简介：N^6-methyladenosine(m^6A)isanessentialRNAmodificationthatregulateskeycellularprocesses,includingstemcellrenewal,cellulardifferentiation,andresponsetoDNAdamage.Unsurprisingly,aberrantm6Amethylationhasbeenimplicatedinthedevelopmentandmaintenanceofdiversehumancancers.Alteredm6AlevelsaffectRNAprocessing,mRNAdegradation,andtranslationofmRNAsintoproteins,therebydisruptinggeneexpressionregulationandpromotingtumorigenesis.Recentstudieshavereportedthattheabnormalexpressionofm6Aregulatoryenzymesaffectsm6Aabundanceandconsequentlydysregulatestheexpressionoftumorsuppressorgenesandoncogenes,includingMYC,SOCS2,ADAM19,andPTEN.Inthisreview,wediscussthespecificrolesofm6A“writers",“erasers”,and“readers”innormalphysiologyandhowtheiralteredexpressionpromotestumorigenesis.Wealsodescribethepotentialofexploitingtheaberrantexpressionoftheseenzymesforcancerdiagnosis,prognosis,andthedevelopmentofnoveltherapies.

简介：Glioblastoma(GBM)isoneofthedeadliesttumorsandhasamediansurvivalof3monthsifleftuntreated.Despiteadvancesinrationallytargetedpharmacologicalapproaches,theclinicalcareofGBMremainspalliativeinintent.Sincethemajorityofalteredsignalingcascadesinvolvedincancerestablishmentandprogressioneventuallyaffectcellcycleprogression,analternativeapproachforcancertherapyistodevelopinnovativecompoundsthatblocktheactivityofcrucialmoleculesneededbytumorcellstocompletecelldivision.Inthiscontext,wereviewpromisingongoingandfuturestrategiesforGBMtherapeuticsaimedtowardsG2/Minhibitionsuchasanti-microtubuleagentsandtargetedtherapyagainstG2/Mregulatorslikecyclin-dependentkinases,Aurorainhibitors,PLK1,BUB,1,andBUBR1,andsurvivin.Moreover,wealsoincludeinvestigationalagentsinthepreclinicalandearlyclinicalsettings.Althoughseveraldrugswereshowntobegliotoxic,mostofthemhavenotyetenteredtherapeutictrials.TheuseofeithersingleexposureoracombinationwithnovelcompoundsmayleadtotreatmentalternativesforGBMpatientsinthenearfuture.

简介：Gastrointestinal(GI)cancerisoneofthemostcommoncausesofcancer-relateddeathsworldwide.Tumormarkersarevaluableindetectingpost-surgicalrecurrenceorinmonitoringresponsetochemotherapy.PyruvatekinaseisoformM2(PKM2),aglycolyticenzymecatalyzingconversionofphosphoenolpyruvate(PEP)topyruvate,confersagrowthadvantagetothetumorcellsandenablesthemtoadapttothetumormicroenvironment.Inthisreview,wehavesummarizedcurrentresearchontheexpressionandregulationofPKM2intumorcells,anditspotentialroleinGIcarcinogenesisandprogression.Furthermore,wehavealsodiscussedthepotentialofPKM2asadiagnosticandscreeningmarker,andatherapeutictargetinGIcancer.

简介：目的：评价^99Tc^m-MIBI乳腺显像对乳腺肿瘤和腋窝淋巴结转移的诊断价值。方法：52例女性乳腺肿瘤患者，体检腋窝未扪及肿块。应用^99Tc^m-MIBI740MBq(20mCi)经肘静脉注射，行乳腺和腋窝显像，并用手术、病理加以对照。结果：48例乳腺肿瘤患者中，^99Tc^m-MIBI显像真阳性32例，灵敏度为84％(32／38例)，特异性60％(6／10例)，准确性79%，40例乳腺癌腋窝淋巴结的灵敏度为71％(10／14例)，特异性88％(23／26例)，准确性83％。结论：^99Tc^m-MIBI乳腺显像既可以显示乳腺肿瘤又能了解腋窝淋巴结的灵敏度为71％(10／14例)，特异性88％(23／26例)，准确性83％。结论：^99Tc^m-MIBI乳腺显像既可以显示乳腺肿瘤又能了解腋窝淋巴结，是核素乳腺显像的首选方法之一。

