简介：AIM:Toinvestigatethediversecharacteristicsofdifferentpathologicalgradingsofgastricadenocarcinoma(GA)usingtumor-relatedgenes.METHODS:GAtissuesindifferentpathologicalgradingsandnormaltissuesweresubjectedtotissuearrays.Expressionsof15majortumor-relatedgenesweredetectedbyRNAinsituhybridizationalongwith3’terminaldigoxin-labeledanti-sensesinglestrandedoligonucleotideandlockednucleicacidmodifyingprobewithinthetissuearray.Thedataobtainedwereprocessedbysupportvectormachinesbyfourdifferentfeatureselectionmethodstodiscovertherespectivecriticalgene/genesubsetscontributingtotheGAactivitiesofdifferentpathologicalgradings.RESULTS:IncomparisonofpoorlydifferentiatedGAwithnormaltissues,tumor-relatedgeneTP53playsakeyrole,althoughothersixtumor-relatedgenescouldalsoachievetheAreaUnderCurve(AUC)ofthereceiveroperatingcharacteristicindependentlybymorethan80%.ComparingthewelldifferentiatedGAwithnormaltissues,wefoundthat11tumor-relatedgenescouldindependentlyobtaintheAUCbymorethan80%,butonlythegenesubsets,TP53,RBandPTEN,playakeyrole.Onlythegenesubsets,Bcl10,UVRAG,APC,Beclin1,NM23,PTENandRBcoulddistinguishbetweenthepoorlydifferentiatedandwelldifferentiatedGA.Noneofasinglegenecouldobtainavaliddistinction.CONCLUSION:Differentfromthetraditionalpointofview,thewelldifferentiatedcancertissueshavemorealterationsofimportanttumor-relatedgenesthanthepoorlydifferentiatedcancertissues.

简介：interleukin-24(IL-24)能在人的癌症的一个大系列导致apoptosis，是记录得好的MDA-7/IL-24基因的导出的房间线，而是效果在未知的老鼠黑瘤房间遗体上转。IL-24(pEGFP-IL-24)的真核细胞的表示plasmid被DNA再结合技术构造。再结合plasmid和空向量是进B16F0房间的transfected，IL-24的表情被LSM决定，B16F0房间的增长被MTT试金，和apoptosis率测量，B16F0房间的房间周期分发被FCM测量。在老鼠固体肿瘤的IL-24基因transfection的禁止的效果被观察并且测量。与控制相比，B16F0房间的增长被transfection与pEGFP-IL-24禁止，transfected房间的G2/M阶段也是increased.Moreover，在与pEGFP-IL-24与B16F0房间transfected接种以后，有可检测的肿瘤的鼠标的百分比被减少。在老鼠模型的肿瘤的生长率显著地与控制相比在IL-24基因治疗组被禁止。B16F0细胞的增长被pEGFP-IL-24的pEGFP-IL-24transfection.Theintratumor注射禁止能显著地在老鼠禁止稳固的肿瘤的生长。

简介：在表面上co有教养的肝正常房间和癌症房间由不同的化学的功能的组修改了，包括mercapto(-SH),氢氧根(-OH)和甲基(-CH3个)组。结果证明不同房间响应不同表面展出了变化。正常房间在上当癌症房间不能在-CH3组织，它也死了。在合作文化系统，-CH3组展出了它能触发癌症房间的死亡并且没在正常房间上有效果的唯一的效果。我们的调查结果为有效、安全的再生药材料的设计在策略上提供有用信息。

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简介：AIM:ToinvestigatewhethertheevaluationoftumorbuddingcancomplementK-RASanalysistoimprovetheindividualizedpredictionofresponsetoanti-epidermalgrowthfactorreceptorbasedtherapiesinmetastaticcolorectalcancer(mCRC)patients.METHODS:Forty-threepatientswithmCRCtreatedwithcetuximaborpanitumumabwereenteredintothisstudy.AccordingtotheResponseEvaluationCriteriainSolidTumorscriteria,30patientshadstableorprogressivedisease(non-responsive),while13patientshadapartialresponse.Tumorbudswereevaluatedfromwholetissuesectionsstainedforpan-cytokeratin,evaluatedinthedensestregionusinga40×objectiveand'high-grade'tumorbuddingwasdefinedas15buds/high-powerfield.RESULTS:TumorbudsandK-RASmutationbothcorrectlyclassified68%ofpatients.AllpatientswithK-RASmutation(n=7)orhigh-gradetumorbudding(n=11)werenon-responsive,ofwhich4patientshadbothfeatures.All13partialresponderswereK-RASwild-typewithlow-gradetumorbudding.Combined,thepredictivevalueofK-RASandtumorbuddingwas80%.Additionally,high-gradetumorbuddingwassignificantlyrelatedtoworseprogression-freesurvival[HR(95%CI):2.8(1.3-6.0,P=0.008)].CONCLUSION:Ifconfirmedinlargercohorts,theadditionoftumorbuddingtoK-RASanalysismayrepresentaneffectiveapproachforindividualizedpatientmanagementinthemetastaticsetting.

