简介:甲醇摘录ofStellerachamaejasmeL被antitumor为antitumor活动估计对鼠科的白血病P388invivo的活跃生物鉴定。摘录的bioassay-directcd分离供应了七diterpene混合物(stellerarin,stelleramacrin,gnidimacrin,pimelea因素P2,subtoxin,huratoxin,simplexin)并且二biflavanone混合物(neochemae茉莉属A和B)。在他们之中,gnidimacrin,stellerarin和stelleramacrin(新奇混合物)被发现对P388,L1210和K562invivoandinvitro有高antitumor和细胞毒素的活动。结果建议diterpene混合物是有势力antitumorprinciplesofStellerachamaejasmeL。
简介:目的探讨残胃癌的诊断和治疗体会?方法回顾性分析2002年1月至2007年12月收治的28例残胃癌患者的临床资料。结果患者中22例获手术治疗,根治性手术12例,姑息性手术10例:消化道重建方式为空肠“P”袢代胃、胃空肠Roux—en—Y吻合。手术组中6例术后发生并发症,肺部感染4例,切1:3裂开2例,均经治疗后痊愈出院。未行手术组生存时间为3~6个月,中位生存时间为4.5个月;姑息性切除者生存时间为6~18个月,中位生存时间为12.8个月;根治性切除患者生存时间为12~68个月,中位生存时间为27.5个月。结论定期胃镜检查是早期诊断残胃癌的关键,根治性切除是治疗残胃癌的有效方法,病期及根治性切除是决定残胃癌预后的关键因素。
简介:Cancerevadeshostimmunesurveillancebyusingimmunecheckpoints,whichareinhibitorypathwayscrucialformaintainingself-tolerance1.Tumorcellsexpressmultipleinhibitoryligands,andtumor-infiltratinglymphocytes(TIL)expressavarietyofinhibitoryreceptors.InhibitoryreceptorscytotoxicT-lymphocyte-associatedprotein4(CTLA-4)andprogrammeddeath-1
简介:目的:探讨EZH2对胃癌MKN-28细胞生物学的影响。方法:siRNA干扰EZH2;MTT法检测沉默EZH2后细胞的增殖情况;Transwell小室观察细胞的侵袭情况;Realtime-PCR检测细胞中相关基因的表达情况。结果:siRNA有效干扰了EZH2的表达;沉默EZH2细胞组的细胞增殖明显受到抑制(P〈0.05);细胞的侵袭情况,沉默EZH2明显抑制了细胞的侵袭,与其他两组比较差异显著(P〈0.05);siEZH2细胞组E-cadherinmRNA、β-cateninmRNA的表达水平高于其他两组,Bcl-2mRNA的表达水平低于其他两组(P〈0.05)。结论:沉默EZH2抑制了胃癌MKN-28细胞的增殖,抑制了细胞的侵袭和抗凋亡基因的表达,可能是通过调控E-cadherin的表达水平和Wnt信号途径实现的,为寻找有效的靶点和肿瘤的靶向治疗提供一定的理论依据。
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:目的:评价国产吉西他滨(gemcitabine,GEM)联合顺铂方案治疗晚期非小细胞肺癌的疗效和不良反应。方法:对经病理组织学或细胞学证实的28例晚期非小细胞肺癌患者采用GP方案化疗:GEM1000mg/m^2ivdrip第1、8日,DDP30mg/m^2ivdrip第1-3日,21日为1周期。结果:CR0例,PR12例,SD14例,PD2例,总有效率为42.8%,初治、复治各14例,均有6例PR,有效率均为42.8%,不良反应以消化道反应及白细胞、血小板下降为主,均可耐受。结论:国产吉西他滨联合顺铂对晚期非小细胞肺癌有较好疗效,毒副反应可以耐受,可作为一线或二线化疗方案。
简介:目的:研究幽门螺杆菌L型(helicobacterpyloriL—form,Hp—L型)感染对胃癌BGC-823细胞增殖的影响,并探讨其作用机制。方法:将胃癌BGC-823细胞与Hp—L型以不同比例(1:20、1:100、1:500)共培养,以不加Hp—L型为对照组,在不同时段进行以下实验:倒置显微镜观察细胞形态学变化;四甲基噻唑氮蓝(MTT)法检测细胞生长增殖率;流式细胞仪(FCM)检测细胞凋亡率;免疫组化(SP法)检测癌基因(skp2)、抑癌基因(p53)和核增殖指数(Ki-67)的表达情况。结果:Hp—L型作用BGC-823细胞后,倒置显微镜观察到细胞分裂增多,增殖旺盛,瘤巨细胞增多,出现明显的生长加速现象;MTT法测定细胞生长曲线显示,Hp—L型对胃癌BGC-823细胞增殖有促进作用;FCM检测可见,lip—L型影响胃癌BGC-823细胞周期的分布,使G0/G1期比例降低,S期比例升高;免疫组化可见细胞中Skp2、p53和Ki-67蛋白表达阳性率逐渐增加;以上作用均呈细菌浓度和作用时间依赖性。结论:Hp—L型可促进胃癌BGC-823细胞增殖,其机制与上调skp2、p53和Ki-67蛋白的表达有关。
