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：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：阿司匹林在预防中风及心脏疾病中已有广泛应用，近据英国牛津大学一项针对14，000名该组人群20余年回顾性研究资料显示，服用阿司匹林使肠癌的发生率降低1／4，死亡率减少1，3。虽然长期，服用阿司匹林会有发生一些副作用的危险，

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简介：Cancerevadeshostimmunesurveillancebyusingimmunecheckpoints,whichareinhibitorypathwayscrucialformaintainingself-tolerance1.Tumorcellsexpressmultipleinhibitoryligands,andtumor-infiltratinglymphocytes(TIL)expressavarietyofinhibitoryreceptors.InhibitoryreceptorscytotoxicT-lymphocyte-associatedprotein4(CTLA-4)andprogrammeddeath-1

简介：L-氨基酸氧化酶（LAAO）作为蛇毒中的一个重要成分，有着多样的生物学活性，近年来许多文献报道LAAO的生化作用和药理作用，提供了许多关于其对血小板活性、诱导细胞凋亡、细胞毒性、抗菌等方面的资料，本文就蛇毒L-氨基酸氧化酶（SV-LAAO）的理化性质、生物学特性及其可能的抗肿瘤作用及作用机制作一综述。

简介：目的检测正常胃黏膜细胞株GES-1和胃癌细胞株GnT-V的mRNA和蛋白质的表达水平。方法体外培养胃癌细胞株BGC823、SGC7901、MKN45和正常胃黏膜细胞株GES-1，应用RT-PCR、Real-timePCR、Westemblot等技术检测胃癌细胞株及正常胃黏膜细胞GnT-VmRNA和蛋白质表达的水平。结果检测显示3株胃癌细胞（BGC823、SGC7901、MKN45）均表达CmT-VmRNA，其中BGC823、SGC7901呈高表达，MKN45则低表达GnT-V（P〈0．05）。各细胞相对正常对照组GnT-V的相对表达倍数分别为18．25，13．36，9．25。Westernblot结果显示3株胃癌细胞均不同程度的GnT-V蛋白表达，而正常对照组不表达GnT-V蛋白。结论胃癌细胞不同程度表达GnT-V，各细胞中以BGC823表达量最高，SGC7901表达量居中，MKN45呈低表达，提示GnT-V可能对于胃癌的发生发展有一定的影响。

简介：Prostatecancergene3(PCA3,alsoknownasDD3)isanewbiomarkerthatcouldimprovetheaccuracyofprostatecancerdiagnosis.Itisagreatbiomarkerwithfairlyhighspecificityandsensitivity.Theincidenceofprostatecancerisrisingsteadilyinmostcountries.Thecommonlyusedprostate-specificantigen(PSA)testoncegavepeoplehopeforearlydiagnosisofprostatecancer.However,thelowspecificityofthePSAtesthasresultedinalargenumberofunnecessarybiopsiesandovertreatment.Duringthepastdecade,manynewprostatecancerbiomarkershavebeenfound.Amongthese,PCA3isthemostpromising.Duetoitsgreatperformanceindistinguishingprostatecancerfromotherprostateconditions,PCA3couldlikelybeappliedforearlydiagnosisofprostatecancer,patientfollow-up,prognosisprediction,andtargetedtherapy.Afteryearsofresearch,wehaveobtainedsomeknowledgeaboutthesequenceofPCA3gene.WehavealsodeterminedtherelationshipbetweenPCA3andtheproliferationofprostatecancercellsandlearnedsomeinformationabouthowPCA3affectstumor-relatedgenesandproteins.APCA3scorehasbeencreated,andithasbeenusedinavarietyofstudies.SomeresearchershaveevenappliedPCA3totargetedtherapyandobtainedagoodeffectinvitro.Thisreviewdescribesthecurrentstateofresearch,andexploresthefutureprospectsforPCA3.更多还原

简介：Forelectronicmicroscopicobservation,wefoundSSV-transformedNIH3T3cellsweredifferentfromnon-transformedcells.InSSV-transformedNIH3T3cellsnucleicytoplasmaratiowasincreasedandincytoplasmatheribosomes(polyribosomeswereattachedtotheswollenroughendoplasmicreticulum.Itwaslikelythatribosomeswerelinedtogetherfunctionallyandstructionallytoproducespecificprotein(PDGF-likeprotein).