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简介：Esophagealcancerhasbeenreportedastheninthmostcommonmalignancyandranksasthesixthmostfrequentcauseofdeathworldwide.Esophagealcancertreatmentinvolvessurgery,chemotherapy,radiationtherapy,orcombinationtherapy.Novelstrategiesareneededtoboosttheoncologicoutcome.Recentadvancesinthemolecularbiologyofesophagealcancerhavedocumentedtheroleofgeneticalterationsintumorigenesis.Oncogenesserveapivotalfunctionintumorigenesis.Targetedtherapiesaredirectedattheuniquemolecularsignatureofcancercellsforenhancedefficacywithlowtoxicity.RNAinterference(RNAi)technologyisapowerfultoolforsilencingendogenousorexogenousgenesinmammaliancells.RelatedresultshaveshownthattargetingoncogeneswithsiRNAs,specificallythemRNA,effectivelyreducestumorcellproliferationandinducesapoptoticcelldeath.Thisarticlewillbrieflyreviewstudiesonsilencingtumorenhancergenesrelatedtotheinductionofesophagealcancer.

简介：Theextinctionphenomenoninducedbymultiplicativenon-GaussianL′evynoiseinatumorgrowthmodelwithimmuneresponseisdiscussed.Undertheinfluenceofthestochasticimmunerate,themodelisanalyzedintermsofastochasticdifferentialequationwithmultiplicativenoise.BymeansofthetheoryoftheinfinitesimalgeneratorofHuntprocesses,theescapeprobability,whichisusedtomeasurethenoise-inducedextinctionprobabilityoftumorcells,isexplicitlyexpressedasafunctionofinitialtumorcelldensity,stabilityindexandnoiseintensity.Basedonthenumericalcalculations,itisfoundthatfordifferentinitialdensitiesoftumorcells,noiseparametersplayoppositerolesontheescapeprobability.Theoptimallyselectedvaluesofthemultiplicativenoiseintensityandthestabilityindexarefoundtomaximizetheescapeprobability.

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简介：AIM:Toexaminetheassociationofgeneticpolymorphisms(-308)G/ATNFα,(+250)A/GLtα,(+36)A/GTNFR1,(+1663)A/GTNFR2withthedevelopmentofprimaryopenangleglaucoma(POAG)amongpeopleinCentralRussia.METHODS:Thestudysampleincluded443individuals,ofwhich252patientswithPOAGand191individualsinthecontrolgroup.Genotypingof(-308)G/ATNFα,(+250)A/GLtα,(+36)A/GTNFR1,(+1663)A/GTNFR2wasperformedusingpolymerasechainreaction.ThedistributionofallelesandgenotypesofthestudiedDNAmarkersinthegroupswasexaminedby2×2contingencytablesandχ2withtheYates'scorrectionforcontinuityandoddsratios(OR)with95%confidenceintervals(CI).RESULTS:Allele(-308)GTNFα(Р=0.01,OR=1.78,95%CI1.12-2.85)wasidentifiedasariskfactorforPOAG.Homozygotes(-308)AATNFαareatalowestriskfordevelopmentofthedisease(Р=0.01,OR=0.0005).ThefollowingcombinationofgeneticvariantsofcytokineswereassociatedwithareducedriskofPOAG:(+1663)ATNFR2and(+250)GLtα(OR=0.34)CONCLUSION:Geneticpolymorphisms(-308)G/ATNFα,(+250)A/GLtα,(+1663)A/GTNFR2associatedwiththedevelopmentofPOAGinthepopulationofCentralRussia.

简介：Extragonadalprimaryyolksactumoroftheintestinaltractoriginisexceedinglyrare.Throughamultipledisciplinaryteam,thediagnosisandtreatmentofprimaryintestinalyolksactumorwerefurtherdefined.Wereport2suchcaseswithdetailedhistologicandimmunohistochemicalanalysis.Thetwopatientswerea7-year-oldgirlanda29-year-oldwoman.Bothofthempreoperativelyhadanelevatedserumalphafetoprotein(AFP)level(≥1,210ng/mL).Thetumorsarelocatedintheintestineandimagingexaminationindicatedtherectumastheprimarysite.Grosslythemasswasgrey-whiteandcrisptexture.Microscopicexaminationfeaturedreticular,microcystic,macrocystic,papillary,solid,andsomeglandularpatterns.Immunohistochemically,tumorcellsofbothcaseswerepositiveforSALL4,AFP,pan-cytokeratin(AE1/AE3),andglypican-3.Simultaneously,astainforEMA,OCT4,CD30,HCG,vimentinandCK20werenegativeinall2neoplasms.Thefeaturesofmorphology,immunohistochemistry,laboratoryexaminationsandimagingstudiesconsistofthediagnosisofprimaryyolksactumoroftheintestine.

