慢性粒细胞白血病小鼠动物模型建立的研究进展
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摘要
慢性粒细胞白血病(chronic myeloid leukemia,CML)是造血干细胞(hematopoietic stem cells,HSC)恶性克隆性增殖引起的一种血液系统疾病。动物模型是研究CML发病机制及药物靶向治疗的重要载体和工具。研究表明,CML小鼠模型可以通过逆转录病毒介导、转基因和白血病细胞移植的方法建立。三种方法建立的CML小鼠模型均可用于CML发病机制及药物疗效评估研究。实验动物模型进一步通过血常规、血涂片和骨髓涂片、免疫学、分子生物学及病理学等检测手段,判断模型是否建立成功。本文就近年来CML小鼠模型的建立、鉴定及研究应用进展进行综述。
Chronic myeloid leukemia(CML) is a blood system disease caused by malignant clonal proliferation of hematopoietic stem cells(HSCs). Animal models are important tools for studying the pathogenesis of CML and drug-targeted therapy research. Studies have shown that the CML mouse model can be established by retroviral-mediated, transgenic and leukemia cell transplantation methods.The CML mouse model established by the three methods can be used to research and unravel the pathogenesis mechanism of CML, and to evaluate CML drug efficacy of therapy. The experimental animal model further judges whether the model is successfully established by means of blood routine, blood smear and bone marrow smear, immunology, molecular biology and pathology. In this paper, the advances of the establishment, identification and application of CML mouse models in recent years are reviewed.
Chronic myeloid leukemia(CML) is a blood system disease caused by malignant clonal proliferation of hematopoietic stem cells(HSCs). Animal models are important tools for studying the pathogenesis of CML and drug-targeted therapy research. Studies have shown that the CML mouse model can be established by retroviral-mediated, transgenic and leukemia cell transplantation methods.The CML mouse model established by the three methods can be used to research and unravel the pathogenesis mechanism of CML, and to evaluate CML drug efficacy of therapy. The experimental animal model further judges whether the model is successfully established by means of blood routine, blood smear and bone marrow smear, immunology, molecular biology and pathology. In this paper, the advances of the establishment, identification and application of CML mouse models in recent years are reviewed.
引文
[1]何晓薇,燕玮,杨威.三氧化二砷对慢性髓系白血病细胞Hedgehog通路的影响[J].中国实验血液学杂志, 2015, 3(4):971-975Quintás-Cardama A, Cortes J. Molecular biology of bcr-abl1-positivechronic myeloid leukemia[J]. Blood, 2009, 113(8):1619-1630
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[4] Cattaneo D, Morotti D, Bucelli C, et al. Comprehensive MolecularAnalyses in a Case of Masked Philadelphia Chronic MyeloidLeukemia[J]. Cytogenet Genome Res, 2015, 147(1):35-40
[5]李珍,房佰俊.慢性粒细胞白血病的治疗进展[J].临床荟萃, 2014,29(10):1126-1130
[6]王媛媛,史春雷,费海荣,等.二代酪氨酸激酶抑制剂治疗慢性粒细胞白血病的近期疗效研究[J].山西医药杂志, 2016, 45(24):2912-2914
[7] Li S, Zhang H. Chronic Myeloid Leukemia:Methods and Protocols[J].Methods in Molecular Biology, 2016, 1465
[8] Carella, AM, Saglio G, Mahon XF, et al. Present results and futureperspectives in optimizing chronic myeloid leukemia therapy[J].Haematologica, 2018, 103(6):928-930
[9]张佳,杨文华,杨向东,等.尾静脉注射K562细胞建立慢性髓系白血病小鼠模型及其鉴定[J].中国实验血液学杂志, 2012, 20(3):773-776
[10]张欣,于亮. NOD/SCID小鼠白血病模型在白血病研究中的应用现状及进展[J].临床血液学杂志, 2015, 28(5):451-454