简介:Havingbeenpassedfor160generations,acelllinedesignatedasH22-F25/LwasestablishedfromamurinetumorlymphaticmetastatlcmodelH22-F25whichhadbeensetupinourcollege.Thecelllinewasinsuspensionculturewitharapidproliferationandstablegrowth.Thepeaktuneofcelldivisionandproliferationwas48and96hoursafterculture.Inaweek,thecellnumberwasIncreasedby25tunes.H22-F25/Lstillkeepsthefeaturesofapoorlydifferentiatedcancer.Itstumorinducingrate(invivo)was100%in615mice.Lymphnodemetastasisratewas50%andpulmonarymetastasisrate10%.H22-F25/LIsapopulationofheterogenetlctumorcellsIncluding2stemcelllines(themodelnumberofchromosomesbeing43in40%tumorcellsand86in32%)andsomesidelines.ThecommonmarkerchromosomesM1,M2,M3andM4werepresentinallstemandsidelines.
简介:TheresponsetosingleheattreatmentandStep-downheat(SDH)treatmentinvitroofV79andLcellswasstudied.Colony-formingabilitywasassayedinmediumaftertreatmentinvitro.Time-responsecurveswereestablishedandsubjectedtoArrheniusanalysis.TheArrheniuscurvesshowedinflectionpointsat43℃forV79cellsandat42℃forLcells.Theactivationenergieswere145kcal/moleand400kcal/moleaboveandbelow43℃(P<0.05),respectively,forV79cells,while160kcal/moleand300kcal/moleaboveandbelow42℃(P<0.05),respectively,forLcells.ThermosensitivityofLcellsaremarkedlyhigherthanV79cells.BothV79andLcellsweresensitizedbySDH.TheSDHeffectwascharacterizedbyareductioninshoulder(anadditioneffecttosublethaldamage),anincreaseinslope(thermosensitization),andthedelayanddisappearanceofthermotolerant"tail"forV79andLcellsat45℃to40℃and44℃to42℃SDHtreatmentrespectively.Particularly,42℃to39℃or42℃to40℃SDHforLc
简介:Objective:Epidermalgrowthfactorreceptor(EGFR)activationwasreportedtoupregulateprogrammeddeath-ligand1(PD-L1)expressioninlungcancercellsandsubsequentlycontributetoimmuneescape,indicatingitscriticalroleinEGFR-drivenlungtumors.ThisstudycharacterizedPD-L1expressioninpatientswithsurgicallyresectedEGFR-mutantnon-smallcelllungcancer(NSCLC).TheeffectofPD-L1expressiononclinicaloutcomeswasalsoinvestigatedinadvancedEGFR-mutantNSCLCtreatedwithEGFR-tyrosinekinaseinhibitors(TKIs).Methods:Intotal,73patientswithsurgicallyresectedNSCLCandEGFRmutationswereidentified.PD-L1expressionandCD8+tumor-infiltratinglymphocyte(TIL)densitywereassessedbyimmunohistochemistry.AliteraturereviewofpublicationsthatassessedthepredictiveandprognosticvalueofPD-L1expressioninadvancedEGFR-mutantNSCLCpatientstreatedwithEGFRTKIswasperformed.Results:Nineteen(26.0%)patientswerepositiveforPD-L1expression,whichwassignificantlyassociatedwithconcomitantKRASmutation(P=0.020)andmarginallyassociatedwithhigherCD8+TILsdensity(P=0.056).PositivePD-L1expressionwasassociatedwithmarkedlyinferioroverallsurvival(OS)inmultivariateanalysis(P=0.032).ThecombinationofPD-L1andCD8+TILsexpressioncouldbeusedtostratifythepopulationintothreegroupswithdistinctprognoses.Ameta-analysisofsixpublicationsshowedthatpositivePD-L1expressionwasnotassociatedwithOS[hazardratio(HR)=0.90;95%confidenceinterval(CI),0.42–1.38]orprogression-freesurvival(HR=1.03;95CI,0.73–1.33)inadvancedEGFR-mutantNSCLCpatientsreceivingEGFR-TKIs.Conclusions:PD-L1expressiontendedtocorrelatewithCD8+TILexpression,concomitantKRASmutation,andpoorsurvivalinsurgicallyresectedEGFR-mutantNSCLC.PD-L1expressionwasneitherthepredictivenortheprognosticfactorinadvancedEGFR-mutantNSCLCpatientstreatedwithEGFR-TKIs.
