简介：基因治疗为癌症的治疗提供一条新途径。编码immunostimulatorycytokines的基因的转移与显著成功被使用了在动物消除癌症。然而，在有这策略的病人的临床的试用限制了功效。因此，基因转移向量系统的改进是必要的。混合病毒的向量，与鼠科的IL-12或记者LacZ基因由SFVreplicon组成，被构造。这混合向量在vitro并且在vivo在HCC显示出表示的特性和高水平。在一个老鼠orthotropic肝肿瘤模型，没有伴随毒性，由有mIL-12基因的混合向量的确定的肿瘤的治疗导致了一项强壮的反肿瘤活动。随后，助手依赖者侵入人体气管粘膜的病菌包含mifepristone(RU486)的向量可诱导的系统被构造为控制并且人的interleukin的肝特定的表示12(hIL-12)(HD-Ad/RUhIL-12)并且鼠标IL-12(mIL-12)(HD-Ad/RUmIL-12)。数据证明hIL-12的高、支撑的浆液层次能被继续RU486的管理达到每12或24h。hIL-12的重复正式就职能被获得在上，至少在HD-Ad/RUhIL-12的单个注射以后的48个星期的一个时期。肝转移与的处理HD-Ad/RUmIL-12，正RU846在所有动物导致了完全的肿瘤回归。然后，不同cytokine基因被插入到有条件的replicative侵入人体气管粘膜的病菌向量(也叫的oncolytic侵入人体气管粘膜的病菌)。在肿瘤房间的侵入人体气管粘膜的病菌的复制将杀死肿瘤房间和版本病毒，它感染包围肿瘤房间。由oncolytic侵入人体气管粘膜的病菌的cytopathic效果和transgene的生物效果的联合将施加强壮的反肿瘤活动。向量的这些新类型可以为癌症基因治疗提供一个有势力和安全工具。

简介：ChinahasrecognizedthethreatofHIVtoitspopulationandrespondedwithanationalantiretroviraltreatment(ART)program.However,highARTfailureratesandthespreadofresistancewithinpopulationsareimportantrealitiestoconsiderwhendevelopingandmanagingARTprogramsinChinaandworldwide.Conceptswhichwilldefinetreatmentsuccessandlocalandnationalprogrammaticgoalsare1)accesstoART,2)durabilityofARTatthepatientlevel,3)scalabilityoftreatmentmodalities,andthe4)sustainabilityoftheprogramatthecommunityornationallevel.Inthefaceoflimitedresources,ChinamustalsoconsiderwhentostartARVtherapy,whichagentstouse,whentoswitchthem,andhowtotreathighlyexperiencedpatientswithdrugresistance.TheoptimalARVregimentostartwithischangingfrequentlywiththeintroductionofnewagentsandthepresentationofnewdata.Currently,aregimenincludingtenofovir,emtricitabineorlamivudineandanonnucleosidereversetranscriptaseinhibitorappearstohaveoptimalcharacteristicstotreatHIV/AIDSinChina.However,criticaltoallofthesechoicesistheevaluationofprogramsimplementedtoinsurewidescalesuccess.Chinahaswiselybegunthisprocessofevaluatingtheperformanceoflocalprogramsthroughsystematicmonitoringandevaluationoftreatmentoutcomes.Thiswillallowregimensandprogramsthatworktobeexpanded,andprogramswithhighfailureratestobeeliminated.Intheend,evidencebaseddatasupportingtreatmentstrategieswillallowChinatosuccessfullyconfrontitsAIDSepidemicearlyandpreventitstragicconsequences

简介：Monoclonal(mAb)成功地被用于长期的疾病的治疗，例如癌症，发炎和有免疫力的疾病。与在抗体工程的技术进展，当有减少的immunogenicity的高亲密关系治疗学在聚光灯下面变得，小重组体抗体的开发碎裂。设计重组体抗体碎片的一种流行格式是单个链的改正变量(scFv)分子，父母抗体的VH和VL区域被一个多肽连接器一起在连接。scFv碎片保留目标特性和未经触动的抗体，和罐头的抗原绑定亲密关系被在房间从单个cDNA表示VH和VL区域的宫外的联盟者遗传上在大数量设计并且生产。由于它的更小的尺寸，scFv分子表演在肿瘤穿入改进了pharmacokinetics并且被主人免疫系统更好容忍。

简介：Thetherapeuticeffectofherpessimplexvirusthymidinekinase/ganciclovir(HSV-tk/GCV)systemonhepatocellularcarcinomawasstudiedinthisexperiment.Thetk-containingretroviralrecombinantswereusedtoinfecthepatomacells(BEL-7402)andthecellsweretreatedwithganciclovir(0-100μg/ml).TheresultsshowedthatHSV-tkgenecouldbeefficientlytransferredinvitrointohepatomacellsandstablyexpressed.Thegrowthpotentialofthetk-containingcellswassignificantlyinhibitedbyGCV(P<0.01)ascomparedtothenon-tk-containingcells.TheantitumoreffectofHSV-tk/GCVsystemwasalsoproducedexvivointk-containingtumorofnudemiceascharacterizedbyamarkeddecreaseintumorgrowthafterGCVtreatmentcontrarytoaprogressiveenlargementofnon-tk-containingtumors.Althoughthehistologicalexaminationdemonstratedthattheefficiencyofthegenetransferwaslessthan30%,thekillingeffectofHSV-tk/GCVsystemonhepatocellularcarcinomawasstillsignificantlygenerated.ThegropermechanismofHSV-tkgenetherapyonhepatictumorreferredas“bystandereffect”intherapeuticapproachhasnotbeenfoundinthisstudyandrequiredtobeexploredfurther.

简介：OverexpressionandactivationofHER-2/neu(alsoknownasc-erbB-2),aproto-oncogene,wasfoundinabout30%ofhumanbreastcancers,promotingcancergrowthandmakingcancercellsresistanttochemo-andradio-therapy.Wild-typep53iscrucialinregulatingcellgrowthandapoptosisandisfoundtobemutatedordeletedin60-70%ofhumancancers.Andsomecancerswithawild-typep53donothavenormalp53function,suggestingthatitisimplicatedinacomplexprocessregulatedbymanyfactors.Inthepresentstudy,weshowedthattheoverexpressionofHER-2/neucoulddecreasetheamountofwild-typep53proteinviaactivatingPI3Kpathway,aswellasinducingMDM2nucleartranslocationinMCF7humanbreastcancercells.BlockageofPI3KpathwaywithitsspecificinhibitorLY294002causedG1-Sphasearrest,decreasedcellgrowthrateandincreasedchemo-andradio-therapeuticsensitivityinMCF7cellsexpressingwild-typep53.However,itdidnotincreasethesensitivitytoadriamycininMDA-MB-453breastcancercellscontainingmutantp53.OurstudyindicatesthatblockingPI3KpathwayactivationmediatedbyHER-2/neuoverexpressionmaybeusefulinthetreatmentofbreasttumorswithHER-2/neuoverexpressionandwild-typep53.