简介:Objective:Toinvestigatetheimmunotherapyefficacyoffusioncells(dendritic-C6anti-TGF-β1cells)inthetreatmentofintracranialgliomas.Methods:Dendriticcellswereisolatedfromratbone-marrowprecursorsstimulatedinvitrowithgranulocyte-macrophagecolony-stimulatingfactor(GM-CSF)andInterleukin-4(IL-4).C6anti-TGF-β1cellsoriginallyfromC6celllineofaratglioblastomaweretransfectedwithplasmidofTGF-β1anti-sensegene.FusionsofdendriticcellsandC6anti-TGF-β1cellswerepreparedbypolyethyleneglycol(PEG).TheDC/C6anti-TGF-β1fusioncellswereobservedandconfirmedbylightmicroscopyandscanningelectronmicroscopy.Experimentalratsweredividedintothreegroupsatrandom:C6cells(I),dendritic-C6anti-TGF-β1fusioncellsandC6cells(II)andIMDMmediumonly(III).Thecellswereinjectedintorightparietalloberegionoftheratwithstereotaxictechnique.Histology,tumornecrosisandsurvivaltimewereevaluated.Results:ComparedwiththeratsthatreceivedC6cells(survivalmediantimewaslessthan20days,tumorregionwasseeninallfieldsofobserved),theratsinjectedwithdendritic-C6anti-TGF-β1fusioncellsandC6cellsgotamoreprolongedlifespan(morethan59days),aswellaslesstumorregion(5.01%-6.2%).Therewasnotumornecrosis,butsomegliaswereseeninsurroundings.Allratsweresurvivedandnonecrosiswasobservedinnegativecontrolgroup.StatisticalanalysisshowedthatgroupIIhadsignificantdifferencecomparedwithgroupI.Conclusions:Dendritic-C6anti-TGF-β1fusioncellscouldprolongthelifespanofrats,providingastrategytoachieveanantitumorresponseagainsttumorsinthecentralnervoussystem.
简介:客观:为了与M-CSFR验证MAF-J6-1受体的抗原协会并且进一步学习M-CSF和它的受体的角色,调停了在支持白血病的房间增长的juxtacrine。方法:MAF-J6-1RRE2的Monoclonal抗体(McAb)和rhM-CSFR的polyclonal抗体(PolyAb)被准备。到M-CSFR的McAbRE2的特性被ELISA被间接ELISA,有J6-1房间殖民地形成的跨neutralizing试金和中立化测试证实。结果:到M-CSFR的净化的RE2的反应活动是超过1:16000。M-CSFR和MAF-J6-1R的禁止的活动能被RE2和anti-M-CSFR抗体堵住。到M-CSFR的RE2的反应能被M-CSFR减少。结论:到M-CSFR的RE2的特性被证实,有M-CSFR的MAF-J6-1R的抗原协会被证明。它建议M-CSF和它的受体调停了auto-juxtacrine刺激能是在白血病或nonhematological恶意的起作用的机制。
简介:目的探讨Dishevelled-1(Dvl1)、CyclinD1和CD44v6蛋白在儿童骨肉瘤组织中的表达及其与骨肉瘤临床病理特征的关系。方法采用免疫组化法检测Dvl1、CyclinD1和CD44v6在47例儿童骨肉瘤组织中的表达情况。分析3者表达的关系及其与临床病理特征的关系。结果Dvl1、CyclinD1和CD44v6在儿童骨肉瘤组织中的高表达率为76.60%(36/47)、72.34%(34/47)和68.09%(32/47)。Dvl1表达与肿瘤直径(P=0.020)和Ennecking分期(P=0.032)有关;CyclinD1和CD44v6的表达也分别与肿瘤直径(P=0.007,P=0.036)和Ennecking分期(P=0.024,P=0.020)有关。Dvl1表达与CyclinD1(r=0.332,P=0.023)和CD44v6表达(r=0.376,P=0.009)呈正相关。结论Dvl1、CyclinD1和CD44v6在儿童骨肉瘤中呈高表达,其高表达能够促进儿童骨肉瘤的恶性进展。
简介:目的通过研究CD44v6、MMP2和β1integrins在CINⅡ-Ⅲ、宫颈鳞形细胞癌组织中的表达,探讨细胞外基质降解在宫颈鳞形细胞癌发生发展中的作用。方法收集宫颈鳞形细胞癌组织切片20例,CINⅡ-Ⅲ组织切片15例,正常宫颈组织切片10例,免疫组化法检测CD44v6、MMIr2和β1integrins表达。结果CD44v6低表达与CINⅡ-Ⅲ、病变有相关性(P〈0.05),与宫颈鳞形上皮癌变有高度相关性(P〈0.001);β1integrins低表达与CINⅡ-Ⅲ、病变有高度相关性(P〈0.001);MMP2高表达与宫颈鳞形上皮癌变有高度相关性(P〈0.001),但与CINⅡ-Ⅲ病变无相关性(P〉0.05)。结论CD44v6、MMIr2和plintegrins和MMP2的异常表达与宫颈鳞癌的发生发展有关,细胞外基质作用减弱有利于宫颈癌变的发生,其本身结构的破坏有利于宫颈癌的浸润。
简介:PROMOTIONOFINVITROGROWTHOFHUMANMEDULLOBLASTOMACELLSBYEXOGENEOUSIL-6LiuJiai刘佳;LiHong李宏;HamouMarie-France;NicolasdeTribolet(1Di...
