growth-promoting activity, a cDNA encoding the growth factor was isolated through functional expression cloning in COS-1 cells from a cDNA library prepared from T3M-11 cells. The nucleotide sequence encoded by the cDNA proved to be identical with that of insulin-like growth factor II.     

Human Embryonic Stem Cells - a Potential Vaccine for Ovarian Cancer

Objective: To investigate the therapeutic potential of human embryonic stem cells (hESCs) as a vaccine toinduce an immune response and provide antitumor protection in a rat model. Methods: Cross-reactivity ofantigens between hESCs and tumour cells was screened by immunohistochemistry. Fischer 344 rats were dividedinto 7 groups, with 6 rats in each, immunized with: Group 1, hESC; Group 2, pre-inactivated mitotic NuTu-19;Group 3 PBS; Group 4, hESC; Group 5, pre-inactivated mitotic NuTu-19; Group 6, PBS; Group 7, hESC only.At 1 (Groups 1-3) or 4 weeks (Groups 4-6) after the last vaccination, each rat was challenged intraperitoneallywith NuTu-19. Tumor growth and animal survival were closely monitored. Rats immunized with H9 and NuTu-19 were tested by Western blot analysis of rat orbital venous blood for cytokines produced by Th1 and Th2 cells.Results: hESCs presented tumour antigens, markers, and genes related to tumour growth, metastasis, and signalpathway interactions. The vaccine administered to rats in Group 1 led to significant antitumor responses andenhanced tumor rejection in rats with intraperitoneal inoculation of NuTu-19 cells compared to control groups.In contrast, rats in Group 4 did not display any elevation of antitumour responses. Western blot analysis foundcross-reactivity among antibodies generated between H9 and NuTu-19. However, the cytokines did not showsignificant differences, and no side effects were detected. Conclusion: hESC-based vaccination is a promisingmodality for immunotherapy of ovarian cancer.     

Overexpression of Hiwi Promotes Growth of Human Breast Cancer Cells

The Piwi subfamily comprises two argonaute (Ago) family proteins, which are defined by the presence of PAZand Piwi domains, with well known roles in RNA silencing. Hiwi, a human Piwi subfamily member, has beenshown to play essential roles in stem cell self-renewal and gametogenesis. Recently, accumulating reports haveindicated that abnormal hiwi expression is associated with poorer prognosis of multiple types of human cancers,including examples in the breast. However, little is known about details of the oncogenic role of hiwi in breastcancers. In present study, we confirmed overexpression of hiwi in breast cancer specimens and breast cancercell lines at both mRNA and protein levels. Thus both RT-qPCR and Western blot data revealed significantlyhigher hiwi in intratumor than peritumor specimens, overexpression being associated with tumor size, lymphnode metastasis and histological grade. Hiwi overexpression was also identified in breast cancer cell lines, MDAMB-231 and MCF-7, and gain-of-function and loss-of-function strategies were adopted to identify the role ofhiwi in the MCF-7 cell growth. Results demonstrated that hiwi expression in MCF-7 cells was significantly up- ordown- regulated by the two strategies. We next evaluated the influence of hiwi overexpression or knockdownon the growth of breast cancer cells. Both cell count and colony formation assays confirmed promoting rolesof hiwi in MCF-7 cells, which could be inhibited by hiwi specific blockage by siRNAs. In summary, the presentstudy confirmed overexpression of hiwi in breast cancer specimens and breast cancer cell lines, and providede vidence of promotion by hiwi of cell growth. The results imply an oncogenic role of hiwi in breast cancers.     

重组人粒细胞巨噬细胞集落刺激因子活性测定标准品的研制

目的建立效价测定用的重组人粒细胞巨噬细胞集落刺激因子(GM-CSF)国家标准品.方法标准品按WHO有关要求进行制备、分装、冻干、检测,用GM-CSF国际标准品为标准进行协作标定.结果冻干重组GM-CSF标准品经检测外观,无菌实验合格,水分为0.93%,加速热稳定实验表明其生物学活性在温度为-20℃,4℃和25℃,37℃条件下23个月保持稳定.该标准品经3家实验室协作标定共21次测定,几何平均效价为1.77×105IU/支.实验均数的95%可信区间为(1.64～1.90)×105IU/支,单次实验的95%参考值范围为(1.23～2.34)×105IU/支,平均可信限率为6.962%.结论该批重组GM-CSF国家标准品各项指标均符合要求,可作为国家标准品使用,效价定为1.8×105IU/支,编号为98/01.     

