STI571用于慢性髓细胞性白血病的疗效和安全性

ＳＴＩ5 71是人工合成的酪氨酸激酶抑制物 ,可以通过竞争性抑制酪氨酸激酶ＡＴＰ结合位点发挥作用 ,抑制酪氨酸磷酸化 ,使表达ｂｃｒ ａｂｌ的造血细胞停止生长或凋亡。临床前期试验已证明ＳＴＩ5 71的抗白血病活性 ,在此基础上 ,选择经α 干扰素治疗失败ＣＭＬ患者进行ＳＴＩ5 71的Ⅰ期试验。方法 :选择 83例慢性期慢性髓细胞性白血病(ＣＭＬ)患者 ,分为 14个剂量组 (2 5ｍｇ/ｄ～ 10 0 0ｍｇ/ｄ)口服ＳＴＩ5 71。 80 0ｍｇ/ｄ和 10 0 0ｍｇ/ｄ组每日口服 2次 ,每次分别为 4 0 0ｍｇ和 5 0 0ｍｇ ,余治疗组为每日口服 1次。在最初 4周内 ,…     

STI571在慢性髓细胞白血病急变期造血干细胞移植治疗中的作用

目的：探讨STI571在慢性髓细胞白血病(CML)急变期外周血干细胞移植中的应用价值。方法：CML急变期患者接受STI571治疗,然后进行异基因造血干细胞移植,同时进行临床观察。结果：3例CML急变期患者均获得临床血液学缓解,STI571对异基因造血干细胞移植后的造血恢复无影响。结论：STI571对CML急变期有治疗作用,可应用于造血干细胞移植前治疗,二者结合有可能使患者生存期延长。     

STI571治疗慢性髓系白血病的临床疗效与毒副作用观察

背景与目的:bcr-abl融合基因翻译的蛋白产物P210bcr-abl的酪氨酸激酶(proteintyrosinekinase,PTK)活性异常增高被认为是导致慢性髓系白血病(chronicmyeloidleukmeia,CML)发病的根本原因。STI571能高效特异性抑制P210bcr-abl的PTK活性,在临床应用中获得了显著的疗效,但对急变期患者的治疗效果维持时间短。本研究观察和比较了STI571治疗慢性期与加速/急变期CML患者的临床疗效和所发生的不良反应,并从细胞遗传学的角度对急变期患者STI571耐药机制进行初步的分析。方法:选择接受STI571治疗的CML患者22例,其中慢性期6例,加速/急变期16例。按照血液学缓解和细胞遗传学缓解的标准,结合骨髓细胞形态学分析、骨髓细胞G显带技术分析和间期荧光原位杂交检测结果,对患者STI571治疗前和治疗3个月后的血液学和细胞遗传学缓解情况进行分析,并对3个月内出现耐药复发的患者进行核型演化分析。同时密切观察各系统发生的不良反应及严重程度。结果:6例(100%)慢性期CML患者获血液学完全缓解和细胞遗传学缓解,4例(25%)加速/急变期CML患者获血液学完全缓解,8例(50%)获不同程度的细胞遗传学反应。获血液学完全缓解和细胞遗传学反应的百分率两组比较均有统计学差异(P<0.05)。3例急变期CML患者出现耐药复发,其中2例可见2Ph和其它新     

抗肿瘤新药STI571研究新进展

STI571是近年开发的用于治疗慢性髓细胞性白血病(CML)的酪氨酸激酶抑制剂，对bcr-abl激酶有高度特异性的抑制作用。由于该药物是在理解疾病分子机制的基础上，针对CML特异的分子异常进行的一种靶向治疗，因而与传统化疗药物有很大的不同，从而引起了人们的普遍关注。现介绍其作用机制、体内外抗瘤作用、临床试验结果及耐药性等的最新进展。     

STl571治疗慢性粒细胞白血病急变缓解后发生髓外急变1例

1病例介绍 患者,男性,47岁,因疲乏无力,消瘦,腹胀,四肢骨骼疼痛1a于1992年8月20日收治入院.体检:体温36.5℃,P80次/min,R16次/min,BP15.96/931 kPa,慢性病容,轻度贫血外貌,全身皮肤无出血点,浅表淋巴结无肿大,胸骨下段压痛,心肺检查未见异常,肝脏未触及,脾脏肋下6 cm,质硬,无压痛.     