简介:Objective:TolookforthefurtherevidenceforHPVL1HPV16E6,HPV18E6andEBVascarcinogenicfactorsinlaryngealcarcinoma.Method:weexaminedrepresentativenumbersofspecimensfromlaryngealcancerwithhighlysensitivePCRtechniqueforthepresenceofHPVL1andhigh-risktypesHPV16E6,HPV18E6andEBVLMP1.Results:UsingPCRdetection,7.3%sampleswereHPVL1positive,52.03%wereHPV16E6positive,30.89%wereHPV18E6positiveand9.13%wereEBVLMP1positive.ThelowincidenceofHPVL1andhighincidenceofHPV-16E6andHPV18E6genessuggestthatHPVmightbeintegratedintotumorcells.OurresultssupportaroleofHPV-16andHPV-18infectioninthepathogenesisoflaryngealcarcinomainChina.Conclusion:IntegrationofE6intohostgenomeandstableexpressionofthesegenesmaybeassociatedwiththecarcinogenesisoflaryngealcarcinoma.HPV-16andHPV-18maysynergisticallyfunctiononthepathogenesisoflaryngealcarcinoma.Ourresultssuggestanassociationoflaryngealcarcinogenesisandinfectionwiththehigh-riskHPVtypes16,HPV18andEBV.
简介:Objective:ToinvestigatetheeffectsofE7080andN5-(1-iminoethyl)-L-ornithinedihydrochloride(L-NIO)oncolorectalcanceraloneandincombination.Methods:HT29colorectalcancercelllinefromSapInstitutewasused.Real-timecellanalysis(xCELLigencesystem)wasperformedtodeterminetheeffectsofE7080andL-NIOoncolorectalcellproliferation.WhileapoptosiswasdeterminedwithAnnexinVstaining,andtheeffectofagentsonangiogenesiswasdeterminedwithchorioallantoicmembrane(CAM)model.Results:WefoundthatE7080hasastrongantiproliferativeeffectwithanhalfmaximuminhibitionofconcentration(IC50)valueof5.60×10–8mol/L.AlsoithasbeenobservedthatE7080showedantiangiogenicandapoptoticeffectsonHT29colorectalcancercells.AntiangiogenicscoresofE7080were1.2,1.0and0.6for100,10and1nmol/LE7080concentrations,respectively.Furthermore,apoptosishasbeendetectedin71%ofHT29colorectalcancercellsafteradministrationof100nmol/LE7080whichmayindicatestrongapoptoticeffect.MeanwhileadministrationofL-NIOalonedidnotshowanyeffect,butthecombinationofE7080withL-NIOincreasedtheantiproliferative,antiangiogenicandapoptoticeffectsofE7080.Conclusions:ResultsofthisstudyindicatethatE7080maybeagoodchoiceintreatmentofcolorectaltumors.FurthermoretheincreasedeffectsofE7080whencombinedwithL-NIOraisethepossibilitytousealowerdoseofE7080andthereforeavoid/minimizethesideeffectsobservedwithE7080.
