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刊名:中国实验血液学杂志
曾用名:实验血液学杂志
主办:中国病理生理学会
主管:中国科学技术协会
ISSN:1009-2137
CN:11-4423/R
语言:中文
周期:双月刊
影响因子:0.610899984836578
被引频次:34668
数据库收录:
北大核心期刊(2011版);北大核心期刊(2014版);化学文摘(网络版);生物医学检索系统;文摘与引文数据库;中国科技核心期刊;期刊分类:临床医学
期刊热词:
白血病,多发性骨髓瘤,急性髓系白血病,细胞凋亡,骨髓增生异常综合征,急性白血病,K562细胞,间充质干细胞,急性淋巴细胞白血病,造血干细胞移植,

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实验血液学架起实验室与临床的桥梁血液学的希

来源:中国实验血液学杂志 【在线投稿】 栏目:期刊导读 时间:2021-07-09 12:49

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【摘要】实验血液学架起实验宣与临床的桥梁——血液学的希望80Kantalji锄H,GilesF,Wunder】eL,“df.Nilotinib in imatinib— resistantCML and philadelphia chromosome—positiVeALLNEnglJMed,2006:354:2542—Ca丌D11 w

实验血液学架起实验宣与临床的桥梁——血液学的希望80Kantalji锄H,GilesF,Wunder】eL,“df.Nilotinib in imatinib— resistantCML and philadelphia chromosome—positiVeALLNEnglJMed,2006:354:2542—Ca丌D11 wL,BhojwaniD,MinDJ,“af.Pedia试c acute lymph— oblastic leukemia.HematologyAmSocHematolEducPrograrn2003;2003:102一】3l82Pui cH,EValls wE.Treatment of acute lymphoblastic leukernia.NEnglJMed,2006;354:166—Carrol】wL,BhojwaniD,MinDJ,甜日Z.PediatricAcuteLymphoblasticLeukemia.HematologyAmSocHematolEducProgram2003;2003:102~KauTR,WayJC,SilVerPA.Nuclear tmnspon and cancer:from mechanism to interventionNatRevCancer,2004;4:106一EsteyEHTherapeutic options for acute myelogenous leukeIrⅡaCancer.200l:92:1059—MecucclC.RosatiR.StarzaRL.1eukemia.RevC1inExpHemat01,Genetic pro础e of acute myeloid2002;6:3—2587LichtJD,StembergDW.The molecu】ar pathology of acute myeloidIeukemiaHematologyAmSocHematolEducPmgraHl,2005;2005:137一PLIiCH.JehaSNew therapeutic strategies forche treatment of acute lymphoblasticIeukaenlia.NatReVDrugDiscoV,2007;6:149一ZhouGB,ZhangJ,WangZY,订础.Treatment of acute promye一10cytic leukaemia with a11一trans retinoic acid and arsenic trioxide:a paradigm of synergistic molecular targeting therapy.PhilosTransRSocLondBBioISci2007;362:959—ZhouGB,ChenSJ,ChenZ.Acute promyelocytic leukemia:a model of molecular target based ther印y.Hematology,2005;1O(SupplI):270—2809lDouerD,Preston—Manin s,changE,“以Z.H唔h fI.equency of acute promyelocyticJeukemia aITlongLatinos with acute myeloid leukemiaBlood.1996;87:308—teroJc, santillana s,FereyrosG.Hi曲f嘲uency of acute promyelocytic1eukemia amongLatinos with acute myeloid leukemiaB100d.1996;88:TomasJF,Femandez—RanadaJM.About the increased行equency of acute promyelocytic leukemia amongLatin08: the experience from a center inSpain.BIood,1996;88:2357—RowleyJD.GolombHM,DoughenyC15/17 tmnslocation,a consistent chromosomal change in acute pmmyelocytic leukaemia.Lancet,1977;l(8010):549— de—TheH.ChomienneC,LanotteM,Pf甜The t(15;17) translOcation of acute promyelocytic1eukaemia t’uses the retinoic acid receptor alpha gene to a noVel