抗肿瘤新药STI571研究新进展

STI571是近年开发的用于治疗慢性髓细胞性白血病（CML）的酪氨酸激酶抑制剂，对bcr-abl激酶有高度特异性的抑制作用。由于该药物是在理解疾病分子机制的基础上，针对CML特异的分子异常进行的一种靶向治疗，因而与传统化疗药物有很大的不同，从而引起人们的普遍关注。现介绍其作用机制、体内外抗瘤作用、临床试验结果及耐药性等的最新进展。     

慢性粒细胞白血病对STI571耐药机制的研究进展

STI571是近年开发的一种治疗慢性粒细胞白血病（CML）的有效药物。它以白血病细胞的bcr-abl为靶标,通过抑制其酪氨酸激酶活性,阻断信号传导机制,诱导细胞凋亡。但随着STI571在临床的广泛应用,对其耐药的病例报告日益增多。就多种机制引发的STI571耐药进行了阐述。     

STI571诱导K562细胞红系分化及其机制的初步研究

目的 :探讨 STI5 71诱导 K5 6 2细胞向红系分化的可能机制。方法 :单用 STI5 71及联用信号传导阻滞剂处理 K5 6 2细胞 ,采用联苯胺染色法检测 K5 6 2细胞向红系分化比例变化 ,流式细胞术检测细胞周期改变 ,Western blot检测 Rb、p- Rb、Erk、p- Erk、p2 7蛋白改变 ,RT- PCR检测 GATA1、GATA2、p2 7m RNA水平变化。结果 :STI5 71诱导 K5 6 2细胞向红系分化 ,呈时间剂量依赖性改变。K5 6 2细胞经 STI5 71处理后 1 2 h即可发生 G1 期阻滞 ,随时间延长趋于明显 ,伴随 p2 7,p- Rb水平下降。p- Erk水平升高。STI5 71与信号传导阻滞剂 U0 1 2 6联合应用后 ,K5 6 2细胞联苯胺阳性率明显下降 (P<0 .0 5 )。STI5 71作用后 ,GATA1、GATA2、m RNA水平未见明显变化。结论 :STI5 71通过上调p2 7,降低 p- Rb水平 ,诱导 K5 6 2细胞发生 G1 期阻滞 ,活化 Erk促使 K5 6 2细胞向红系分化     

STI571联合非清髓性外周血干细胞移植治疗高危慢粒

慢性粒细胞性白血病(慢粒)是一种起源于多能干细胞的肿瘤增生性疾病，异基因干细胞移植是最有希望的疗法。因移植后复发率较高，加速期(AP)、急变期或第二次慢性期(CP2)的患被认为是高危患。2002年4月～2002年7月，2例高危慢粒患在我院接受了非清髓性异基因外周血干细     

流感疫苗促进髓系白血病骨髓细胞来源树突状细胞的功能

目的: 研究流感疫苗对髓系白血病骨髓源性树突状细胞（dendritic cells,DCs）功能的影响及其机制。方法：分离髓系白血病患者\[急性髓细胞白血病(acute myeloid leukemia, AML)19例, 慢性髓细胞白血病（chronic myeloid leukemia,CML) 8例\]骨髓单个核细胞（mononuclear cell,MNC）,用GMCSF和IL4诱导7 d,获得未成熟白血病DCs,然后加入全病毒灭活流感疫苗（whole inactivated influenza vaccine, WIV）、裂解病毒流感疫苗（split influenza vaccine,SIV）或TNFα继续培养24 h。R显带法分析DCs染色体核型,流式细胞仪检测DCs表型,ELISA法测定DCs培养上清IL12的水平,CCK8法检测DCs诱导的CTL对自体白血病细胞的细胞毒作用。结果：19例AML患者中的15例及8例CML患者的MNC全部成功诱导出DCs。与TNFα刺激的白血病DCs相比,流感疫苗刺激的白血病DCs表面分子（CD80、CD83、CD86、HLADR）表达明显上调（P<005）,培养上清中IL12的分泌水平明显增加（P<0.05）,其诱导的CTL可显著杀伤自体白血病细胞（P<0.05）;WIV刺激的DCs在表型、IL12分泌水平及细胞毒作用方面均较SIV刺激的DCs显著增高（P<0.05）。结论： 流感疫苗促进髓系白血病源DCs表型成熟及IL12的分泌,增强其诱导的CTL对自体白血病细胞的杀伤作用。     

