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：RecentinsituhybridizationstudiesshowedthatmRNAlevelsofOLIGlandOLIG2transcriptionfactorsareelevatedinoligodendrogliomas.Weraisedpolyclonalantibodiesagainstasyntheticpeptidehomologoustothehumantran-scriptionfactorOliglandstudiedbyimmunohistochemistrytheexpressionofOliglin84braintumorsandinnon-neoplasticbraintissues.Alloligodendrogliomas,oligoastrocytomas,anddysembryoplasticneuroepithelialtumorsshowedmoderatetostrongintranuclearimmunoreactivityincellsmorphologicallyidentifiedasoligodendrocytes.In

简介：Transforminggrowthfactor-β(TGF-β)isakeyfactorincancerdevelopmentandprogression.TGF-βcansuppresstumorigenesisbyinhibitingcellcycleprogressionandstimulatingapoptosisinearlystagesofcancerprogression.However,TGF-βcanmodulatecancer-relatedprocesses,suchascellinvasion,distantmetastasis,andmicroenvironmentmodificationthatmaybeusedbycancercellstotheiradvantageinlatestages.Correspondingmechanismsincludeangiogenesispromotion,anti-tumorimmunitysuppression,andepithelial-to-mesenchymaltransition(EMT)induction.ThecorrelationbetweenTGF-βexpressionandcancerprognosishasalsobeenextensivelyinvestigated.ResultssuggestthatTGF-βpathwaycanbetargetedtotreatcancer;assuch,thefeasibilityofthistreatmentisinvestigatedinclinicaltrials.

简介：Ovariancanceristhesecondmostlethalgynecologicalcancerworldwideandwhilemostpatientsrespondtoinitialtherapy,theyoftenrelapsewithresistantdisease.Humanepidermalgrowthfactorreceptors(especiallyHER1/EGFRandHER2/ERBB2)areinvolvedindiseaseprogression;hence,strategiestoinhibittheiractioncouldproveadvantageousinovariancancerpatients,especiallyinpatientsresistanttofirstlinetherapy.Monoclonalantibodiesandtyrosinekinaseinhibitorsaretwoclassesofdrugsthatactonthesereceptors.Theyhavedemonstratedvaluableantitumoractivityinmultiplecancersandtheirpossibleuseinovariancancercontinuestobestudied.Inthisreview,wediscussthehumanepidermalgrowthfactorreceptorfamily;reviewemergingclinicalstudiesonmonoclonalantibodiesandtyrosinekinaseinhibitorstargetingthesereceptorsinovariancancerpatients;andproposefutureresearchpossibilitiesinthisarea.

简介：在细胞的增长和内长的脉管的endothelial生长因素(VEGF)上调查melatonin的效果的目的在胰腺的癌房间(PANC-1)的表示。方法PANC-1房间为这研究是有教养的。在文化媒介的分泌VEGF集中用ELISA方法被决定，在肿瘤房间的VEGF生产被immunocytochemistry，和VEGFmRNA表示检测被RT-PCR决定。更高结果melatonin集中显著地禁止了细胞的增长，与展出最高禁止的效果的1mmol/L集中(P<0.01)。在房间文化上层清液和intra小房的VEGF集中都显著地在melatonin(1mmol/L)以后被减少孵化(P<0.05)。VEGFmRNA表示在观察时期期间以一种时间依赖者方式显著地减少了(P<0.05)。结论高melatonin集中显著地禁止了胰腺的癌房间的增长。内长的VEGF表示被melatonin孵化也压制。