简介:客观:为了改进倔强的脸中部的外部T房间non-Hodgkin鈥檚的功效,有L天门冬氨酰胺酶(LASP)的淋巴瘤(MPTC-NHL)基于抢救化疗。方法:有倔强的MPTC-NHL的21个病人被分析,11patients(LASP组)收到了L天门冬氨酰胺酶基于的抢救化疗由L天门冬氨酰胺酶,长春新碱和dexame-thosone组成。没有L天门冬氨酰胺酶,10个病人(控制组)收到了抢救联合化疗。结果:完全的宽恕率为LASP组是45.6%,0.0%为控制组织(P<0.05)。全面反应率(CR+PR)为LASP组是63.6%,10.0%为控制组织,分别地(P<0.05)。2年的幸存率为LASP组是45.5%,0.0%为控制组织(P<0.05)。LASP的主要不利效果是白细胞减少,浆液bilirubin和多糖症的举起。结论:LASP基于的初步的临床的学习表演抢救化疗可以与倔强的MPTC-NHL改进反应率和病人的2年的幸存率。进一步继续学习是必要的。
简介:Objective:Tostudytheeffectofactivecompound6FandAfromPterissemipinnataL.(PsL)ontheactivitiesofDNAtopoisomerase(TOPO)IandII,activitiesofcytosolicandmembraneTPK,andexpressionofoncogenec-mycinlungadenocarcinomacells.Methods:Theeffectofcompound6FandAonactivitiesofcytosolicandmembraneTPKwasmeasuredbyscintillationcounting;theeffectofcompoundAonexpressionofoncogenec-mycwasdeterminedbyflowcytometryindirectfluorimetry.Results:compound6FandAcouldinhibittheactivitiesofTOPOI,andtheystronglyinhibitedtheTOPOIIin0.01mg/Land10.0mg/Lrespectively.CompoundAslightlyinhibitedtheactivitiesofmembraneTPK,butnotthecytosolicone.CompoundAcouldinhibittheexpressionofoncogenec-myc.Conclusion:Topoisomerasesaretargetofcompound6FandA.CompoundAcouldslightlyinhibittheactivitiesofTPK,andshowedaninhibitoryeffectontheexpressionofoncogenec-myc.
简介:Blockadeofimmunecheckpointshasrecentlyemergedasanoveltherapeuticstrategyinvarioustumors.Inparticular,monoclonalantibodiestargetingprogrammedcelldeath1(PD-1)oritsligand(PD-L1)havebeenmoststudiedinlungcancer,andPD-1inhibitorsarenowestablishedagentsinthemanagementofnon-smallcelllungcancer(NSCLC).ThereportsonhighprofileclinicaltrialshaveshowntheassociationofPD-L1expressionbyimmunohistochemistry(IHC)withhigheroverallresponseratestothePD-1/PD-L1axisblockadesuggestingthatPD-L1expressionmayserveasapredictivemarker.Unfortunately,however,eachPD-1orPD-L1inhibitoriscoupledwithaspecificPD-L1antibody,IHCprotocolandscoringsystemforthebiomarkerassessment,makingthehead-to-headcomparisonofthestudiesdifficult.Similarly,multipleclinicalseriesthatcorrelatedPD-L1expressionwithclinicopathologicand/ormolecularvariablesand/orsurvivalhavereportedconflictingresults.Thediscrepancycouldbeexplainedbythedifferencesinethnicityand/orhistologictypesincludedinthestudies,butitappearstobeattributedinparttothedifferencesinPD-L1IHCmethods.Thus,orchestratedeffortstostandardizethePD-L1IHCarewarrantedtoestablishtheIHCasapredictiveand/orprognosticbiomarkerinNSCLC.