α-干扰素与慢性髓性白血病来源的树突状细胞

 各种临床观察肯定了α-干扰素（IFN-α）治疗慢性髓性白血病的疗效,其可明显延长白血病的慢性期及患者生存时间。树突状细胞（DC）作为功能最强的专职抗原递呈细胞,能有效递呈白血病抗原,逆转机体对白血病抗原的耐受,启动特异抗白血病的T细胞应答。IFN-α用于诱导慢性髓性白血病来源的DC,已经取得一定成绩,用IFN-α诱导慢性髓性白血病细胞分化成为具有较强功能的"临床型"DC被寄予厚望。     

抑制吲哚胺2，3-双加氧酶活性促进慢性粒细胞白血病源树突状细胞的功能

目的: 研究吲哚胺2,3双加氧酶（indoleamine 2,3dioxygenase,IDO）在慢性粒细胞性白血病源性树突状细胞（dendritic cells derived from chronic myeloid leukemia,CMLDCs）中的表达,及抑制IDO活性对CMLDCs免疫刺激功能的影响。方法: RTPCR检测17例患者CMLDCs的IDO mRNA的表达情况,流式细胞仪检测CMLDCs免疫表型。在有或无IDO抑制剂1甲基色氨酸（1methyltroptophan,1MT）作用下,分别以不成熟CMLDCs（imDCs）和成熟CMLDCs（mDCs）为刺激细胞,完全缓解期（complete remission,CR）CML患者外周T淋巴细胞为反应细胞建立混合淋巴细胞反应体系,ELISA法检测CMLDCs上清液IL12水平,MTT法检测CMLDCs刺激自体T淋巴细胞的增殖能力。结果: 随着CMLDCs的诱导分化和成熟,IDO mRNA表达逐渐上调;经TNFα诱导的DCs免疫表型除CD1a外,CD80、CD86、CD83、HLADR的表达均明显上调(P<005),且上述分子的表达不受1MT的影响。用1MT抑制IDO活性后的imDCs和mDCs,其IL12水平均明显增加(P<005,P<001),且激发自体T淋巴细胞增殖的能力也明显增强(P<0.05,P<0.01)。结论: 抑制IDO活性可提高CMLDCs的IL12分泌水平,增强其对自体T细胞增殖的刺激能力,IDO对DCs的负性调节为白血病生物治疗提供了新的思路。     

α干扰素促进急性髓性白血病来源的树突状细胞的成熟分化

目的:研究α干扰素(interferon alpha,IFN-α)对不同亚型的急性髓性白血病(acute myeloid leukemia,AML)细胞来源的树突状细胞(dendritic cell,DC)免疫表型及功能的影响。方法:5例初发AML患者(其中M2 1例、M4 2例、M5 2例)的外周血单个核细胞,在含GM-CSF、IL-4、TNF-α的无血清培养液中培养11 d,其后加入IFN-α-2a(1 000 U/ml)继续培养3 d,获得DC(IFN-AML-DC),光镜下观察细胞形态,流式细胞仪测定细胞免疫表型,同种异体混和淋巴细胞反应检测DC的免疫功能。结果:所有患者白血病细胞培养14 d后均转化为IFN-AML-DC,与正常人外周血单核细胞由GM-CSF IL-4 TNF-α培养获得的DC(monocyte-derived DC,MoDC)及AML细胞由GM-CSF IL-4 TNF-α培养获得的DC(AML-DC)相比,IFN-AML-DC具有典型成熟形态的细胞明显增多,表达CD83 细胞的比例显著增加,HLA-DR、CD86分子的表达水平增高,对同种异体T淋巴细胞的激活能力明显高于MoDC及AML-DC。结论:IFN-α能够促进AML-DC的体外成熟,形成更强的免疫激活能力,为AML的免疫治疗提供更有力的手段。     

Toll样受体7及9在慢性粒细胞白血病患者浆细胞样树突状细胞内的表达

目的:研究Toll样受体7(Toll-like receptor 7,TLR7)mRNA及TLR9 mRNA在慢性粒细胞白血病(chronic myeloid leukemia,CML)患者外周血浆细胞样树突状细胞(plasmacytoid dendritic cell,pDC)内的表达及pDC分泌干扰素-α(interferon-α,IFN-α)的能力。方法:收集兰州大学第二医院血液科2010年11月至2011年7月间收治的30例CML患者(初诊未治组15例,缓解组15例)和体检中心的15例健康对照者,运用免疫磁珠法分选外周血pDC,利用real time-PCR检测pDC内TLR7及TLR9 mRNA表达水平。CpG ODN 2216刺激pDC 24 h后,ELISA检测上清液中IFN-α水平。结果:初诊组CML患者外周血pDC内TLR7 mRNA表达水平显著低于缓解组[(0.34±0.11)vs(0.93±0.21),P<0.05],初诊CML患者TLR9 mRNA表达水平显著低于缓解组[(0.44±0.15)vs(0.94±0.18),P<0.05]。CpG ODN 2216刺激后,初诊组pDC产生的IFN-α明显低于缓解组及健康对照组[(408.61±77.11)vs(611.39±84.86)、(651.67±93.39)ng/L,P<0.05]。结论:CML患者pDC内TLR7和TLR9 mRNA明显降低可能是pDC功能缺陷的主要原因,提示TLR7和TLR9可能参与CML的发病。     