transcribed10cus.Nature,1990:347(6293):558—KaJ(izukaA.MillerWH.Jr.UmesonoK,“以Z.Chromosomal trallslocationI(15;l7) in human acute promyelocytic leukemia fusesRAR alpha witll a novel putative tmnscription factor,PMLCell.1991:66:663—MelnickA,LichtJDDeconstructing a disease:RARalpha,its fusion pa咖ers, and their r01es in山e pathogenesis of acute pmmye】ocytic1eukellliaBIood,1999;93:3167—ChenSJ,ZelentA,TongⅢ,甜甜.Rearrallgements ofthe retinoic acid receptor alpha and pmmyelocytic leukemia zinc finger genes resulting t-Tom t(1l;17)(q23;q21)in a patient with acute promyelocytic leukemia.JC1inInVest,1993;9l:2260—ChenZ,GuidezF,ROusselotP,Pf dZPLZF—RAR alpha fhsion proteins generated from theVariaIlt t(11;17)(q23;q21) translocation in acute promyelocytic leukelllia inhibit1幢and— dependent tfansac“Vation of wild—type retinoic acid佗ceptors.ProcNatlAcadSciUSA.1994;91:1178一ChenZ,BralldNJ,ChenA,甜口f.Fusion between a novelKruppel—like zinc nnger gene and也e re“noic acid receptor-alpha10cus due to a v撕ant t(11;17)trallslocation associated with acute promyelocytic leukaemia.EM:BOJ,1993;12:116l—lZhangT,XiongH,KanLX,ef nf.Genomic sequence,stmctural o唱anization,m01ecular eV01ution,a11d abe嗽nt rearrangement of pmmyelocytic leukemia zinc finger gene.ProcNatlAcadSciUSA,1999;96:—ChengGX,ZhuXH,MenXQ,甜们Djstinct leukemia phenotypes in transgenic mice aIld difhent corepressor interactions generated by promyelocytic1eukemiaVariaI】t fusion genesPLZF-RARalpha andNPM—RARalpha.ProcNatlAcadSciUSA,1999;—CoreySJ,LockerJ,OliVeriDR,甜口,.A non—classical trans— location inVolVing17q12(reⅡnoic acid receptor alpha)in acute promyelocytic leukemia(APM吐) with atypical featuresLeukemia.1994:8:1350一WellsRA.HummelJL,De—KovenKA, translocation in acute pmmyelocytic“以Z.A leukaeIIlia: neWVanant mOIecular ch锄cterization aIld clinical conelationLeukerIlia,】996;10:735—HuangME,YeYC,ChenSR,“以A11一虹ans retinoic acid witll or withoutIow dose cytosine arabinoside in acute promyelocytic leukemia.Report of6 cases.chinMedJ(En91).1987;100:949—HuangSL,GuOAX,XiangY,“口f.Clinjcal study on the treatment of acute pmmyelocytic leukemia withCompositeIndigoNaturalis tablets.ChinJHemat01,1995;16:26—NiuC,YanH,YuT,甜酬.Studies on treatment of acute promyelocytic1eukemia with arsenic trioxide: remission induction, f01low—up, and molecular monitoring in11 newly diagnosed and47 relapsed acute promyelocytic leukernia patients.Blood.1999:94:3315—ZhangP,WangSY,HuLH acute pmmyelocytic1eukemiaArsenic trioxide treated72 cases ofChinJHemat01,1996:17:58—ShenZX,ChenGQ.NiⅢ,盯酬.Use of arsenic trioxide(A8203) in the treatment of acute promyelocytic leukemja(APL):II.C1inical emcacy and phanllacokinetics in relapsed p atjentsB100d,1997;89:3354—Sun皿,MaL,HuXC,酣Ⅱ,.Ai—LinI treated32 cases of acute