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简介：Objective:Previousworkindicatedthataneuploidyofchromosome8incirculatingtumorcells(CTCs)correlatedwiththerapeuticefficacyforadvancedgastriccancer(AGC)patients.Inthisfollow-upstudyperformedonthesamepopulationofAGCpatients,weinvestigatedwhetherandhowaneuploidyofchromosome8inCTCscorrelateswithpatients'clinicalprognosis.Methods:Theprospectivestudywasperformedon31patientswithnewlydiagnosedAGC.Previouslyestablishedintegratedsubtractionenrichment(SE)andimmunostaining-fluorescenceinsituhybridization(iFISH)platformwasappliedtoidentify,enumerateandcharacterizeCTCs.QuantificationofCTCsandanalysisoftheiraneuploidyofchromosome8wereperformedonpatientsbeforeandaftertherapy.Results:CTCsweremeasuredin93.5%ofAGCpatients,andtwoCTCsubtypeswithdiversethresholdvalueswereidentified,multiploidCTCswiththethresholdof≥2per7.5mLandmultiploidplustriploidCTCswiththethresholdof≥4,whichwerefoundtosignificantlycorrelatewithpoorprogression-freesurvival(PFS)andoverallsurvival(OS).Inparticular,patientswith≥10%increasedmultiploidCTCsafteraninitial6weeksoftherapyhadpoorPFSandOS,whereasimprovedPFSandOSwereobservedonthosewhohad≥10%decreasedmultiploidCTCs.Afteradjustingforclinicallysignificantfactors,≥10%increasedpost-therapymultiploidCTCswastheonlyindependentpredictorofPFSandOS.Conclusions:AneuploidyofCTCscorrelateswithprognosisofAGCpatients.QuantitativecomparisonmonitoringmultiploidCTCsbeforeandaftertherapymayhelppredictimprovedorinferiorprognosisandchemoresistance.

简介：AbstractToinvestigatetheroleofCD4^+helperT(Th)cellsinthememoryCTL-mediatedanti-tumorimmunity,theRAG-1geneknockoutmicewereadoptivelytransferredwithOT-1cellstogeneratethememoryCTL,theC57B1/6miceimmunizedwiththeepitopepeptideofOVAspecificThcellsandwithdifferentadjuvantswereadopfivelytransferredwiththesememory-CTLs,andthentheanimalswerechallengedwithtumorcellsEGT.ItwasfoundthatalthoughthesimpleimmunizationofmicewiththeepitopepeptideoftheOVAspecificThcellscouldgeneratemoreeffectCTL,butthiseffectwasnotsostrongenoughtoresistcompletelythechallengeswithtumorcells.Nevertheless,thememoryCTL-mediatedanti-tumorimmuneeffectrequiredthehelpsofTh1andTh2cells.Thecross-regulationbetweenThlandTh2cellsseemedtobebeneficialforthehosttogeneratemoreeffectorCTLformountinganefficientanti-tumorresponse.ItconcludedthattheinteractionbetweenThlandTh2cellsmightbemoreimportantthanthesinglesubsetofThcellsinthememoryCTL-mediatedanti-tumorimmuneresponse.Moreattentionshouldbepaidinthisregardforthefuturestudies.

简介：A29-year-oldmanwasadmittedforerythema,papulesanderosions.Erosionsandpurulentsecretionswereseeninthecircumferenceofthemouth,eyes,oralmucosa,tongue,andpreputium.Conjunctivaswereswollenandtheurethralorificewasred,bothwereaccompaniedbypurulentsecretions.Multiplevesicleswereshowninthepenis.Thepatientwasdiagnosedwith:①Stevens-Johnsonsyndrome;②gonococcalophthalmoblennorrhea;③nongonococcalurethritis,gonococcalurethritis;④genitalherpes;⑤mediastinaltumor.

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简介：Objective:ResponseEvaluationCriteriainSolidTumors(RECIST)guidelineversion1.0(RECIST1.0)wasproposedasanewguidelineforevaluatingtumorresponseandhasbeenwidelyacceptedasastandardizedmeasure.WithanumberofissuesbeingraisedonRECIST1.0,however,arevisedRECISTguidelineversion1.1(RECIST1.1)wasproposedbytheRECISTWorkingGroupin2009.ThisstudywasconductedtocompareCTtumorresponsebasedonRECIST1.1vs.RECIST1.0inpatientswithadvancedgastriccancer(AGC).Methods:Wereviewed61AGCpatientswithmeasurablediseasesbyRECIST1.0whowereenrolledinotherclinicaltrialsbetween2008and2010.Thesepatientswereretrospectivelyre-analyzedtodeterminetheconcordancebetweenthetworesponsecriteriausingtheκstatistic.Results:ThenumberandsumoftumordiametersofthetargetlesionsbyRECIST1.1weresignificantlylowerthanthosebyRECIST1.0(P<0.0001).However,therewasexcellentagreementintumorresponsebetweenRECIST1.1andRECIST1.0(κ=0.844).Theoverallresponserates(ORRs)accordingtoRECIST1.0andRECIST1.1were32.7%(20/61)and34.5%(20/58),respectively.Onepatientwithpartialresponse(PR)basedonRECIST1.0wasreclassifiedasstabledisease(SD)byRECIST1.1.OftwopatientswithSDbyRECIST1.0,onewasdowngradedtoprogressivediseaseandtheotherwasupgradedtoPRbyRECIST1.1.Conclusions:RECIST1.1providedalmostperfectagreementwithRECIST1.0intheCTassessmentoftumorresponseofAGC.