细胞凋亡检测用于卵巢癌实体瘤体外化疗药物敏感试验

目的 评价细胞凋亡检测用于实体瘤体外化疗药物敏感试验的可行性。方法 对Ⅲｃ期原发性上皮性卵巢癌实体瘤细胞行体外分离培养,使用６种不同的抗肿瘤药物对其进行处理,经５天培养后,制成细胞涂片,末端标记法观察不同药物作用后细胞凋亡情况。结果 发现源一示同病例的卵巢癌实体瘤细胞对不同抗癌药物的敏感性存在差异,同一种抗癌药物对不同病人卵巢癌实体瘤细胞产生的凋亡程度不同。结论 细胞凋亡检测用于肿瘤的药物敏感试验     

糖皮质激素对人卵巢癌HO-8910细胞TβR-Ⅱ的上调作用

目的：研究转化生长因子－β1（TGF-β1）通路，是否参与人工合成的糖皮质激素地塞米松（Dex）对人卵巢癌细胞系HO－8910的增殖抑制过程。方法：分别采用细胞计数和流式细胞分析方法检测细胞增殖和细胞周期分布；采用定量RT－PCR，酶联免疫吸附法（ELISA）和（或）免疫细胞化学法，检测TGF－β1及其I型受体（TβR-I）和Ⅱ型受体（TβR－Ⅱ）的表达水平。结果：Dex可引起HO－8910细胞周期G0／G1期进展停滞，并可明显上调TβR－ⅡmRNA的表达，且具有浓度依赖性特点，Dex作用HO－8910细胞8h时作用最强，此时10^-7mol/L Dex组TβR－ⅡmRNA水平比对照组高1．4倍（P＜0．01）；相应地，TβR－Ⅱ的蛋白表达水平也增高，糖皮质激素受体（GR）阻断剂RU486能够逆转这些作用，而Dex对TGF－β1和TβR－ImRNA的表达无调节作用。结论：Dex抑制HO－8910细胞增殖的机制可能包括上调TβR－Ⅱ的表达，该作用是由GR介导的。     

Expression of Vascular Endothelial Growth Factor and E-Cadherin in Human Ovarian Cancer: Association with Ascites Fluid Accumulation and Peritoneal Dissemination in Mouse Ascites Model

Ascites formation and peritoneal dissemination are critical problems in patients with advanced ovarian cancer. Vascular endothelial growth factor (VEGF), also known as angiogenic growth factor, is a potent mediator of peritoneal fluid accumulation and angiogenesis of tumors. E-Cadherin is an adhesion molecule that is important for cell-to-cell interaction. To elucidate the molecular mechanism of ascites formation and peritoneal dissemination of ovarian cancer, we examined the expression of VEGF and E-cadherin in different ovarian cancer cell lines and utilized nude mice to compare the biological characteristics of ovarian cancer cells. Three human ovarian cancer cell lines (AMOC-2, HNOA and HTBOA) were used in this study. Expression of genes was analyzed by northern blotting and RT-PCR methods. AMOC-2 expressed E-cadherin, but not VEGF. HNOA expressed VEGF without E-cadherin expression. HTBOA expressed both VEGF and E-cadherin. Each human ovarian cancer model revealed a specific feature. The AMOC-2 mouse had a single large peritoneal tumor without ascites or remarkable peritoneal dissemination. HTBOA and HNOA mice had bloody ascites and marked peritoneal dissemination. Introduction of VEGF antisense into HTBOA cells could inhibit the ascites formation. It is suggested that VEGF is important for the ascites formation via the increased vascular permeability effect. The deregulation of E-cadherin expression might be involved in the peritoneal dissemination. These molecules are important for the formation of specific features of advanced ovarian cancer. Ovarian cancer cell lines that had different gene expression patterns produced nude mouse human ovarian cancer models with different characteristics.     

卵巢癌细胞和脐血树突状细胞融合瘤苗抗肿瘤免疫效应的初步研究

目的：将脐血来源的树突状细胞（DC）与人卵巢癌细胞株SKOV3细胞相融合，获得SKOV3/DC融合细胞，分析其生物学特性及体外诱导抗卵巢癌肿瘤免疫的能力.方法：1）将用PKH26红色荧光染料标记脐血来源的DC后，聚乙二醇法（PEG）融合DC与人卵巢癌细胞株SKOV3细胞，流式细胞仪分选融合细胞.2）应用细胞培养技术、流式细胞术及光学显微镜检测SKOV3/DC的生长特性和形态学特征 四甲基偶氮唑蓝（MTT）法观察融合细胞体外刺激混合淋巴细胞反应的能力及诱导特异性肿瘤免疫的能力.结果：1）DC和SKOV3按10∶1比例融合，融合率约为8.5%.融合细胞可在体外缓慢增殖，CA125抗原及CD1a、CD80、CD86、HLA-DR、MHC-Ⅰ分子表达阳性.2）SKOV3/DC在体外能有效的激发混合淋巴细胞增殖反应，可明显激活细胞毒性T淋巴细胞（CTL），对卵巢癌细胞株SKOV3有特异性杀伤效应.结论：利用PEG法制备的SKOV3/DC融合细胞兼具两种亲本细胞的部分特性，在体外能够诱导特异性抗肿瘤免疫.本研究将SKOV3/DC作为肿瘤疫苗，为其在卵巢癌主动免疫治疗研究中的进一步应用打下了基础.     