pmmyelocytic】eukemia.ChinJIntegratChinWestMed.I992;12.170—MervisJAncient remedy pe怕ms new砸cks.Science,(5275):LiuYF,ZhuYM,ShenSH,甜以f.Mo】ecular response in acute promyelocytic leukemia:a direct comparison of regular a11d real‘ timeRT.PCR.Leukemia.2006:20:1393—LiuYF,ZhuYM,ShiZZ,甜Ⅱ,Long—tenTl fbllow—up confirms the beneflt of a11-trans retinoic acid(ATRA)and arsenic trioxide(As203) as f如nt1ine therapy fbr newly diagnosed acute promyelocytic leukefnia.Blood,2006;108:l70a(abstmct565)114ShenZX,ShiZZ,FangJ.甜以Z.All—trans retinoic acid/A5203 combination yieIds a high quality relllission and surviVal in newly diagnosed acute promyelocytic1eukemiaProcNatlAcadSciUSA,2004:10l:5328—DegosLThe histOry of acute promyelocytic leukaemia.BrJHaematol,2003;122:539—HillestadLKAcute promyelOcytic leukeIIlia.ActaMedScalld,1957;159:189—DraphnRL,GeeTs,DowlingMD,甜以Prophylactic h印arin therapy in acute pmmyelocytic1eukemia.Cancer,1978;41:2484—BemardJ,WeilM,BoironM,ef“f.Acute pmmyelocytic leukemia:results()t t陀atment by daunorubicinBlood,1973;4l:489—TallmallMS,NabhanC,FeusnerⅢ,甜“.Acute promyelocytic leul(e111ia:eV01Ving t11erapeutic s岫舱gies.B100d,20【)2;99:759—SlackJL,WaxmanS,TricotG.甜讲.Advances in the management of acute pmmyelocytic leukemia and other hemat0109ic malignancies wim arsenic trioxideOncologist,2002;7(Suppj1):l—ChanKW,SteinherzPG,M川erDR.Acute promyelocytic leukemia in childremMedPediatr oncol,198l:9:5—CordollllierC,VemalltJP,BrunB,甜以f.Acute pmmyelocyⅡcIeukernia in57 preViously un廿eated pmients.Callcer,1985;55:18—25 l23KantaIjianHM.KeatingMJ,WaltersRS,甜以Acute pmmyel—Ocytic leukemiaM.D.AndersonHospital experience.AmJMed,1986:80:789—SallzMA,Jarque l,ManinG,d以f.Acute pmmyelocytic1euke—111ia.Therapy results and prognostic f沁torsCallcer1988;6l:7— sachsL control of nonllal cell differentiation and the phenotypic reVersion of malignancy in myeloid1eukaemia.Nature,1978;274-535—Hofhnan—LiebemannB.SachsL proteins in the difkrentiationOf1978:14:825—834RegulatiOn of actin aIldOther myelOid1eukemic cells.Cell,127LotemJ.SachsL m v如D induction of no丌11al dif艳rentiation in myeloid1eukemia cellsProcNatlAcadScjUSA.1978;75:378l一BreitmanTR.SeIonickSE.CollinsSJInduction of differen. tiation of the human pmmyelocytic1eukemia cell une(HL_60)by retinoic acid.ProcNatlAcadSciUSA,1980;77:2936—BreitmanTR.CollinsSJ.KeeneBRTemlinal difkrentiation of human pronlyelocytic1eukemic ce¨s in primary cuJture in response to retinoic acid.Blood,198l;57:1000—F1ynnPJ,MillerWJ,WeisdorfDJ,“nf.Retinoic acid treatment of acute promyelocytic1eukemia:加 v打m and抽 v如D obserVations.B100d,1983:62:121l—lF0ntanaJA,RogersJS,DurhamJP.The mle of13 cis—retinoic acid in山e remission induction of a patient wjth acute promyelocytic leukemia.Cancer,1986;57:209—NilssonBPmbable加VfVD induction of differentiation