骨髓微环境调控骨髓增生异常综合征的作用及相关机制

doi:10.16150/j.1671-2870.2016.06.002

摘要/Abstract

中图分类号:

R715.2

赵智刚, 王金焕. 骨髓微环境调控骨髓增生异常综合征的作用及相关机制[J]. 诊断学理论与实践, 2016, 15(06): 550-555.

[1] Balderman SR, Li AJ, Hoffman CM, et al.Targeting of the bone marrow microenvironment improves outcome in a murine model of myelodysplastic syndrome[J]. Blood,2016,127(5):616-625.
[2] Greenberg PL.Synergistic Interactions of molecular and clinical advances for characterizing the myelodysplastic syndromes[J]. J Natl Compr Canc Netw,2015,13(7):829-832.
[3] Xiong H, Yang XY, Han J, et al.Cytokine expression patterns and mesenchymal stem cell karyotypes from the bone marrow microenvironment of patients with myelodysplastic syndromes[J]. Braz J Med Biol Res,2015, 48(3):207-213.
[4] Schepers K, Pietras EM, Reynaud D, et al.Myeloproli-ferative neoplasia remodels the endosteal bone marrow niche into a self-reinforcing leukemic niche[J]. Cell Stem Cell,2013,13(3):285-299.
[5] Bakker E, Qattan M, Mutti L, et al.The role of microenvironment and immunity in drug response in leukemia[J]. Biochim Biophys Acta,2016,1863(3):414-426.
[6] Hanoun M, Zhang D, Mizoguchi T, et al.Acute myelogenous leukemia-induced sympathetic neuropathy promotes malignancy in an altered hematopoietic stem cell niche[J]. Cell Stem Cell,2014,15(3):365-375.
[7] Wang L, Zhang H, Rodriguez S, et al.Notch-dependent repression of miR-155 in the bone marrow niche regulates hematopoiesis in an NF-κB-dependent manner[J]. Cell Stem Cell,2014,15(1):51-65.
[8] Zhao ZG, Xu W, Yu HP, et al.Functional characteristics of mesenchymal stem cells derived from bone marrow of patients with myelodysplastic syndromes[J]. Cancer Lett,2012,317(2):136-143.
[9] Geyh S, Oz S, Cadeddu RP, et al.Insufficient stromal support in MDS results from molecular and functional deficits of mesenchymal stromal cells[J]. Leukemia,2013, 27(9):1841-1851.
[10] Greenbaum A, Hsu YM, Day RB, et al.CXCL12 in early mesenchymal progenitors is required for haematopoietic stem-cell maintenance[J]. Nature,2013,495(7440):227-230.
[11] Sochacki AL, Fischer MA, Savona MR.Therapeutic approaches in myelofibrosis and myelodysplastic/myeloproliferative overlap syndromes[J]. Onco Targets Ther,2016, 9:2273-2286.
[12] Jia P, Xu YJ, Zhang ZL, et al.Ferric ion could facilitate osteoclast differentiation and bone resorption through the production of reactive oxygen species[J]. J Orthop Res,2012,30(11):1843-1852.
[13] Raaijmakers MH, Mukherjee S, Guo S, et al.Bone progenitor dysfunction induces myelodysplasia and secondary leukaemia[J]. Nature,2010,464(7290):852-857.
[14] Kode A, Manavalan JS, Mosialou I, et al.Leukaemogenesis induced by an activating β-catenin mutation in osteoblasts[J]. Nature,2014,506(7487):240-244.
[15] Teofili L, Martini M, Nuzzolo ER, et al.Endothelial progenitor cell dysfunction in myelodysplastic syndromes: possible contribution of a defective vascular niche to myelodysplasia[J]. Neoplasia,2015,17(5):401-409.
[16] Kim CK, Han DH, Ji YS, et al.Biomarkers of angiogenesis as prognostic factors in myelodysplastic syndrome patients treated with hypomethylating agents[J]. Leuk Res,2016,50:21-28.
[17] Ding L, Saunders TL, Enikolopov G, et al.Endothelial and perivascular cells maintain haematopoietic stem cells[J]. Nature,2012,481(7382):457-462.
[18] Ohmori S, Ohmori M, Yamagishi M, et al.MDS-macrophage derived inhibitory activity on myelopoiesis of MDS abnormal clones[J]. Br J Haematol,1993,83(3):388-391.
[19] Saito T, Usui N, Asai O, et al.Pseudo-Gaucher cell proliferation associated with myelodysplastic syndrome[J]. Int J Hematol,2007,85(4):350-353.
[20] Allampallam K, Shetty V, Mundle S, et al.Biological significance of proliferation, apoptosis, cytokines, and monocyte/macrophage cells in bone marrow biopsies of 145 patients with myelodysplastic syndrome[J]. Int J Hematol,2002,75(3):289-297.
[21] Nybakken G, Gratzinger D.Myelodysplastic syndrome macrophages have aberrant iron storage and heme oxygenase-1 expression[J]. Leuk Lymphoma,2016,57(8):1893-1902.
[22] Powers MP, Nishino H, Luo Y, et al.Polymorphisms in TGFbeta and TNFalpha are associated with the myelodysplastic syndrome phenotype[J]. Arch Pathol Lab Med,2007,131(12):1789-1793.
[23] Velegraki M, Papakonstanti E, Mavroudi I, et al.Impaired clearance of apoptotic cells leads to HMGB1 release in the bone marrow of patients with myelodysplastic syndromes and induces TLR4-mediated cytokine production[J]. Haematologica,2013,98(8):1206-1215.