简介:N^6-methyladenosine(m^6A)isanessentialRNAmodificationthatregulateskeycellularprocesses,includingstemcellrenewal,cellulardifferentiation,andresponsetoDNAdamage.Unsurprisingly,aberrantm6Amethylationhasbeenimplicatedinthedevelopmentandmaintenanceofdiversehumancancers.Alteredm6AlevelsaffectRNAprocessing,mRNAdegradation,andtranslationofmRNAsintoproteins,therebydisruptinggeneexpressionregulationandpromotingtumorigenesis.Recentstudieshavereportedthattheabnormalexpressionofm6Aregulatoryenzymesaffectsm6Aabundanceandconsequentlydysregulatestheexpressionoftumorsuppressorgenesandoncogenes,includingMYC,SOCS2,ADAM19,andPTEN.Inthisreview,wediscussthespecificrolesofm6A“writers",“erasers”,and“readers”innormalphysiologyandhowtheiralteredexpressionpromotestumorigenesis.Wealsodescribethepotentialofexploitingtheaberrantexpressionoftheseenzymesforcancerdiagnosis,prognosis,andthedevelopmentofnoveltherapies.
简介:胃癌是导致癌症患者死亡的主要疾病之一,而现有的治疗手段有限。当前免疫检测点抑制剂在肿瘤的治疗中取得了突破进展,相关研究迅速覆盖到胃癌。针对免疫检查点抗程序性死亡分子1(PD-1)/PD-1配体(PD-L1)抗体的临床研究正在广泛开展。本文对胃癌发生的免疫机制,PD-1/PD-L1表达,抗PD-1/PD-L1抗体早期临床研究及抗PD-1/PD-L1抗体预测疗效的生物标志物的研究进行文献复习。
简介:Objective:Toexploretheprobabilityofvascularendothelialgrowthfactor(VEGF)antisenseoligodeoxynucleotidesasadevelopingnewtherapeuticstrategyforglioma.Methods:VEGFproteinexpressionwasdetectedbyS-Pimmunohistochemicaltechnique.TumorcellapoptosiswasobservedbyTUNELmethod.Results:Comparedwithcontrol,VEGFproteinexpressionwasinhibitedbyantisenseoligodeoxynucleotidesinvitro.Andtheinhibitoryeffectsincreasedwiththeincreasingconcentration.VEGFpositiveratewas82.10%incontrolgroup,whilein2.5,5,10(mol/LAODNgroups,theywere70.00%,57.85%,53.20%respectively.Noinhibitioneffectwasfoundinthecelllinestreatedwithmissenseandsenseoligodeoxynucleotides.Invivo,antisenseoligodeoxy-nucleotidestherapyalsoinhibitedVEGFproteinexpressionandinducedtheincreaseofapoptotictumorcells.However,ithasnoeffectontumorcellproliferation.Conclusion:ItishopefulthatVEGFantisenseoligodeoxynucleotidesmaybeanewgenetherapymethodtogliomathroughitsantiangiogenesiseffectbyinhibitionofVEGF.