简介：Objective:ToexploretheeffectsofnuclearM-CSFontheprocessoftumorigenesis.Methods:FunctionalpartofM-CSFcDNAwasinsertedintoaneukaryoticexpressionplasmidpCMV/myc/nuc,whichcanaddthreeNLStotheC-terminaloftheexpressedproteinanddirecttheproteinintothecellnuclei.TheconstructedplasmidwastransferredintoNIH3T3cellsandthecellcloneswereselectedbyG-418selection.CellclonesstableexpressingtargetproteinwereidentifiedbyRT-PCR,ABCimmunohistochemistryassayandWesternblot.Cellgrowthkineticsanalysesthroughgrowthcurves,celldoublingtime,MTTtestandanti-senseoligodeoxynucleotide(ASODN)inhibitingcellgrowthtestwereperformedtoidentifycellsproliferationpotential.Results:Thetransfectedcellsshowedelevatedproliferationpotentialoverthecontrolcells.Conclusion:AbnormalappearanceofM-CSFinnucleuscouldenhancecellproliferation,whichsuggeststhatcytokineisoformswithincellnucleusmightplaytranscriptionfactor-likerole.

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：指深屈肌腱撕脱性损伤俗称＂运动衣，Jersey＂损伤，常伴有肌腱止点处的撕脱骨折，是一种少见的损伤。国外报道较多，国内也偶见报道[1-2]。Leddy等[3]早在1977年就根据损伤后肌腱所在的位置，将此种损伤分为3种类型，I型：撕脱的肌腱回缩到手掌部，肌腱长短腱纽均断裂。II型：肌腱回缩到近端指间关节，短腱纽断裂，长腱纽完整，肌腱断端常带有小片撕脱骨折。III型：指屈肌腱止点处撕脱骨折，骨折片较大，常累及关节面，短腱纽完整，骨折片移位到远端指间关节。1981年，Smith[4]对此分型做了新的补充，也就是IV型，即：肌腱止点处撕脱骨折，同时肌腱又从骨折片上撕脱，并向近端回缩。2001年，Al-Qattan[5]报道了4例不同于前几型的损伤，即：屈指深肌腱止点撕脱骨折同时合并末节基底的骨折，他称之为V型损伤，并根据撕脱骨折是否涉及关节面，分为Va和Vb不同类型。2002年，潘勇卫等[1]报道的14例屈指深肌腱撕脱性损伤中有4例是此种类型的损伤。2012年10月29日，我们收治2例非运动性损伤的V型屈指深肌腱撕脱伤患者的诊断和治疗进行探讨。

简介：目的：探讨14—3—3β基因（酪氨酸3-加单氧矽色氨酸5-加单氧酶激活蛋白基因）对卡波氏肉瘤（Kaposigsarcoma，KS）细胞迁移的影响。方法：采用脂质体法将14—3—3β基因稳定转染入BCBL—1（HHV-8positiveandEBVnegativehumanBcells）细胞，Western—Blot检测14—3—3β蛋白的表达，最后利用Transwell法分析14—3—3β基因对BCBL-1细胞迁移的影响（设立空载体组和阴性对照组）。结果：pcDNA3．1／myc—His（-）A-14—3—3β组细胞迁移数目明显高于pcDNA3．1／myc—His（-）A组和阴性对照组，差异具有统计学意义（P〈0．05）；pcDNA3．1／myc—His（-）A组和阴性对照组细胞迁移数目相比差异无统计学意义（P〉0．05）。结论：14—3—3β基因能促进KS细胞的迁移。

简介：TheeffectofTPA,apotenttumorpromoter,onSSV-NIH3T3cellsinserum-freemediumwasinvestigated.TPAstimulatedDNAsynthesisofSSV-NIH3T3cellsonthethirddayofcultureinSFM.InSDS-PAGFofmediumconditionedbyTPA-treatedSSV-NIH3T3cells(inSFM+TPA),theamountsoffourproteinsof31.0Kd,28.5Kd,25.5Kdand13.5Kdstrikinglyincreasedoverthatofnon-TPA-treatedcounterpart(inSFM).ThePDGF-likeactivitywasalsodetectedinCMofSFM+TPA.WheninsulinandEGFweredrownofftheSFM+TPA(SFM-Ins-EGF+TPA),TPAlostitsabilitytostimulateDNAsynthesisofSSV-NIH3T3cellsonthethirddayandSDS-PAGEoftheconditionedmediumshowedthattheamountsofthefourproteinsnotedabovegratelyreduced.However,cellsinSFM-Ins-EGF+TPAwereinalmostthesamegrowthconditionascellsincompleteSFM+TPAonthethirddayofculture.Resultswerediscussedinthepaper.

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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：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.