by retinoic acidOf pmmyelocytes in acute pmmyelocytic leukaemia.BrJHaematOl,1984;57:365—RundeV,AulC,SudhoffT,甜ⅡZ.RetinOic acid in the treatment中国实验血液学杂志,E甲胁优n加z2008;16(1) of acute promyelocytic leukemia: inemcacy of山e13一cis isomer and induction of complete remission by山e a11一trans isomer complicated by山romboemb01ic eVents.AnnHemat01,1992;64:270一WarrellRPJr.de—TheH.1eukemia.NEn91JMed,WangZY,甜酬.Acute promyelocytic1993;329:177—Slack几.WaxmanS.TricotG.订ⅡfAdv arIces in山e man— agement of acute pmmyelocytic leukemia and other hematologic malignancies with arsenic moxide.Onc0109ist,2002;7:l一WaIlgZYHam—Wasse丌nan lecture:treatment of acute leukemia by inducing differentiation a11d apoptosisHematolOgyAmSocHematolEducProgram,2003:1—13 l37NerViC,FerraraFF,FanelliM,甜n1.Caspases medi ate retinoic acid—induced degradationOf the acute promyelocytic leukemiaPML/RARalpha t’usion protein.Blood1998;92:2244—225 l138ZhuJ,GiallniM,KopfE,甜“f.Retinoic acid induces proteasome—dependent degradation of retinoic acid receptor ajpha(RARalpha)and oncogenicRARalpha fusion pmteins.ProcNatlAcadSciUSA.1999:96:—KitareewanS.PⅢ1a—RoweI.SekulaD.甜以,.UBElL is a retinoid target that triggersPML/RARalpha degradation and apoptO如s in acute promyeIocytic leukemia.ProcNatlAcadSciUSA,2002:99:3806—38Il140TylerJK,Kadonaga几.The“dark side”of chromatin remo— deling:repressiVe eft色cts on transcription.Cell,】999;99:443—lLinRJ,NagyL,InoueS,订口, complex in acute promyelocytic(6669):81】一814Role of the histone deacetylase eukaemia.Nature.1998:GrignaniF,De·MatteisS,NerviC,甜n,.Fu sjon proteins of tbe retinoic acid recepto卜alpha recn】it histone deacetylase in promyelocytic leukaemia.Nature,1998;391(6669):815—GuidezF,IvinsS,ZhuJ.“Ⅱf.Reduced retinOic acid—sensi— tiVities of nuclear receptOr corepT℃ssor binding toPML—andPLZF—RARalpha underlie molecular pathogenesis a11d treatment of acute promyelocytic1eukemiaBlood,1998;9 l:2634— wangJ,SaunthararajallY,RednerRL,P,d,.Inhibitors of histone deacetyIase relieVeETO—mediated repression and induce dif-ferentiation ofAMLl_ETo1eukemia cellsCancerRes.1999:59.2766—WaxmanS.Differentiation therapy in acute myeIogenous leukemia(non—APL)Leukemia,2000:J4:491—ZhengPz,wangKK,ZhangQY,P,以fSystems analysis of transcriptome and proteome in retinOic acid/arsenic moxide— induced cel|diff色rentiatioll/apoptosjs of promye】ocytic leukemia.ProcNatlAcadSciUSA,2005:102:7653—MaoM,YuM,TongJH,出以,RIG—E,a human hom0109 ofthe munneLy_6 famjly, is induced by retinoic acid during the diff色rentiatiOnOf acute prOmyelocytic1eukemia cell.ProcNat】AcadSciUSA,1996;93:5910—YuM,TongJH,MaoM,Pr以Z.C10ning of a gene(RIG—G) associated with r℃tinoic acid—induced dif佗rentiation of acute promye—locytic leukemia cells and representing a new member of a family