[24] Cachaço AS, Carvalho T, Santos AC, et al.TNF-alpha regulates the effects of irradiation in the mouse bone marrow microenvironment[J]. PLoS One,2010,5(2):e8980.
[25] 张翼鷟, 达万明, 赵丹丹, 等. 骨髓基质细胞衍生因子1及其受体在骨髓增生异常综合征患者中的表达[J]. 中华医学杂志,2011,91(46): 3275-3277.
[26] Yang R, Pu J, Guo J, et al.The biological behavior of SDF-1/CXCR4 in patients with myelodysplastic syndrome[J]. Med Oncol,2012,29(2):1202-1208.
[27] Wang J, Xiao Z.Mesenchymal stem cells in pathogenesis of myelodysplastic syndromes[J]. Stem Cell Investig,2014, 1:16.
[28] Legros L, Slama B, Karsenti JM, et al.Treatment of myelodysplastic syndromes with excess of blasts by bevacizumab is well tolerated and is associated with a decrease of VEGF plasma level[J]. Ann Hematol,2012,91(1):39-46.
[29] Teofili L, Martini M, Nuzzolo ER, et al.Endothelial progenitor cell dysfunction in myelodysplastic syndromes: possible contribution of a defective vascular niche to myelodysplasia[J]. Neoplasia,2015,17(5):401-409.
[30] 费成明, 顾树程, 赵佑山, 等. Notch配体Delta-like-1和Jagged-1 mRNA在骨髓增生异常综合征患者骨髓间充质干细胞中表达研究[J]. 中国实验血液学杂志,2014, 22(6):1656-1660.
[31] Qi X, Chen Z, Liu D, et al.Expression of Dlk1 gene in myelodysplastic syndrome determined by microarray, and its effects on leukemia cells[J]. Int J Mol Med,2008,22(1):61-68.
[32] Xu J, Suzuki M, Niwa Y, et al.Clinical significance of nuclear non-phosphorylated beta-catenin in acute myeloid leukaemia and myelodysplastic syndrome[J]. Br J Haematol,2008,140(4):394-401.
[33] Reins J, Mossner M, Neumann M, et al.Transcriptional down-regulation of the Wnt antagonist SFRP1 in haematopoietic cells of patients with different risk types of MDS[J]. Leuk Res,2010,34(12):1610-1616.
[34] Li S, Fan R, Zhao XL, et al.CXXC4 mRNA levels are associated with clinicopathological parameters and survival of myelodysplastic syndrome patients[J]. Leuk Res,2014,38(9):1072-1078.
[35] Lin S, Li J, Zhou W, et al.BIIB021, an Hsp90 inhibitor, effectively kills a myelodysplastic syndrome cell line via the activation of caspases and inhibition of PI3K/Akt and NF-κB pathway proteins[J]. Exp Ther Med,2014,7(6):1539-1544.
[36] Falconi G, Fabiani E, Fianchi L, et al.Impairment of PI3K/AKT and WNT/β-catenin pathways in bone marrow mesenchymal stem cells isolated from patients with myelodysplastic syndromes[J]. Exp Hematol,2016,44(1):75-83.
[37] Zou J, Hong Y, Tong Y, et al.Sonic hedgehog produced by bone marrow-derived mesenchymal stromal cells supports cell survival in myelodysplastic syndrome[J]. Stem Cells Int,2015,2015:957502.
[38] da Costa SV, Roela RA, Junqueira MS, et al. The role of p38 mitogen-activated protein kinase in serum-induced leukemia inhibitory factor secretion by bone marrow stromal cells from pediatric myelodysplastic syndromes[J]. Leuk Res,2010,34(4):507-512.
[39] 王静雅,秦铁军,徐泽锋,等. 环孢素联合沙利度胺治疗IPSS低危/中危-1骨髓增生异常综合征远期疗效影响因素分析[J]. 中华血液学杂志,2015,36(11):942-946.
[40] Medyouf H, Mossner M, Jann JC, et al.Myelodysplastic cells in patients reprogram mesenchymal stromal cells to establish a transplantable stem cell niche disease unit[J]. Cell Stem Cell,2014,14(6):824-837.
[41] Chen X, Eksioglu EA, Zhou J, et al.Induction of myelodysplasia by myeloid-derived suppressor cells[J]. J Clin Invest,2013,123(11):4595-4611.
[42] Ueda Y, Kondo M, Kelsoe G.Inflammation and the reciprocal production of granulocytes and lymphocytes in bone marrow[J]. J Exp Med,2005,201(11):1771-1780.
[43] Bouchliou I, Miltiades P, Nakou E, et al.Th17 and Foxp3(+) T regulatory cell dynamics and distribution in myelodysplastic syndromes[J]. Clin Immunol,2011,139(3):350-359.
[44] Mailloux AW, Epling-Burnette PK.Effector memory regulatory T-cell expansion marks a pivotal point of immune escape in myelodysplastic syndromes[J]. Oncoimmunology,2013,2(2):e22654.
[45] Zou JX, Rollison DE, Boulware D, et al.Altered naive and memory CD4+ T-cell homeostasis and immunosenescence characterize younger patients with myelodysplastic syndrome[J]. Leukemia,2009,23(7):1288-1296.
[46] Yue QF, Chen L, She XM, et al.Clinical prognostic factors in 86 Chinese patients with primary myelodysplastic syndromes and trisomy 8: A single institution experience[J]. Yonsei Med J,2016,57(2):358-364.
[47] Epling-Burnette PK, Bai F, Painter JS, et al.Reduced natural killer (NK) function associated with high-risk myelodysplastic syndrome (MDS) and reduced expression of activating NK receptors[J]. Blood,2007,109(11):4816-4824.
[48] Olnes MJ, Sloand EM.Targeting immune dysregulation in myelodysplastic syndromes[J]. JAMA,2011,305(8):814-819.