简介：Objective:Thepredictiveandprognosticroleofprognosticnutritionalindex(PNI)ingastriccancerpatientswithperitonealdisseminationremainsunclear.ThisstudyaimstoexploretheroleofthePNIinpredictingoutcomesofgastriccancerpatientswithperitonealdissemination.Methods:Atotalof660patientsdiagnosedwithgastricadenocarcinomawithperitonealmetastasisbetweenJanuary2000andApril2014atSunYat-senUniversityCancerCenterandtheSixthAffiliatedHospitalofSunYatsenUniversitywereretrospectivelyanalyzed.Theclinicopathologiccharacteristicsandclinicaloutcomesofpatientswithperitonealdisseminationwereanalyzed.Results:ComparedwithPNI-highgroup,PNI-lowgroupwascorrelatedwithadvancedage(P=0.036),worseperformancestatus(P<0.001),higherfrequencyofascites(P<0.001)andhigherfrequencyofmultisitedistantmetastasis(P<0.001).Kaplan-MeiersurvivalcurvesshowedthatPNI-highgrouphadasignificantlylongermedianoverallsurvivalthanPNI-lowgroup(13.13vs.9.03months,P<0.001).MultivariatesurvivalanalysisrevealedthatBorrmanntypeIV(P=0.014),presenceofascites(P=0.017)andlowerPNI(P=0.041)wereindependentpoorprognosticfactors,andpalliativesurgery(P<0.001)andfirst-linechemotherapy(P<0.001)weregoodprognosticfactors.Forpatientsreceivingpalliativesurgery,thepostoperativemorbidityratesinthePNI-lowgroupandPNIhighgroupwere9.1%and9.9%,respectively(P=0.797).ThepostoperativemortalityratewasnotsignificantlydifferentbetweenPNI-lowandPNI-highgroups(2.3%vs.0.9%,P=0.362).Conclusions:PNIisausefulandpracticaltoolforevaluatingthenutritionalstatusofgastriccancerpatientswithperitonealdissemination,andisanindependentprognosticfactorforthesepatients.

简介：ＴＵＭＯＲＮＥＣＲＯＳＩＳＦＡＣＴＯＲ－αＡＬＴＥＲＳＰＲＯＴＥＩＮＭＥＴＡＢＯＬＩＳＭＡＮＤＣＥＬＬ－ＣＹＣＬＥＫＩＮＥＴＩＣＳＩＮＭＡＬＩＧＮＡＮＴＴＵＭＯＲＹｅＳｈｅｎｇｌｏｎｇ叶胜龙；ＴａｎｇＺｈａｏｙｏｕ汤钊猷；ＢｒｕｃｅＲＢｉｓｔｒｉａｎ...

简介：

简介：Objective:Toexploretheprobabilityofvascularendothelialgrowthfactor(VEGF)antisenseoligodeoxynucleotidesasadevelopingnewtherapeuticstrategyforglioma.Methods:VEGFproteinexpressionwasdetectedbyS-Pimmunohistochemicaltechnique.TumorcellapoptosiswasobservedbyTUNELmethod.Results:Comparedwithcontrol,VEGFproteinexpressionwasinhibitedbyantisenseoligodeoxynucleotidesinvitro.Andtheinhibitoryeffectsincreasedwiththeincreasingconcentration.VEGFpositiveratewas82.10%incontrolgroup,whilein2.5,5,10(mol/LAODNgroups,theywere70.00%,57.85%,53.20%respectively.Noinhibitioneffectwasfoundinthecelllinestreatedwithmissenseandsenseoligodeoxynucleotides.Invivo,antisenseoligodeoxy-nucleotidestherapyalsoinhibitedVEGFproteinexpressionandinducedtheincreaseofapoptotictumorcells.However,ithasnoeffectontumorcellproliferation.Conclusion:ItishopefulthatVEGFantisenseoligodeoxynucleotidesmaybeanewgenetherapymethodtogliomathroughitsantiangiogenesiseffectbyinhibitionofVEGF.

