简介：MicroRNAs(miRNAs)aresmall,non-codingsingle-strandedRNAsthatcanmodulatetargetgeneexpressionatposttranscriptionallevelandparticipateincellproliferation,differentiation,andapoptosis.Tcellshaveimportantfunctionsinacquiredimmuneresponse;miRNAsregulatethisimmuneresponsebytargetingthemRNAsofgenesinvolvedinTcelldevelopment,proliferation,differentiation,andfunction.Forinstance,miR-181familymembersfunctioninprogressionbytargetingBcl2andCD69,amongothers.MiR-17tomiR-92clustersfunctionbybindingtoCREB1,PTEN,andBim.ConsideringthatthesuppressionofTcell-mediatedimmuneresponsesagainsttumorcellsisinvolvedincancerprogression,weshouldinvestigatethemechanismbywhichmiRNAregulatesTcellstodevelopnewapproachesforcancertreatment.

简介：目的探讨肿瘤组织中调节性T细胞(Tregs)浸润与患者临床病理特征的关系及其对患者预后的影响.方法免疫组织化学法检测76例肝癌患者肿瘤和癌旁组织中Tregs浸润情况,分析Tregs高表达、低表达与患者临床病理特征之间的关系,采用Kaplan-Meier生存分析法评估Tregs浸润对肝癌患者预后的影响.结果肿瘤组织中Tregs浸润与患者性别和门静脉癌栓显著相关(P＜0.05),而与肝内多发瘤灶、HBV感染、血清AFP水平、肿瘤大小、肝硬化、肿瘤包膜完整性、Edmonson分级等无相关性(P＞0.05).Tregs低表达组DFS和TS均显著高于Tregs高表达组(P=0.012和P=0.022).生存分析显示,肝内多发病灶、包膜有无、门静脉癌栓形成(PVTT)和瘤内Tregs浸润显著影响患者无瘤生存率(P＜0.05),其他因素如年龄、性别、乙肝状态、AFP水平、Child-pugh分级、肝硬化有无、Edmonson分级、癌旁和瘤内CD4+、CD8+T细胞浸润等均对患者DFS无显著影响(P＞0.05).上述因素中,仅PVTT和瘤内Tregs浸润显著影响患者总体生存率(P＜0.05).多因素风险模型分析,包膜完整与否(OR=1.816,95％CI:1.084-3.041,P=0.023)和瘤内Tregs浸润(OR=1.931,95％CI:1.153-3.233,P=0.012)是影响患者DFS的独立预后因素;瘤内Tregs浸润(OR=1.843,95％CI:1.073-3.166,P=0.027)是影响患者OS的独立预后因素.结论肿瘤组织中Tregs高表达的肝癌患者预后不良,Tregs高表达有可能促进PVTT形成,Tregs有可能成为肝癌免疫治疗的作用靶点.

简介：Objectives:Toinvestigatetheeffectsofadenovirus-mediatedinduciblenitricoxidesynthasegenetransfectiononbladdertransitionalcellcarcinomaT24cells,andtoprovidenovelinsightsandapproachestoclinicaltherapiesagainstbladdertransitionalcellcarcinoma.Methods:Firstly,constructrecombinantadenovirusvectorpAd-iNOSofiNOS,followedbytransfectionofpAd-iNOSintoHECK293packagingcells.Thirdly,harvestrecombinantadenovirusrAd-iNOSafteramplificationandpurificationprocedures.Finally,transfecttherecombinantadenovirusrAd-iNOSintohumanbladdercarcinomaT24cellsandexaminetheeffectofrAd-iNOStransfectiononapoptosisofT24andpossiblemechanism.Results:Asshownbythisstudy,therecombinantadenovirusrAd-iNOSwasconstructedsuccessfully.Thevirustiterwas5.8×108PFU/mLandrecombinantwasverifiedbyPCRanalysis.TransfectionofadenovirusrAd-iNOSintoT24cellscouldinducesecretionofhighNOconcentration,P53proteinexpressionupregulation,aswellaspromotionofT24cellapoptosis.Conclusions:ThetransfectionofhumanbladdercarcinomaT24cellsfromrecombinantadenovirusrAdiNOSwasconfirmedtoinduceintracellulariNOSover-expression,highproductionofNO,up-regulationofintracellularP53expressionandpromotionofcellapoptosis.

简介：Theacquisitionofsecondarychromosomalaberrationsinchronicmyeloidleukemia(CML)patientswithPhiladelphiachromosome-positive(Ph+)karyotypesignifiesclonalevolutionassociatedwiththeprogressionofthediseasetoitsacceleratedorblasticphase.Therefore,theseaberrationshaveclinicalandbiologicalsignificance.T(3;12)(q26;p13),whichisarecurrentchromosomalaberrationobservedinmyeloidmalignancies,istypicallyassociatedwithdysplasiaofmegakaryocytes,multilineageinvolvement,shortdurationofanyblasticphase,andextremelypoorprognosis.Wehaveidentifiedarecurrentreciprocaltranslocationbetweenchromosomes3and12withdifferentbreakpointatbands3q21inthemalignantcellsfroma28-year-oldman.ThepatientwasinitiallydiagnosedashavingPh+CMLinthechronicphase.Thet(3;12)(q21;p13)translocationoccurred4yearsafterthepatientwasfirstdiagnosedwithCMLwhileundergoingtyrosinekinaseinhibitortherapy.Weconfirmedthet(3;12)(q21;p13)translocationviafluorescenceinsituhybridizationassaybyusingwhole-chromosomepaintprobesforchromosomes3and12.Ourfindingsdemonstratethat,similartootherrecurrenttranslocationsinvolving3q26suchast(3;3)andt(3;21),thet(3;12)(q21;p13)translocationisimplicatednotonlyinmyelodysplasticsyndromeandacutemyeloidleukemiabutalsointheprogressionofCML.Thesefindingsextendthediseasespectrumofthiscytogeneticaberration.