of inte他ron—stimulated genes.PmcNaclAcadSclUSA,1997;94:7406—741 l149 xiaoS,LjD,ZhuHQ,“nZ.RIG—G as a key mediator o“he antipmliferatiVe actiVity of inle盹ron—related pathways thmu曲实验血液学架起实验室与临床的桥梁——血液学的希望 enhancing p2I and p27 pmteins.ProcNatlAcadSciUSA,:一KiniAR.PetersonLA,TallmanMS,甜甜Angiogenesis in acute promyelocytic1eukemia:induction byVascular endothelial gmwth factor and inhibition by a11一trans retinoic acidBlood,2001:97:3919—3924StreuliCExtracellular matrix remodelling and cellular differen tia“onCurr opinCellBiol,1999;ll:634—CharradRS,LiY,DelpechB,甜Ⅱf.Ligation of theCI)44 adhesion molecule reVerses blockageOf dif话rentiation in humall acute myeloid leukemia.NatMed,1999;5:669—硒ncadePW.Blasting away leukemla.NatMed,1999;5:619—ZhuQ,ZhangJw,ZhuHQ,甜n,.Synergic efkcts of arsenicⅢoxide and cAMP during acute pmmyelocytic leukemia cell maturation subtends a noVel signaling cross—talkBlood2002;99: lOl4—KamasheVD,VitouxD,de—TheH.PML—RARA—RXR01igomers mediate retinoid and rexinoid/cAMP cross—ta】k in acute pmmyelo— cytic leukemia cell difllerentiationJExpMed,2004;199:1163一 lJChelbi—A1ixMK.PelicanoL1ing cmss talk in nomlal and1999:13:1167一1174Retinoic acjd a11d interfemn signaRA—resistantAPL cells.Leukemia157LippmanSM,LotanR,SchIeunigerURetinoid.interferon the. rapy of soIid tumors.IntJCancer,1997;70:48l一ZhuJ,ChenZ,Lallemand—BreitenbachV.订酬.How acute promye— locytic1eukaemia revived arsenic.NatRevCancer.2002;2:705—ZhuJ,LalJemand—BreitenbachV,de—TH.Pathways of retinoic acid—or arsenic trioxide—inducedPML/RARalpha catabolism,role of oncogene degradation in disease remissionOncogene,2001;20:7257— zhuJ,KokenMH,Quignon targe—ting onto nuclear bodies acute promyelocytic1eukemia.94:3978—3983F.Ff nf.Arsenic.inducedPML implicatiOns t10r me“℃atment ofPmcNatlAcadSciUSA.】997:16lIshoVAM,SotnlkovAG,NegorevD,“以Z.PML is critical forNDlO fbnnation and rec nIits thePML-interacting protein daxx to this nuclear structure when modjned bySUMo—1.JCellBi01.1999:】47:22l一MannKK.Mi】lerWHJr sumoylationCancerCell,Death by arsenic:implications ofPML2004:5:307—MillerWHJr,SchipperHM,LeeJS,“ⅡZ.Mechallisms of action of arsenic moxideCancerRes,2002;62:3893—LazoG,KantarjianH,EsIeyE,甜以,Use of arsenic tnoxide(A82 oj) in che treacmeⅢof patients with acute pmmyeJocytic leukemia:theM.D.Anderson experience.Cancer,2003;97:2218—SoignetSL,FrankelSR,DouerD,Pf以Z.UnitedStates multi. center study of arsenic triOxide in relapsed acute promyelocytic1eukemia.JC1in onc01,2001;19:3852—JingY,WangL,xiaL,“以Combined ef诧ct of a11.tmns retinoic acid and arsenic trioxide in acute promyelocytic1eukeIIlia cells in v打,订and in vivD.B100d,200l:97:264—EsteyE,Garcia—ManemG,Ferrai01iA,甜ⅡZ.Use of all—trans retinoic acid plus arsenic砸oXide as aI】altemative to chemotherapy in untreated acute pmmyelocytic leuke仃lia.B100d,2006;107:3469—WallgG,LiW,CuiJ,甜以An emcient therapeutic approach to patients with acute pmmyelocytic1eukemia using a combination of arsenic moxide wi山10w—dose a11一trans retinoic acid.Hemat01 onc01,2004;22:63—71 l69Lo。