简介：Objective:Toanalyzetheexpressionofinduciblenitricoxidesynthase(iNOS),endothelialnitricoxidesynthase(eNOS)andvascularendothelialgrowthfactor(VEGF)inhepatocellularcarcinoma(HCC)anditsrelationtoangiogenesis.Methods:Tissuesectionsfrom71HCCpatientswereexaminedimmunohistochemicallyforproteinexpressionofiNOS,eNOS,andVEGF.Microvessaldensity(MVD)wascountedbyendothelialcellsimmunostainedbyanti-CD34antibody.Results:PositiveimmunostainingforiNOS,eNOSwasdetectedin83.1%and85.9%ofHCCrespectively.INOSandeNOSwerenotdetectedinnormalhepatictissue.MVDwas34.3±1.5/HPand38.6±1.6/HPinHCCwithpositivestainingforiNOSandVEGFwhileitwas31.2±2.8/HP,and22.4±2.0/HPinHCCwithnegativestainingforiNOSandVEGF(P<0.01).AcorrelationbetweenNOSexpressionandVEGFinHCCwasnotobserved.Conclusion:iNOSandeNOSmayplayaroleinmalignanttransformationfpost-hepaticcirrhosis.TheexpressionofiNOSandVEGFfavorsangiogenesisofHCC.

简介：Objective:Chroniclymphocyticleukemia(CLL)andmantlecelllymphoma(MCL)cellsover-expressaguanineexchangefactor(GEF),Rasgrf-1.ThisGEFincreasesactiveRasasitcatalyzestheremovalofGDPfromRassothatGTPcanbindandactivateRas.ThisstudyaimstostudythemechanismofactionofRasgrf-1inB-cellmalignancies.Methods:N-terminustruncatedRasgrf-1variantshaveahigherGEFactivityascomparedtothefull-lengthtranscriptthereforeaMCLcelllinewithstableover-expressionoftruncatedRasgrf-1wasestablished.TheB-cellreceptor(BCR)andchemokinesignalingpathwayswerecomparedintheRasgrf-1over-expressingandacontroltransfectedcellline.Results:Cellsover-expressingtruncatedformofRasgrf-1haveahigherproliferativerateascomparedtocontroltransfectedcells.BCRwasactivatedbylowerconcentrationsofanti-IgMantibodyinRasgrf-1over-expressingcellsascomparedtocontrolcellsindicatingthatthesecellsaremoresensitivetoBCRsignaling.BCRsignalingalsophosphorylatesRasgrf-1thatfurtherincreasesitsGEFfunctionandamplifiesBCRsignaling.ThisactivationofRasgrf-1inover-expressingcellsresultedinahigherexpressionofphospho-ERK,AKT,BTKandPKC-alphaascomparedtocontrolcells.BesidesBCR,Rasgrf-1over-expressingcellswerealsomoresensitivetomicroenvironmentstimuliasdeterminedbyresistancetoapoptosis,chemotaxisandERKpathwayactivation.Conclusions:ThisGEFproteinsensitizesB-cellstoBCRandchemokinemediatedsignalingandalsoupregulatesanumberofothersignalingpathwayswhichpromotesgrowthandsurvivalofthesecells.

简介：TheinvivoeffectsofPhytolaccaacinosapoly-saccharidesI(PEP-I)onimmunologiccytotoxicityofmouseperitonealmacrophagesanditsproductionoftumornecrosisfactor(TNF)andinterleukin1(IL-1)werestudied.PEP-I80or160mgkgwasgiveniptwiceevery4day.BothdoseswerefoundtohavesignificantenhancingactivityonmacrophagescytotoxicityagainstS180sarcomacellsandmalignanttransformedfibroblastL929cells.PeritonealactivatedmacrophageswereincubatedwithLPSfor2and24hrstoinduceTNFandIL-1,respectively.TheTNFandIL-1activitiesweretestedfromcytotoxicityagainstL929cellsinanabsorbenceassayofenzymaticreactionandproliferationofthymocytesco-stimulatedassayseparately.TheoptimaltimeforTNFproductionwasfoundonday8.SignificantincreasesinTNFandIL-1wereobserved.IncomparisonoftheeffectofPEP-IonTNFwiththatofknownprimingagentBCG,therewasnodifferencebetweenthem,butPEP-IhadahigheffectonIL-1.Theseresultssug

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：

简介：

简介：这研究试图表示白喉毒素和人的熔化蛋白质的目的在Escherichiacoli的B激活房间的因素(DT388sBAFF)(E。coli)并且在人的B系尖锐成淋巴细胞的白血病调查它的活动1个房间(BALL-1)。