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: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.
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.
简介:背景与目的:脑干是生命中枢,手术中常因损伤脑干而发生死亡或长期昏迷,完善手术中的监护,在尽可能切除肿瘤的同时及时察觉脑干的反应以避免损伤正常脑干组织,是一个迫切需要解决的问题。脑干听觉诱发电位(BAEP),是脑干及其附近手术中很好的监测方法之一,在神经外科手术中有着广泛的应用,对防止术中神经功能损伤、降低并发症及判断预后有着重要的意义。本研究目的就是检测脑干及与相应颅神经功能受损伤时较敏感的电生理指标,为后颅窝肿瘤手术提供精确、准确和安全的术中监测手段。方法:对30例后颅窝肿瘤病人。用同一进口监护仪于手术前、术中及术后分别进行BAEP连续实时监护,测定手术操作对这些指标的影响。结果:后颅窝肿瘤手术操作均可以引起BAEP改变,BAEP的Ⅰ、Ⅲ、Ⅴ波潜伏期(PL),Ⅰ~Ⅴ、Ⅲ~Ⅴ峰间潜伏期(IPL)的明显延长(P<0.01)、Ⅴ波波幅明显降低(P<0.01),其中BAEP的Ⅴ波潜伏期及波幅改变最为显著。结论:BAEP的Ⅴ波潜伏期延长和波幅下降是术中敏感的电生理指标,对其进行监护,可为手术中及手术后避免神经功能损伤提供客观指标,降低手术伤残率,减少或避免病人手术后神经功能损伤。