阿法替尼对卵巢癌阿霉素耐药细胞的增敏作用及其机制

目的 探讨阿法替尼增强耐药性卵巢癌细胞对阿霉素化疗敏感度的作用及机制。方法 MTT法检测联用阿法替尼对阿霉素作用于卵巢癌A2780及A2780T细胞的IC50的影响;不同浓度的阿法替尼干预后,罗丹明123蓄积实验检测ABCB1外排功能;ABCB1-Glo? Assay Systems实验检测ABCB1ATPase活性;Western blot检测A2780T细胞EGFR、p-EGFR、HER-2、p-HER-2及ABCB1的表达;RTPCR实验检测A2780T细胞MDR1 mRNA的表达。结果 无毒浓度的阿法替尼显著降低了阿霉素对耐药卵巢癌A2780T细胞的IC50（P<0.05）,而对A2780细胞没有影响;阿法替尼浓度依赖性地增加罗丹明123在A2780T细胞内的蓄积量及ABCB1 ATPase活性（P<0.05）;阿法替尼下调A2780T细胞ABCB1的编码基因MDR1的mRNA水平及ABCB1的蛋白表达水平,抑制了EGFR及HER-2的磷酸化水平。结论 阿法替尼可能通过抑制ABCB1转运体的外排功能,下调ABCB1的表达,进而增敏耐药卵巢癌细胞A2780T对阿霉素的化疗敏感度,是一种有开发前景的卵巢癌化疗增敏剂。     

Potentiation by Tumor Necrosis Factor of Mitoxantrone Cytotoxicity to Human Ovarian Cancer Cell Lines

The cytotoxic activity of human recombinant tumor necrosis factor (rHuTNF) (from 0.01 to 10000 U/ml) was assayed on six human ovarian cancer cell lines and one human cervical carcinoma cell line using a crystal violet assay. rHuTNF was cytotoxic to four cell lines (A2780, A2774, SW626, PAD, while 3 cell lines (IGROV1, SKOV3, Mel80) were marginally sensitive to its activity. However, under the same experimental conditions rHuTNF markedly enhanced the cytotoxicity of mitoxantrone, a chemotherapeutic drug targeted at DNA topoisomerase II, in six cell lines. The potentiation of mitoxantrone cytotoxicity was not caused by increased drug accumulation after rHuTNF treatment. No significant increase in cytotoxicity to Me180 cell line was seen when rHuTNF was added to mitoxantrone.     

消癌平注射液增敏奥沙利铂抑制卵巢癌Caov-3细胞的增殖

目的研究消癌平是否增敏奥沙利铂（Oxaliplatin,OXA）抑制卵巢癌细胞的增殖,并探讨其药理机制。方法体外培养的卵巢癌Caov-3细胞,分别施以OXA、OXA＋消癌平干预,空白对照组给予PBS,采用MTT法测定OXA 单独应用或与消癌平联合应用的IC50及肿瘤细胞存活率;荧光显微镜观察Caov-3细胞胞核形态变化;流式细胞术检测细胞凋亡;蛋白质免疫印迹方法检测caspase-3蛋白质表达。结果消癌平可明显降低OXA的IC50,抑制Caov-3细胞增殖;消癌平增敏OXA诱导的Caov-3细胞凋亡,增加细胞凋亡率,并促进caspase-3活化。结论消癌平增敏OXA抑制卵巢癌细胞Caov-3增殖,促进caspase-3活化可能是其增敏的机制之一。     