CocoF,CiHⅡnoG,BrecciaM,甜以f.Gemtuzumab ozoga. micin(Mylotarg)as a single agent for moleculady relapsed acute promyelocytic leukemja.B100d,2004;104:1995—JurcicJG,DeBlasioT,DumontL,甜酬.M01ecular remission induction wi山retinoic acid and anti—CI)33 monoclonal antibodvHuMl95 in acute promyelocytic leukeIIlia.C1inCaIlcerRes,2000;6:372—SohalJ,PhanVT,ChanPV.已f nf.A model ofAPL withFLT3 mutation is responsiVe to retinoic acid and a receptor tymsine1(inase inhjbitor,SUll657Blood,2003;101:3188—LichtJD.AMLl a11d山eAMLl一ETo fhsion pmtein in the pathogenesis of t(8;21)AMLOncogene,2001;20:5660一5679 l73RubnitzJE,RaimondiSC.HalbertAR.甜nf.Characteristics and outcome of t(8;21)·positiVe chjldhood acute myeIoid leukemia:a sin91e institution’s experience.I。eukemia,2002;16:2072—MiyagiJ.KakazuN,MasudaM,甜以Acute myeloid leukemia(FAB一Ⅳ您)wim a masked type oft(8;21)translocation revealed by spectral karyotyping.IntJHematol,2002;76:338—GamerdingerU,Tei91e卜SchlegelA,PilsS,“以Cryptic c11romo— somal abemtions leading to anAMLl/ETO rearrangement are frequently caused by small insertions.GenesChmmosomesCancer,2003;36:261—NissonPE,WathnsPC,SaccMN.Trallscriptionally active chimeric gene deriVed f如m the fusion of t11eAMLl gene and a noVel gene on chmmosome8 in t(8;21)leukemic cells.CancerGenetCytogenet,1992;63:81—E^cksonP,GaoJ,ChangKS,Pf“Z.Identi行cation of breakpoints in t(8;21)acute myelogenous leukeIIlia aIld isolation of a fusion transcript,AMLl/ETO, wittI sim们arity toDmsophila segmentation gene,nInt.B100d,1992;80:1825—MiyoshiH,shimizuK,KozuT,“以f.t(8;21)breakpoints on chmmosome2 l in acute myeIoid leukemia are clustered within a1imited region of a single gene,AMLlProcNatlAcadSciUSA,199I:88:1043l一ShimizuK,MiyoshiH,KozuT,甜ⅡZ.Consistent disnIption of theAMLl gene occurs within a single intmn in the t(8;21) chmmosomal translocation.CaJlcerRes,1992;52:6945—HiebenSW,LutterbachB,AmannJ.Role of co—repressors inⅡ仙s criptionalI℃pression mediated by吐le t(8;21),t(16;21),t(12;21) aIld inV(16)fusion pmteins.currOpinHemaf01,200l;8:197—AmannJM,NipJ,StromDK,“Ⅱf.ETO,a target or t(8;2】) in acute leukemia, makes distinct contacts with mu】tiple histone deacetylases and binds mSin3A mrDugh its01igomedza廿on domain.MolCellBiol,2001:21:6470—PabstT,MueUerBU.HarakawaN,甜“fAMLl一ETO down— regulates the granulocytic di】=!fbrentiation tIactorC/EBPalpha in t(8;21)myeloid leukeIuia.NatMed,2001;7:444—45l183VangalaRK,Heiss—Neum arInMS,RangatiaJS,甜以ZThe mye一10id master regulator transcription factorPU.1 is