简介:1901年PrierreCurie成功地研制出放射性粒子,从而开始了组织间种植治疗肿瘤的时代。但由于当时释放出中高能γ射线,防护、质控、植入技术条件差,操作烦琐等因素,故临床应用发展非常缓慢。1979年开始报导125I进入临床治疗脑肿瘤。80年代,由于低能γ射线放射性核素研制成功,以及计算机三维治疗计划系统和CT、MRI等扫描技术的应用,这种组织间近距离粒子治疗,明显提高了脑肿瘤局部控制率和延长了患者生存期,是一种新的治疗方法。90年代,特别是1998年中国原子能研究院解决了纳米焊接技术的难关,国产125I放射微粒开始问世。以及和MRI、CT立体定向手术计划系统的完美结合,解决了放射性粒
简介:Acombinedhistopathological,mucinhistochemi-calandimmunohistochemicalstudyofthetransitionalmucosa(TM)adjacenttocolorectalcancerispresented.Twenty-sixresectedspecimenswerestudiedbyhematoxylinandeosin(HE)andhighirondiamine-alcianblue(HID-AB).Carcinoem-bryonicantigen(CEA)wasdemonstratedbyperoxi-daseantiperoxidass(PAP)technique.TheappearanceoftheTMisusuallythicker,longeranddilatedcryptswithincreasedimmatureandintermediatecells.VariableamountofsialomucinsanddecreasesulphomucinscontentaswellasincreasedCEAcontentarefoundintheTM.Thesechangesarenotseeninnon-transitionalzoneandnormalcolorectalmucosa.ItissuggestedthatthemucinchangesandexpressionofCEAintheTMmayindicateanearlyprimarypremalignantchangesandmaybeoneofthereasonsfortheTMaffectingtheprognosisofpatientswithlargebowelcancerafterradicalresection.
简介:Objective:TumorassociatedantigenencodinggeneHCA520(AF146019)wasidentifiedbyscreeningahumanhepatocellularcarcinomaexpressingcDNAlibraryusingSEREXtechnique.InthisexperimentwestudiedtheeffectofHCA520oncellproliferationandapoptosis.Methods:GeneHCA520wasgainedbyPCRandtransfectedinto293cells.ThestableexpressioncellswereobtainedbyG418selection.Thecellproliferationwasmeasuredby[3H]-TdRuptakeandapoptosisassaywasmeasuredbyFACS.Results:EukaryoticexpressionplasmidpcDNA3-HCA520wasconstructedanditsstabletransfectantswereobtained.OverexpressionofHCA520inhibitedthecellproliferationandenhancedcellapoptosisafterserumdeprivation.Conclusion:HCA520isanoveltumorassociatedantigenthatcanaffectcellproliferationandapoptosis.
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:Objective:Toinvestigatethetreatmentofspontaneousmetastaticlungcancerbytumorantigen-pulsed,interleukin-12(IL-12)gene-modifieddendriticcells(DC).Methods:Thespontaneousmetastaticlungcancermodel,preparedbyinjectionofthe3LLLewislungcancercellsintothefootpadsofC57BL/6mice,wastreatedbysubcutaneousvaccinationwithtumorantigenpeptidemut1-pulsed,IL-12gene-modifieddendriticcells(DC-IL-12/mut1)derivedfromthenormalbonemorrow.Aftertreatment,thelungweight,thenumberoflungmetastaticnodesandthesurvivaltimeofthetumor-bearingmicewereobserved,andtheNKandCTLactivityweredeterminedrespectively.Themiceweredividedinto8groupswith12miceineachgroup.Results:Comparedwithmicetreatedwithmut1-pulsed,controlLacZgenemodifiedDCanduntreatedDC,tumor-bearingmicetreatedwithDC-IL-12/mut1hadthelightestlungweights(P<0.01),theleastlungmetastaticnodenumber(P<0.01),thelongestsurvivaltime(P<0.01),alsowiththeinductionofpotentCTLactivity(P<0.01)andNKactivity(P<0.01).Conclusion:Tumorantigen-pulsed,IL-12gene-modifieddendriticcellshavesignificanttherapeuticeffectsonthespontaneousmetastaticlungcancer,providinganewapproachtotreatmentoflungtumors.