简介:目的研究HPV16E6蛋白及抑癌基因p53在口腔癌中的表达.方法回顾性分析100例口腔癌患者的临床资料和病理切片,采用免疫组织化学方法检测口腔癌组织中p53和HPV16E6蛋白的阳性表达情况,分析其与患者临床分期和病理分级的关系.结果男性口腔癌患者的p53阳性表达率低于女性患者,HPV16E6阳性表达率高于女性患者;年龄﹥50岁口腔癌患者的p53阳性表达率高于年龄≤50岁的患者,HPV16E6阳性表达率低于年龄≤50岁的患者,但差异均无统计学意义(P﹥0.05).口腔癌患者的组织切片显示,p53阳性表达细胞较少,而HPV16E6阳性表达细胞较多.随着患者临床分期的升高(Ⅰ~Ⅳ期),p53阳性表达率呈下降趋势,HPV16E6阳性表达率呈上升趋势,Ⅱ、Ⅲ、Ⅳ期患者与Ⅰ期患者的p53和HPV16E6阳性表达率比较,差异均有统计学意义(P﹤0.05);随着患者病理分级的升高(Ⅰ~Ⅲ级),p53阳性表达率呈下降趋势,HPV16E6阳性表达率呈上升趋势,Ⅱ、Ⅲ级患者与Ⅰ级患者的p53和HPV16E6阳性表达率比较,差异均有统计学意义(P﹤0.05).结论口腔癌患者的p53阳性表达率随患者病理分级与临床分期的升高而降低,HPV16E6阳性表达率随患者病理分级与临床分期的升高而升高,p53阳性表达率的降低和HPV16E6阳性表达率的升高可能与口腔癌的发生和发展有关.
简介:目的:探讨RNAi抑制E6基因的表达对宫颈癌细胞基因表达谱的影响。方法:利用脂质体将已验证有效的表达针对E6基因小发卡RNA(shRNA)的重组质粒转染到宫颈癌细胞CaSKi中,提取宫颈癌细胞总RNA并利用AgilentHuman1A寡核苷酸表达芯片检测RNAi后CaSKi细胞基因表达谱的变化,最后实时PCR检测CDKN2B(p15)和MKI67来验证芯片分析结果。结果:与CaSKi/PSN相比,共有2765个基因表达有明显差异,其中有2709个上调基因(包括代谢相关基因、肿瘤抑制基因、信号转导相关基因、凋亡基因等)和56个下调基因(包括原癌基因、DNA结合和转录基因、代谢相关基因、信号转导相关基因、细胞周期和发育相关基因等)。实时PCR结果表明CDKN2B(p15)和MKI67的变化与基因芯片分析结果一致。结论:联合应用RNAi和基因芯片分析技术可以为研究HPV16E6与宿主细胞相互作用分子机制提够更丰富的资料和信息,并提供新的研究策略和途径。
简介:Someantitumoractivitiesofcomponent(E),extractedfromtherootofFagopynumCymosum(Trev)Meisn(FCTM),haverecentlybeendiscoveredinvivoandinvitro.ThecomponentE(CE)’spatternofactionwithtumorcellularDNAatthemolecularpharmacologicallevelwasinvestigatedbymacromolecularsynthesisexperiment(MSE)andhumanDNAinteractionsystemestablishedinourlaboratory.Theexperimentsdemonstratedthat,invitro,theagentcouldmarkedlyinhibittheincorporationof3H-TdRintothecellularDNA,andtheIC50inP388leukemiacellandinSGC-7901cellwas17.86μg/mland110.4μg/ml,respectively.Theagent,atmg/mllevel,couldproduceanintercalationreversionpatternwithDNAwithinashorttime(2hours).Butwhentheintervalwasprolongedforover4hours,theactionchangedtointercalationirreversiblepattern.Accordingtotheseobservations,theauthorsinferthatCEinteractswithDNAintwoways-directlyandindirectly.Theindirectaction,especiallyinlowconcentr
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: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.