inactivated byAMLl—ETo in t(8;21)myeloid leukemia.Blood,2003;10l:270一277 l84JakubowiakA,PouponnotC,BerguidoF,已f nfInhibition of the transfomling growm factor beta l s培naling pathway by theAMLl/ETO1eukemia—associated fusion protein.JBi01Chem,2000:275:—Lin991B,Mulle卜Tidow c,van—deLochtL,Pf以Z.The t(8;21) fusion pmtein,AMLlETo,specmcaIly represses the trfmscription of the p14(ARF)tumor suppressor in acute myeloid leukemia-NatMed.2002;8:743—KlampferL,ZhangJ,zeIenetzAO,er“TheAMLl/ETo fusion pmtein activates crallscription ofBCL一2ProcNatlAcadSciUSA.1996:93:一E1sasserA,FranzenM,KohlmallnA,订nf.The fusion pmteinAMLl.ETo in acute myeloid leuke皿a with tmnslocation t(8;21) induces c_jun pmtein expression v胁the pmximalAP一1 site of the c_jun promoter in an indirect,JNK—dependent mannerOncogene,2003:22:5646—ShimizuK,Kitabayas|liI,K锄adaN,甜df.AM【L1一~r11G8 leuke‘ mic protein induces山e expression of gr锄ulocyte c010ny—stimulating factor(G—csF)receptor t11mu曲the up—regul撕on of ccAA7I'/ enhaJlcer binding pr()tein印silon.B100d,20()o;96:288—HildebrandD,TiefenbachJ,HeinzelT,甜酬Multiple regions ofETo cOoperate in transcriptiOnal rcpressiOn·JBiolChem,2()()1;276.9889—MulloyJC,CammengaJ,MacKenzieKL,“以Z.TheAMLl一ETo t'usion protein promotes山e expansion of human hematopoietjc stem cells.Blood,2002;99:15—TonksA,PeamL,TonksAJ,甜以f.TheAMI,l—ETo fusion gene pmmotes extensive selt’_renewal of human primary erythroid cells.Blood.2()03;10l: de—GuzmanCG,Warr℃nAJ,ZhangZ,甜以,.Hematopoietic stem cell expansion aJld distinct myeloid deVelopmental abno衄alities in a murine model of theAMLl—ETo translOcatiOn.MOlCellBi01.20()2:22:5506—YergeauDA,HetheringtonCJ,WangQ,町Ⅱf.Embryonic1e山a— lity and impaiment of haematopoiesis in mice heterozygous t’or anAMLl一ETo fusion gene.NatGenet,1997;15:303—kudaT,CaiZ,YangS,已r df.Expression of a knocked—inAMLl一ETo1eukernja gene inhibits the establishment of nonTlal definitiVe hematopoiesis aJld directly generates dysplastic hemato— poietic progenitors.Blood,1998;91:3134—BuchholzF,Ret’aeljY,TmmppA,甜耐.Inducible chromosomal translocation ofAMLl andETO genes thmughCre/IoxP—mediated recombination in ttle mouse.EMBORep,2000;l:133一HiguchiM,0’BrienD,KumaraVeluP,甜甜.Expression of a conditionalAMLl一ETo oncogene bypasses embryonic lethality and establishes a murine model of humall t(8;21) acute myeloid1eukemiaCancerCell.2002:1:63—RhoadesKL.HetheringtonCJ.Ha如kawaN,酣Ⅱ,.Analysis of the role ofAMLl—ETo in leukemogenesis, using an inducible transgenic mouse model.B100d,2000;96:2108—MulloyJC,CaIllmengaJ,BerguidoFJ,“以Maintaining the self_renewal aJld di仟erentiation potential of humanCD34+ hemato—poietic cells using a sin91e genetic e】ement.Blood,2003;102.4369—YuanY,ZhouL,MiyamotoT,P,口Z.AMLl—ET0 expression is directly involved ln the