曲古菌素A和硼替佐米诱导卵巢癌细胞凋亡的协同作用

目的：探讨组蛋白去乙酰化酶抑制剂曲古菌素A与蛋白酶体抑制剂硼替佐米单独及联合应用对人卵巢癌细胞株SKOV3存活率和凋亡率的影响。初步探讨两种药物联合应用对诱导SKOV3细胞凋亡具有的协同作用。 方法曲古菌素A、硼替佐米单独或者联合应用于卵巢癌细胞后,用四甲基偶氮唑蓝（MTT）比色法测定细胞增殖活性,并计算细胞存活率,Annexin-V/PI法流式细胞仪检测细胞凋亡率,蛋白质免疫印迹法（Western blot）检测相关蛋白表达水平。通过检测Caspases-3的活性及其底物多聚ADP核糖聚合酶（PARP）的表达水平进一步说明不同用药组诱导细胞凋亡的情况。 结果联合用药组诱导的细胞凋亡率和单独用药组比较,差异有统计学意义（P<0.05）。几种凋亡相关蛋白Bcl-2、Mcl-1和Bcl-X_L, 在联合用药组的表达显著低于单独用药组。 在相同的时间点,联合用药组Caspase-3的活性和单独用药组比较,差异有统计学意义（P<0.001）。结论：低剂量的曲古菌素A和硼替佐米联合作用人卵巢癌细胞系能诱导凋亡,并且这种作用远远强于相同剂量单独用药引起的凋亡。这两种药物的联合应用可能成为人卵巢癌化疗中的新方案。     

舒林酸对胃癌细胞生长抑制作用的体外观察

背景与目的:体外研究舒林酸对人胃癌BGC-823细胞的生长抑制作用,探讨其作用机制。材料与方法:将舒林酸作用于人胃癌BGC-823细胞,并设置不同的作用浓度和作用时间。以体外药物敏感实验(单核细胞直接细胞毒测定Mono-nuclearcelldireccytotoxicityassay,MTT)检测舒林酸在不同浓度及不同作用时间下对人胃癌BGC-823细胞的增殖抑制效应;流式细胞仪检测胃癌细胞周期分布;透射电镜观察药物作用后细胞凋亡的形态学改变;免疫组化检测细胞增殖(ki-67)、凋亡抑制基因(bcl-2)及还氧合酶(COX-2)蛋白的表达。结果:舒林酸对人胃癌BGC-823细胞有生长抑制作用,使G0/G1期比例增高,S期比例降低;透射电镜观察到细胞凋亡的形态特征及凋亡小体,而ki-67、bcl-2及COX-2蛋白表达阳性率显著降低;上述作用均呈时间和剂量依赖性。结论:舒林酸在体外具有良好的抑制胃癌BGC-823细胞生长的作用,其机制涉及影响细胞周期分布、诱导细胞凋亡及抑制COX-2、ki-67及bcl-2蛋白的表达。     

PDGF-D对人肝癌细胞增殖及VEGF表达影响研究*

目的：研究血小板源性生长因子D（PDGF-D）对人肝癌细胞株BEL-7402增殖及其血管内皮生长因子（VEGF）表达的影响。方法：体外培养肝癌细胞株BEL-7402和肝癌旁非瘤性细胞株QSG-7701,采用RT-PCR 方法检测PDGF-D 与PDGFR βmRNA 在BEL-7402和QSG-7701的表达情况;将浓度分别为0（对照）、5、10、20、50、100、200 μ g/mL 的人重组PDGF-DD蛋白加入BEL-7402中,采用四甲基偶氮唑蓝比色法检测肝癌细胞的生长曲线;流式细胞仪检测细胞周期变化;半定量RT-PCR 检测VEGF及PDGFR β mRNA 表达情况,ELISA 检测PDGF-DD干预细胞后培养上清中VEGF蛋白的表达情况。结果：PDGF-D 及PDGFR βmRNA 在BEL-7402中高表达,与QSG-7701相比差异有统计学意义（P<0.05）。 PDGF-DD干预细胞后,可促进人BEL-7402增殖,浓度为100 μ g/mL 时达最高峰;细胞周期分布变化,G0/G1 期细胞数减少,S 期细胞数增加,与对照组相比差异有统计学意义;RT-PCR 结果显示,VEGF 及PDGFR β RI 值,实验组（除5 μ g/mL 组外）与对照组相比差异有统计学意义;ELISA 结果显示,加入PDGF-DD各浓度组VEGF蛋白浓度较对照组增高,差异有统计学意义,并呈量效依赖性关系。结论：PDGF-DD能促进BEL-7402的增殖,上调PDGFR β 及VEGF的表达。PDGF-D 及其信号传导系统在肝癌的发生、发展中可能发挥重要的作用,可作为肝癌预后预测指标和治疗靶点。     

Growth-inhibitory Effects of N, N-Diethyl-2-[4-(phenylmethyl)phenoxy]-ethanamine-HCl Combined with Cisplatin on Human Ovarian Cancer Cells Inoculated into Nude Mice