骨髓微环境调控骨髓增生异常综合征的作用及相关机制

PDF (PC)

可视化

摘要/Abstract

引用本文

使用本文

参考文献

相关文章 15

编辑推荐

Metrics

本文评价

[1]	王柔嘉, 常春康. 调节性T细胞在骨髓增生异常综合征危险分层中的研究进展[J]. 诊断学理论与实践, 2021, 20(02): 221-224.
[2]	叶成林, 姚永华, 陈真, 贾麟. 骨髓活检塑胶包埋在以单纯血小板减少为表现的骨髓增生异常综合征诊断中的应用价值[J]. 诊断学理论与实践, 2020, 19(02): 177-181.
[3]	吴凌云, 常春康. 骨髓增生异常综合征的诊治最新进展[J]. 诊断学理论与实践, 2019, 18(06): 623-629.
[4]	杜云志, 冯菁华, 常春康. 二代测序技术在骨髓增生异常综合征临床诊断和治疗决策中的应用进展[J]. 诊断学理论与实践, 2019, 18(06): 685-671.
[5]	宋丹丹, 常春康, 郭娟, 许峰, 赵佑山, 吴凌云. 骨髓增生异常综合征患者骨髓巨噬细胞百分比异常及其意义[J]. 诊断学理论与实践, 2018, 17(04): 439-443.
[6]	师蕾, 常春康. 间充质干细胞在骨髓增生异常综合征发病机制中的研究进展[J]. 诊断学理论与实践, 2018, 17(01): 123-126.
[7]	肖志坚. 骨髓增生异常综合征的诊断[J]. 诊断学理论与实践, 2016, 15(06): 545-549.
[8]	宋陆茜, 常春康. 二代测序技术在骨髓增生异常综合征诊治中的临床应用[J]. 诊断学理论与实践, 2016, 15(06): 556-560.
[9]	肖超, 常春康. 骨髓增生异常综合征的铁过载诊断和铁螯合治疗[J]. 诊断学理论与实践, 2016, 15(06): 561-566.
[10]	杨丽艳, 王化泉. 血小板生成素受体激动剂的作用机制及其在骨髓增生异常综合征治疗中的应用[J]. 诊断学理论与实践, 2016, 15(06): 567-572.
[11]	任艳玲, 佟红艳. 骨髓增生异常综合征常用药物治疗的机制[J]. 诊断学理论与实践, 2016, 15(06): 573-577.
[12]	常春康,. 骨髓增生异常综合征WHO(2016)分型的修正[J]. 诊断学理论与实践, 2016, 15(03): 222-225.
[13]	肖超, 常春康,. 白血病微环境的研究进展[J]. 诊断学理论与实践, 2015, 14(03): 288-293.
[14]	盛贤福, 钟华, 万海霞, 钟济华, 陈芳源,. 粒细胞集落刺激因子和AMD3100增加白血病细胞对化疗敏感性的机制研究[J]. 诊断学理论与实践, 2015, 14(02): 120-125.
[15]	常春康,. 骨髓增生异常综合征分类的演变:从FAB到WHO及将来[J]. 诊断学理论与实践, 2014, 13(01): 101-106.