[11]王存邦,白海,葸瑞,等.应用含标记基因K562细胞制备的小鼠白血病模型[J].中国组织工程研究, 2010, 14(19):3550-3553Wang Cun-bang, Bai Hai, Si Rui, et al. Establishment of leukemiamouse models using marker gene-containing K562cell line[J]. ChineseJournal of Tissue Engineering Research, 2010, 14(19):3550-3553
[12]徐玉洁,贾文华,刘苍春,等.人源化慢性髓系白血病小鼠模型的建立[J].中国实验血液学杂志, 2016, 24(5):1329-1333Xu Yu-jie, Jia Wei-hua, Liu Cang-chun, et al. Establishment ofMouse Mode l with Humanized Chronic Myeloid Leukemia[J].Journal of Experimental Hematology, 2016, 24(5):1329-1333
[13] Tomkinson B, Bendele R, Giiles FJ, et al. OSI-211, anovel iposomaltopoisomerase I inhibitor, is active in SCID mouse models of humanAML and ALL[J]. Leuk. Res., 2003, 27(11):1039-1050
[14]宋艳秋,刘敏,李薇,等. K562/NOD-SCID小鼠白血病模型的建立[J].中国实验血液学杂志, 2007, 15(1):16-19
[15]于文俊,杨文华,史哲新,等. NOD-SCID小鼠模型在实验血液学研究中的应用[J].中国实验动物学报, 2008, 16(5):391-395
[16]司志刚,白海,王存邦,等.间充质干细胞影响T淋巴细胞杀伤K562细胞效应的研究[J].中国实验血液学杂志, 2007, 15(6):1216-1219
[17]王亚平.造血干细胞生物学及其研究方法[M].北京:科学出版社,2007, 196-214
[18]王存邦,白海,葸瑞,等.直线加速器小剂量X射线照射对BALB/c小鼠T细胞亚群影响的动态观察研究[J].西北国防医学杂志,2010, 31(2):19-21
[19] Daley GQ, Van Etten RA. Baltimore D Induction of chronicmyelogenous leukemia in mice by the P210bcr/abl gene of thePhiladelphia chromosome[J]. Science, 1990, 47:824-830
[20] Pear WS, Miller JP, Xu L, et al. Efficient and rapid induction of achronic myelogenous leukemia-like myeloproliferative disease inmice receiving P210ber/abl-transduced bone marrow[J]. Bood, 1998,92(10):3780-3792
[21]杨东光,张日.逆转录病毒介导的慢性粒细胞白血病模型研究进展与应用[J].国际输血及血液学杂志, 2006, 29(4):328-330
[22] Zhang X, Ren R. Bcr-Abl efficiently induces a myeloproliferativedisease and production of excess interleukin-3 and granulocyte-macrophage colony-stimulating factor in mice:a novel model forchronic myelogenous leukemia[J]. Blood, 1998, 92(10):3829-3840
[23] Li S, Ilaria RL, Million RP, et al. The P190, P210, and P230 forms ofthe BCR/ABL oncogene induce a similar chronic myeloidleukemia-like syndrome in mice but have different lymphoidleukemogenic activity[J]. J. Exp. Med, 1999, 189(9):1399-1412
[24]潘勤,金红,李婧,等.类人慢性粒细胞性白血病小鼠模型的建立[J].中国病理生理杂志, 2013, 29(8):1530-1536
[25] Cornils K, Thielecke L, Winkelmann D, et al. Clonal competition inBcr Abl-driven leukemia:how transplantations can accelerate clonalconversion[J]. Molecular Cancer, 2017, 16(1):120
[26]张萍,李琛,郑铭喆,等. BCR-ABL1+粒细胞白血病小鼠模型的建立及其鉴定[J].转化医学电子杂志, 2017, 4(10):31-34
[27] Ma W, Ma N, Chen X, et al. An overview of chronic myeloidleukemia and its animal models[J]. Sci. China Life Sci, 2015, 58(12):1202-1208
[28] Gossen M, Bujard H. Tight control of gene expression in mammaliancells by tetracycline-responsive promoters[J]. Proc Natl Acad SciUSA, 1992, 89:5547-5551
[29] Gossen M, Freundlieb S, Bender G, et al. Transcriptional activationby tetracyclines in mammalian cells[J]. Science, 1995, 268:1766-1769
[30] Reynaud D, pietras E, Barry-Holson K, et al. IL-6 controls leukemicmultipotent progenitor cell fate an contributes to chronicmyelogenous leukemia development[J]. Cancer cell, 2011, 20(5):661-673
[31] Zhang B, strauss AC, chu S, et al. Effective targeting of quiescentchronic myelogenous leukemia stem cells by histon deacetylaseinhibitors in combination witn imatinib mesylate[J]. Cancer cell,2010, 17(5):427-442