简介：本组收集2002年9月～2011年2月苏州大学附属第一医院收治的8例CNC中，男性4例、女性4例，年龄22～55岁，中位年龄31-3岁。6例患者因头痛、呕吐及视物模糊等颅高压症状入院。

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简介：Objective:Squamousesophagealcarcinomaishighlyprevalentindevelopingcountries,especiallyinChina.TuBeiMu(TBM),atraditionalfolkmedicine,hasbeenusedtotreatesophagealsquamouscellcarcinoma(ESCC)foralongterm.tubeimosideI(TBMS1)isthemaincomponentofTBM,exhibitinggreatanticancerpotential.Inthisstudy,weinvestigatedthemechanismofTBMS1cytotoxiceffectonEC109cells.Methods:Comparativenuclearproteomicapproachwasappliedinthecurrentstudyandweidentifiedseveralalteredproteinspots.Furtherbiochemicalstudieswerecarriedouttodetectthemitochondrialmembranepotential,cellcycleandcorrespondingproteins’expressionandlocation.Results:SubcellularproteomicstudyinthenucleusfromEC109cellsrevealedthatalteredproteinswereassociatedwithmitochondrialfunctionandcellproliferation.FurtherbiochemicalstudiesshowedthatTBMS1-inducedmoleculareventswererelatedtomitochondria-inducedintrinsicapoptosisandP21-cyclinB1/cdc2complex-relatedG2/Mcellcyclearrest.Conclusions:ConsideringtheconventionalapplicationofTBMinesophagealcancer,TBMS1thereforemayhaveagreatpotentialasachemotherapeuticdrugcandidateforESCC.

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简介：Aseventyeightyearsoldmalepatientunderwentawholebody18F-FDGPET/CTimagingtodiagnosethelesionwhichwasshowedintherightlungbyachestXraytestandCTscanbefore.Besidestheintense18F-FDGuptakeofthelesionintherightlung,alesionintheleftparotidglandalsoshowedintense18F-FDGuptake.Toevaluatethepathologyofthelesionintheleftparotidgland,aparotidglandscintigraphyimagingwithTc-99mpertechnetatewasdoneandrevealedaWarthin'stumor.Laterafineneedleaspiration(FNA)confirmedthatitwasaWarthin'stumor.

简介：目的探讨全反式维甲酸(all-transretinoicacid,ATRA)提高人结肠癌细胞亚株SW480/M5对奥沙利铂(oxaliplatin,L-OHP)敏感性的可能机制.方法MTT法筛选ATRA和L-OHP实验浓度.流式细胞仪检测ATRA对肿瘤细胞周期影响.分别用ATRA、L-OHP、ATRA联合L-OHP作用SW480/M5细胞,MTT法检测药物对肿瘤细胞抑制率,流式细胞仪检测肿瘤细胞周期及凋亡率,原子光谱吸收仪检测肿瘤细胞DNA含铂(Pt)量.结果L-OHP抑制SW480/M5细胞增殖的GI50为58.0mg/L,主要阻滞肿瘤细胞在S和G2/M期.ATRA8.0μmol/L作用24小时后,G1期细胞减少,S期细胞增多；作用72小时后,S期和G2/M期细胞增加并明显抑制肿瘤细胞增殖.8.0μmol/LATRA作用至48小时后联合L-OHP,两药联合由相加作用转变为协同作用；联合用药后S期和G2/M期细胞明显增多,细胞DNA含Pt量显著增加,呈时效依赖性.相对于单独用药,联合用药并不上调肿瘤细胞凋亡率.结论ATRA通过改变SW480/M5细胞周期和提高细胞DNA含Pt量,明显增加肿瘤细胞对L-OHP敏感性.