In 5-day incubation of an estrogen receptor-negative human ovarian cancer cell line (KF) with diethyl-2-[4-(phenylmethyl)phenoxy]ethanamine-HCl (DPPE), the concentration of DPPE required for 50% inhibition of KF cell proliferation (IC₅₀) was 1.7 μM. The IC ₅₀ of DPPE for inhibition of protein kinase C (PKC) activity was 3.0 μM, a similar value to those of other antiestrogens such as tamoxifen and clomiphene. DPPE also inhibited phosphorylation of mitogen-activated protein kinase in KF cells. When treatment with DPPE was started 7 days after inoculation of KF cells into nude mice, 50 mg/kg DPPE alone resulted in a significant growth retardation in the early stage of tumor growth. Although 25 mg/kg DPPE showed a similar effect to 2 mg/kg cisplatin (CDDP), the combination had the most marked tumor growth-inhibitory effect. Nude mice treated with combinations of CDDP and DPPE survived significantly longer than not only untreated, but also CDDP-alone-treated mice, while 50 mg/kg but not 25 mg/kg DPPE alone had an effect comparable to that of 2 mg/kg CDDP alone. If treatment with DPPE was begun from the day after tumor inoculation, the inhibitory effect of DPPE was further enhanced, especially when combined with CDDP. If treatment with DPPE was started in nude mice with a lower tumor burden, 25 mg/kg as well as 50 mg/kg DPPE had a similar effect to 2 mg/kg CDDP, in terms of survival. When DPPE was combined with CDDP, the effect was significantly enhanced, compared to that of either alone. These treatments could be done without any adverse side effect. Thus, we conclude that DPPE has an antiestrogen action and its tumor growth-inhibiting activity is enhanced on administration in combination with CDDP.     

卵巢癌组织中VEGF及MVD表达及其临床意义

目的 分析微血管密度(MVD)以及卵巢上皮性肿瘤血管内皮生长因子(VEGF)的表达与卵巢癌临床病理因素的关系及两者的相关性.方法 选取手术切除的卵巢上皮性肿瘤标本88例以及正常卵巢组织标本35例,采用免疫组化染色方法检测所有标本中VEGF及MVD的表达情况,分析两者相关性及与卵巢上皮性肿瘤临床病理因素的关系.结果 VEGF在卵巢癌组织中的表达阳性率为92.0％及MVD平均值为(30.26±8.69),显著高于良性卵巢上皮性肿瘤组织VEGF的阳性表达率[52.6％,(11.52±3.46)] (P ＜0.05);而良性卵巢上皮性肿瘤组织中VEGF阳性表达率及MVD平均值均高于正常对照组(P＜0.05).VEGF阳性表逸的卵巢癌组织中MVD平均值显著高于VEGF阴性表达者,VEGF阳性表达与MVD平均值呈正相关(P＜0.05).卵巢癌组织中VEGF阳性表达与肿瘤临床分期及细胞分化程度存在明显相关性(P＜0.05),而与肿瘤直径、组织学类型以及患者年龄无明显相关性(P＞0.05).MVD与肿瘤临床病理特征无明显相关性(P＞0.05).结论 VEGF及MVD均能反映卵巢上皮性肿瘤的良恶性和恶性进展程度,并可能成为卵巢癌临床生物学治疗的参考指标.     

卵巢癌SKOV3细胞中侧群细胞的生物学特性

目的 分选人卵巢癌细胞系SKOV3中的侧群（side population, SP）细胞,并探讨其是否具有肿瘤干细胞的生物学特性。方法 流式细胞仪检测、分选经DNA染料Hoechst 33342染色后SKOV3中的SP细胞,并对侧群细胞（SP）与非侧群细胞（non-SP）作细胞生物学鉴定,包括增殖能力、克隆形成能力、侵袭及迁移能力、自我更新能力及细胞周期。结果 SKOV3细胞系中SP细胞比例为（1.12±0.104）%,SP细胞增殖速度快于non-SP细胞,差异有统计学意义（P<0.05）。接种相同数量的细胞,SP细胞克隆形成率高于non-SP细胞（P<0.05）。Transwell实验显示,SP细胞侵袭与迁移的细胞数与non-SP相比均明显增多（P<0.05）。SP细胞体外能分化为Non-SP细胞,具有自我更新能力。SP细胞大多处于细胞周期的G0/G1期。结论 卵巢癌细胞系SKOV3中的SP细胞具有肿瘤干细胞的生物学特性,SP细胞表型可考虑作为富集卵巢癌干细胞样细胞的有效方法。