[32]林燕,付伟,梁英民. SCL-tTA/BCR-ABL转基因慢性髓系白血病小鼠模型的建立及鉴定[J].中国实验血液学杂志, 2017, 25(1):24-29
[33] Koschmieder S, Gottgens B, Zhang P, et al. Inducible chronic phaseof myeloid leukemia with expansion of hematopoietic stem cells in atransgenic model of BCR-ABL leukemogenesis[J]. Blood, 2005, 105(1):324-334
[34]施琳,王月英,陈赛娟.逆转录病毒介导的髓系白血病小鼠模型研究的最新进展[J].中国实验血液学杂志, 2011, 19(04):1058-1063
[35] Hao S, Ren R. Expression of interferon consensus sequence bindingprotein(ICSBP)Is downregulated in Bcr-Abl-induced murine chronicmyelogenous leukemia-like disease, and forced coexpression ofICSBP inhibits Bcr-Abl-induced myeloproliferative disorder[J]. Mol.Cell.&Biol, 2000, 20:1149-1161
[36] Ramirez M, Diaz MA, Madero L, et al. Transplantation of marrowcells from children with standard risk acute lymphoblastic leukemia atthe end of therapy into NOD/SCID mice for detecting residualleukemia cells with in vivo growth potential[J]. Leuk. Res, 2003, 27(12):1153-1157
[37] Wei X, Ning MA, Chen XH, et al. An overview of chronic myeloidleukemia and its animal models[J]. Science China Life Sciences,2015, 58(12):1202-1208
[3] Ben-Neriah Y, Daley GQ, Mes-Masson AM, et al. The chronicmyelogenous leukemia-specific P210 protein is the product of thebcr/abl hybrid gene[J]. Science, 1986, 233(4760):212-214
[4] Cattaneo D, Morotti D, Bucelli C, et al. Comprehensive MolecularAnalyses in a Case of Masked Philadelphia Chronic MyeloidLeukemia[J]. Cytogenet Genome Res, 2015, 147(1):35-40
[5]李珍,房佰俊.慢性粒细胞白血病的治疗进展[J].临床荟萃, 2014,29(10):1126-1130
[6]王媛媛,史春雷,费海荣,等.二代酪氨酸激酶抑制剂治疗慢性粒细胞白血病的近期疗效研究[J].山西医药杂志, 2016, 45(24):2912-2914
[7] Li S, Zhang H. Chronic Myeloid Leukemia:Methods and Protocols[J].Methods in Molecular Biology, 2016, 1465
[8] Carella, AM, Saglio G, Mahon XF, et al. Present results and futureperspectives in optimizing chronic myeloid leukemia therapy[J].Haematologica, 2018, 103(6):928-930
[9]张佳,杨文华,杨向东,等.尾静脉注射K562细胞建立慢性髓系白血病小鼠模型及其鉴定[J].中国实验血液学杂志, 2012, 20(3):773-776
[10]张欣,于亮. NOD/SCID小鼠白血病模型在白血病研究中的应用现状及进展[J].临床血液学杂志, 2015, 28(5):451-454
[11]王存邦,白海,葸瑞,等.应用含标记基因K562细胞制备的小鼠白血病模型[J].中国组织工程研究, 2010, 14(19):3550-3553Wang Cun-bang, Bai Hai, Si Rui, et al. Establishment of leukemiamouse models using marker gene-containing K562cell line[J]. ChineseJournal of Tissue Engineering Research, 2010, 14(19):3550-3553
[12]徐玉洁,贾文华,刘苍春,等.人源化慢性髓系白血病小鼠模型的建立[J].中国实验血液学杂志, 2016, 24(5):1329-1333Xu Yu-jie, Jia Wei-hua, Liu Cang-chun, et al. Establishment ofMouse Mode l with Humanized Chronic Myeloid Leukemia[J].Journal of Experimental Hematology, 2016, 24(5):1329-1333
[13] Tomkinson B, Bendele R, Giiles FJ, et al. OSI-211, anovel iposomaltopoisomerase I inhibitor, is active in SCID mouse models of humanAML and ALL[J]. Leuk. Res., 2003, 27(11):1039-1050
[14]宋艳秋,刘敏,李薇,等. K562/NOD-SCID小鼠白血病模型的建立[J].中国实验血液学杂志, 2007, 15(1):16-19
[15]于文俊,杨文华,史哲新,等. NOD-SCID小鼠模型在实验血液学研究中的应用[J].中国实验动物学报, 2008, 16(5):391-395
[16]司志刚,白海,王存邦,等.间充质干细胞影响T淋巴细胞杀伤K562细胞效应的研究[J].中国实验血液学杂志, 2007, 15(6):1216-1219
[17]王亚平.造血干细胞生物学及其研究方法[M].北京:科学出版社,2007, 196-214
[18]王存邦,白海,葸瑞,等.直线加速器小剂量X射线照射对BALB/c小鼠T细胞亚群影响的动态观察研究[J].西北国防医学杂志,2010, 31(2):19-21
