[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.