简介:目的研究E-cad在食管鳞状细胞癌中的表达及意义。方法免疫组化SABC法检测76例食管癌E-cad的表达。结果正常食管粘膜细胞膜E-cad表达呈阳性。在癌组织中,E-cad细胞膜表达减弱。E-cad减弱表达率为65.8%(50/76),E-cad表达与病理分化程度(P=0.02)、漫润深度(P=0.024)、静脉侵犯(P=0.04)、淋巴结转移(P=0.022)和临床分期(P=0.04)具有相关性;而与年龄、性别、病理类型无关(P>0.05)。在无淋巴结转移组E-cad表达降低占56.25%(27/48),有淋巴结转移组占82.14%(23/28),两者之间表达差异有显著性;有静脉侵犯组E-cad表达降低率为92.86%(13/14)和无静脉侵犯组为59.68%(37/62),两者之间差异有显著性。结论E-cad减弱表达与食管癌生物学行为有关,可能为食管癌预后差的因素之一。
简介:背景与目的:原发性椎管内淋巴瘤十分罕见,本研究旨在总结原发椎管内淋巴瘤的临床特点,影像学特征及治疗手段,以提高对此病的认识。方法:对北京天坛院神经外科三病房2000年1月至2006年12月间收治的6例经病理证实为椎管内恶性淋巴瘤的患者进行回顾性分析,并文献复习。结果56例患者中,男性4例,女性2例,中位年龄38.5岁。4例患者首发症状为疼痛,平均病程10.9个月。所有患者术前均行MRI检查.肿瘤位于颈段4例,胸段1例,骶段1例。本组患者均采取显微手术治疗,术中辅以电生理监测,肉眼全切1例,近全切除4例,大部分切除1例,无手术死亡。术后4例症状缓解,出院后全部患者均行放射治疗.效果满意。结论:原发性椎管内淋巴瘤是椎管内的罕见肿瘤,缺乏特异性的影像学表现。椎板切除减压,肿瘤切除.术后辅以局部放疗和全身化疗是其主要治疗手段.预后较好。
简介:Objective:Tostudytheroleofconnexingene(Cx43)onthedevelopmentofgliomaandthefeasibilityofusingCx43cDNAasatargetofgenetherapyofgliomas.Methods:ParentalratC6cellsandC6cellstransfectedwithCx43cDNAwereimplantedintorightcaudatenucleusofSDratsascontrolandtransfectedgroup.RatsbearingcerebralC6gliomasweretreatedwithCx43cDNAandemptyvectorastreatedgroupandemptyvectorgroup.Thegeneralmanifestation,survivaltime,MRIdynamicscanningandhistopathologicalchangesofallratswereobserved.Insituhybridizationandimmunohisto-chemistrywereusedforexaminationofCx43mRNAanditsproteiningliomas.AveragenumberofAgNORstainingwasusedfordetectionofcellproliferationactivity,andTUNELmethodfordeterminationofcellapoptosis.Results:Allratsincontrolandemptyvectorgroupdiedofcerebralgliomaswithin3weeksafterimplantationofC6cells.Sixoutofnineratsinthetransfectedgroupandeightoutoftenratsintreatedgroupkeptalivebeyond120dayswithtotallydisappearingofthetumorfoci,exceptonetreatedrathavingalittleresidueoftumor.IngliomasoftransfectedandtreatedgroupsCx43geneexpressionwasupregulated,proliferationactivitywaslowered,However,theapoptoticcellsdidnotincrease.Conclusion:ThepresentstudyindicatesthatCx43geneisofcrucialimportanceinthedevelopmentofmalignantglioma.Itcanbeaneffectivetargetforgenetherapyofgliomas.
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:探讨血管内皮生长因子(VEGF)、CD44v6在非小细胞肺癌(NSCLC)的表达及其临床意义。方法:采用SP免疫组织化学方法观察VEGF、CD44v6在62例NSCLC组织的表达。结果:VEGF、CD44v6在NSCLC组织中表达阳性率分别为72.6%、69.4%,均明显高于癌旁正常组织,P<0.01。VEGF、CD44v6的表达与临床分期及有无淋巴结转移有明显相关,有淋巴结转移组其阳性率明显高于无淋巴结转移组,Ⅲ-Ⅳ期NSCLC组织中VEGF、CD44v6均明显高于Ⅰ-Ⅱ期,P<0.05。VEGF、CD44v6阳性的患者3a生存率均明显低于阴性者,P<0.05。通过COX回归分析发现TNM临床分期、CD44v6阳性表达、有无淋巴结转移及VEGF阳性表达可以作为独立的因素影响NSCLC患者术后的3a生存率。结论:通过这两个指标的检测,可以初步预测NSCLC患者的预后及指导其临床治疗。