developmentOf acute myeloid1eukemia in中国实验血液学杂志,£甲HPm以幻f2008;16(1) the presence of additiOnal mutations.PmcNatlAcadSciUSA2001:98:一l()CarrollM.TomassonMH,BarkerGF,以以,.TheTEL/platelet— derived gmwth f-actor beta receptor(PDGF betaR) t、usion in chronic mvelomonocytic leukemia is a transtomllng proteln that self-associates a11d activatesPDGF betaR kinase—dependent sIgna一1ing pathways.ProcNatlAcadSciUSA,1996;93:一YanM.BurelSA,PetersonLF,P,d,Deletion of anAMLl—ETOC—tenninalNcoR/SMRT—interacting region strongly induces leukemia development.ProcNatlAcadSciUSA,2(m4;10l:—1719l202Sakal(umC,Yamaguchi—1waiY,Satal(eM,甜df.Gmwth inhibi— tion and induction of d¨krentiation of t(8;21) acute myeloid leukemia cells by theDNA—binding domain ofPEBP2 and theAMLl/MTG8(ETo)一specinc antisense oligonucleotide.PmcNatlAcadSciUSA.1994:9l:—MatsushitaH,KobayashiH,MoriS,甜n!Ribozymes cleaVe theAMLl/MTG8 fusion franscript and inhibit pr01iferation of leukemic cells with t(8;21)BiochemBiophysRcsCommun,】995:215:431—4372【)4MatsushitaH,KizakiM,KobayashiH,“以f.Induction of apOptosis in myelo|d leukaemic cells by ribozymes targeted againstAMLl/MTG8BrJCancer.1999:79:1325一Heidenreich o.KrauterJ.RiehleH.甜“Z.AMLl/MT(摁Onco— gene suppression by sma“ interferingRNAs supports myeloid dif诧ren“ation of t(8;21)一posiciVe leukemic cellsBlood,2【)()3;101:3157—Da—SilraN,Meye卜MonardS,MenotML,已,以,.FunctionalG—CSF pathways in t(8;21)Ieukernjc ceIls allow for differentiat呈on induction and degradation ofAML】一ET0HematolJ,20()O;1:316—RednerRL,WangJ,LiuJM.Chmmatin remodeling and1euk emla:new thempeuIic paradigmsB100d1999;94:417—FerraraFF,FaziF,BiallchiniA,订ⅡfH商one deacetylase— targeted treatment restores retinoic acid signaling and differentiation in acute myeloid leukemiaCancerRes,200l;61:2—7209DrukerBJ.TalpazM,RestaDJ.e“lf.Emcacy and safety of a specific inhibitor of theBCR—ABL tyrosine kinase in chronic myeloid leukemia.NEnglJMed,200l;344:103I—DrukerBJ,sawyersCL,KanlarjjanH,甜以f.ActiVity of a specmc inhibitor of theBCR—ABL tyrosine kjnase in the blast crisis of chmnic myeloid leukemia and acute lymphoblastic leukemia with thePhiladelphia chmmosome.NEn91JMed,2001:344:1038一PeggsK,MackinnonSImatinib mesylate—the new gold standard for treatment of chronic myeloid1eukemia.NEn91JMed,2003;348:1048— o7BrienSG,GuilhotF,LarsonRA,订df.Imannib compared with intemmn and10w—dose cytarabine t、or newly diagnosed chIDnic—phase chmnic myeloid leukemia.NEnglJMed,20()3;348:994—KerkelaR,GrazetteL.YacobiR.订ⅡfCardiotoxiclty of the caJlcer therapeutic agent imatinib mesylate.NatMed,2006;12:908—YinT,WuYL,SunHP,盯Ⅱ,.Combined efkcts ofA84S4 and imatinib on chronic mveloidJeukemia ce】ls andBCR—ABL oncopmtein.B100d,2()04;104:4219—4225

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