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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：Next-generationsequencing(NGS)technologyiscapableofsequencingmillionsorbillionsofDNAmoleculessimultaneously.Therefore,itrepresentsapromisingtoolfortheanalysisofmoleculartargetsfortheinitialdiagnosisofdisease,monitoringofdiseaseprogression,andidentifyingthemechanismofdrugresistance.OnbehalfoftheTumorBiomarkerCommitteeoftheChineseSocietyofClinicalOncology(CSCO)andtheChinaActionableGenomeConsortium(CAGC),thepresentexpertgroupherebyproposesadvisoryguidelinesonclinicalapplicationsofNGStechnologyfortheanalysisofcancerdrivergenesforprecisioncancertherapy.Thisgroupcomprisesanassemblyoflaboratorycancergeneticists,clinicaloncologists,bioinformaticians,pathologists,andotherprofessionals.Aftermultipleroundsofdiscussionsandrevisions,theexpertgrouphasreachedapreliminaryconsensusontheneedofNGSinclinicaldiagnosis,itsregulation,andcompliancestandardsinclinicalsamplecollection.Moreover,ithaspreparedNGScriteria,thesequencingstandardoperationprocedure(SOP),dataanalysis,report,andNGSplatformcertificationandvalidation.

简介：Objective:Weretrospectivelyanalyzedtheclinicalprognosticvalueofthe8theditionoftheAmericanJointCommitteeonCancer(AJCC)stagingsystemforluminalAbreastcancer.Methods:Usingboththeanatomicandprognosticstaginginthe8theditionofAJCCcancerstagingsystem,werestagedpatientswithluminalAbreastcancertreatedattheBreastDiseaseCenter,PekingUniversityFirstHospitalfrom2008to2014.Follow-updataincluding5-yeardiseasefreesurvival(DFS),overallsurvival(OS)andotherclinic-pathologicaldatawerecollectedtoanalyzethedifferencesbetweenthetwostagingsubgroups.Results:Thisstudyincluded421patientswithluminalAbreastcancer(medianfollow-up,61months).The5-yearDFSandOSrateswere98.3%and99.3%,respectively.Significantdifferencesin5-yearDFSbutnotOSwereobservedbetweendifferentanatomicdiseasestages.Significantdifferenceswereobservedinboth5-yearDFSandOSbetweendifferentprognosticstages.Applicationoftheprognosticstagingsystemresultedinassignmentof175of421patients(41.6%)toadifferentgroupcomparedtotheiroriginalanatomicstages.Intotal,102of103patientswithanatomicstageIIAchangedtoprognosticstageIB,and24of52patientswithanatomicstageIIBchangedtoprognosticstageIB,while1changedtoprognosticstageIIIB.Twenty-twoof33patientswithanatomicstageIIIAweredown-stagedtoIIAwhenstagedbyprognosticstagingsystem,andtheother11patientsweredown-stagedtoIIB.TwopatientswithanatomicstageIIIBweredown-stagedtoIIIA.AmongsevenpatientswithanatomicstageIIICcancer,twoweredown-stagedtoIIIAandfourweredown-stagedtostageIIIB.Conclusions:The8theditionofAJCCprognosticstagingsystemisanimportantsupplementtothebreastcancerstagingsystem.Moreclinicaltrialsareneededtoproveitsabilitytoguideselectionofpropersystemictherapyandpredictprognosisofbreastcancer.

简介：Objective:Thisstudyaimedtodetermineifgastriccardiaadenocarcinoma(GCA)riskwasassociatedwiththelys(Aor*2)alleleatthers671(glu504lys)polymorphismwithinthealdehydedehydrogenase2(ALDH2)geneinaChineseHanpopulation.WealsoaimedtoinvestigateALDH2genotypicdistributionsbetweensubjectsfromhigh-andlow-incidenceareasforbothGCAandesophagealsquamouscellcarcinoma(ESCC).Methods:Wedesignedacase-controlstudyincluding2,686patientswithGCAand3,675controlsubjectsfromhigh-andlowincidenceareasforbothGCAandESCCinChina.TaqManallelediscriminationassaywasusedtogenotypethers671polymorphism.χ~2testandbinarylogisticregressionanalysiswereusedtoestimatetheoddsratiosforthedevelopmentofGCA,andmultivariateordinallogisticregressionwasusedtoanalyzeALDH2genotypicdistributionsamongdifferentgroups.Results:ComparedwithALDH2*1/*1homozygotes,ALDH2*1/*2andALDH2*2/*2carriersdidnotincreasetheriskforGCAintheChineseHanpopulation(P>0.05).Interestingly,theratioofhomozygousorheterozygousALDH2*2carriersinhighincidenceareasforbothGCAandESCCwaslowerthanthatinlow-incidenceareas(P<0.001).Conclusions:Genotypesofrs671atALDH2maynotincreaseGCAsusceptibilityinChineseHanpopulations.Inaddition,theALDH2genotypicdistributiondiffersbetweenChineseHanpopulationsfromhigh-andlow-incidenceareasforbothGCAandESCC.OurfindingsmayshedlightonthepossiblegeneticmechanismforthedramaticgeographicdifferencesofGCAoccurrenceinChina.

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