[19] Daley GQ, Van Etten RA. Baltimore D Induction of chronicmyelogenous leukemia in mice by the P210bcr/abl gene of thePhiladelphia chromosome[J]. Science, 1990, 47:824-830
[20] Pear WS, Miller JP, Xu L, et al. Efficient and rapid induction of achronic myelogenous leukemia-like myeloproliferative disease inmice receiving P210ber/abl-transduced bone marrow[J]. Bood, 1998,92(10):3780-3792
[21]杨东光,张日.逆转录病毒介导的慢性粒细胞白血病模型研究进展与应用[J].国际输血及血液学杂志, 2006, 29(4):328-330
[22] Zhang X, Ren R. Bcr-Abl efficiently induces a myeloproliferativedisease and production of excess interleukin-3 and granulocyte-macrophage colony-stimulating factor in mice:a novel model forchronic myelogenous leukemia[J]. Blood, 1998, 92(10):3829-3840
[23] Li S, Ilaria RL, Million RP, et al. The P190, P210, and P230 forms ofthe BCR/ABL oncogene induce a similar chronic myeloidleukemia-like syndrome in mice but have different lymphoidleukemogenic activity[J]. J. Exp. Med, 1999, 189(9):1399-1412
[24]潘勤,金红,李婧,等.类人慢性粒细胞性白血病小鼠模型的建立[J].中国病理生理杂志, 2013, 29(8):1530-1536
[25] Cornils K, Thielecke L, Winkelmann D, et al. Clonal competition inBcr Abl-driven leukemia:how transplantations can accelerate clonalconversion[J]. Molecular Cancer, 2017, 16(1):120
[26]张萍,李琛,郑铭喆,等. BCR-ABL1+粒细胞白血病小鼠模型的建立及其鉴定[J].转化医学电子杂志, 2017, 4(10):31-34
[27] Ma W, Ma N, Chen X, et al. An overview of chronic myeloidleukemia and its animal models[J]. Sci. China Life Sci, 2015, 58(12):1202-1208
[28] Gossen M, Bujard H. Tight control of gene expression in mammaliancells by tetracycline-responsive promoters[J]. Proc Natl Acad SciUSA, 1992, 89:5547-5551
[29] Gossen M, Freundlieb S, Bender G, et al. Transcriptional activationby tetracyclines in mammalian cells[J]. Science, 1995, 268:1766-1769
[30] Reynaud D, pietras E, Barry-Holson K, et al. IL-6 controls leukemicmultipotent progenitor cell fate an contributes to chronicmyelogenous leukemia development[J]. Cancer cell, 2011, 20(5):661-673
[31] Zhang B, strauss AC, chu S, et al. Effective targeting of quiescentchronic myelogenous leukemia stem cells by histon deacetylaseinhibitors in combination witn imatinib mesylate[J]. Cancer cell,2010, 17(5):427-442
[32]林燕,付伟,梁英民. SCL-tTA/BCR-ABL转基因慢性髓系白血病小鼠模型的建立及鉴定[J].中国实验血液学杂志, 2017, 25(1):24-29
[33] Koschmieder S, Gottgens B, Zhang P, et al. Inducible chronic phaseof myeloid leukemia with expansion of hematopoietic stem cells in atransgenic model of BCR-ABL leukemogenesis[J]. Blood, 2005, 105(1):324-334
[34]施琳,王月英,陈赛娟.逆转录病毒介导的髓系白血病小鼠模型研究的最新进展[J].中国实验血液学杂志, 2011, 19(04):1058-1063
[35] Hao S, Ren R. Expression of interferon consensus sequence bindingprotein(ICSBP)Is downregulated in Bcr-Abl-induced murine chronicmyelogenous leukemia-like disease, and forced coexpression ofICSBP inhibits Bcr-Abl-induced myeloproliferative disorder[J]. Mol.Cell.&Biol, 2000, 20:1149-1161
[36] Ramirez M, Diaz MA, Madero L, et al. Transplantation of marrowcells from children with standard risk acute lymphoblastic leukemia atthe end of therapy into NOD/SCID mice for detecting residualleukemia cells with in vivo growth potential[J]. Leuk. Res, 2003, 27(12):1153-1157
[37] Wei X, Ning MA, Chen XH, et al. An overview of chronic myeloidleukemia and its animal models[J]. Science China Life Sciences,2015, 58(12):1202-1208