Hematopoietic Stem Cell Transplantation for Patients with Chronic Myeloid Leukemia

OBJECTIVE To evaluate the effects of autologous and allogeneic hematopoietic stem cell transplantation (HSCT) for patients with chronic myeloid leukemia(CML).METHODS Fifty-seven patients with CML were treated by HSCT, including 8 cases treated with autologous transplantation purged in vivo and in vitro of minimal residual disease (MRD), 39 cases with related donor allogeneic HSCT (allo-HSCT) and 10 cases with unrelated donor alIo-HSCT. The conditioning regimen was a TBI (total-body irradiation) CY (cyclophosphamide, CTX) protocol in 32 patients, a modified BuCY (hydroxyurea, busulfan, Ara-C, CTX) protocal in 24 patients, and a MACC ( Melphalan, Ara-C, CTX and chlorethyl cyclohexyl nitrosourea ) protocol in one patient. Cyclosporine (CsA) and methotrexate (MTX) were used in patients with related-donor allo-HSCT, and CsA and MTX were added to mycophenolate mofetil (MMF) and antithymocyte globulin (ATG) in unrelated donor allo-HSCT for graft versus host disease (GVHD) prophylaxis. Otherwise, CsA was only used for GVHD prophylaxis in patients with accelerated phase (AP) and blast crisis (BC). The Kaplan-Meier survival analysis model was used to estimate the overall survival (OS) and the disease-free survival (DSF) at 5 years after transplantation.RESULTS Eight patients with autologous transplantation, except for 1 case who died of transplantation-related complications, obtained cytogenetic part or complete remission (CR) within 3 months after transplantation. One patient, who was in BC and obtained CR in hematology before transplantation, had been in molecular CR for 92 months after autologous transplantation. Among the 49 patients treated with alIo-HSCT, all obtained CR, except for one patient who died of hepatic veno-occlusive disease (VOD) and one who had not obtained CR. The incidence of infection and VOD was 33.3% and 7.0%, respectively, during transplantation. After transplantation the incidence of hemorrhagic cystitis (HC) and cytomegalovirus (CMV) interstitial pneumonia (IP) was 22.8% and 8.8%, respectively. VOD, HC and CMV IP did not occur in patients with autologous transplantation. The incidence of acute GVHD and the frequency of chronic GVHD was 41.0% and 48.6%, respectively, in patients with related and unrelated transplantation. The rate of relapse in patients with autologous and allogeneic transplantation was 57.1% and 12.8%, respectively. The DFS at 5 years after transplantation was 25.0% and 61.7%, respectively, in patients with autologous and related donor transplantation. The DFS at 5 years was 70.7% and 34.1%, respectively, in patients with CP (chronic phase) or AP and BC before transplantation.CONCLUSION AIIo-HSCT may have a higher clinical cure rate for CML patients with CP. The CsA MTX MMF ATG protocol is more effective for acute GVHD prophylaxis and can decrease the incidence and degree of GVHD in patients with unrelated donor transplantation, Autologous transplantation with purged bone marrow can prolong the survival time of CML patients and some may be cured with transplants of this type.     

Generation of dendritic cells from peripheral blood of patients at different stages of chronic myeloid leukemia

We report a method to generate dendritic cells (DC) from frozen leukapheresis products of patients with chronic myeloid leukemia (CML), using sterile culture bags and serum-free culture medium, ie conditions feasible for re-infusion into the patient as part of immunother-apeutic protocols. Leukapheresis products were stored from harvests performed either at diagnosis (13 patients) or after chemotherapy with subsequent granulocyte colony stimulating factor (G-CSF) administration (9 patients), for Peripheral Blood Stem Cell (PBSC) collections. In the presence of optimal concentrations of GM-CSF (50 ng/ml) and IL-4 (40 ng/ml) CML progenitors differentiated on day 7 and 14 of culture to DC, expressing CD1a, HLA-DRand CD86 surface antigens. Mature DCs exhibited on average 12-fold higher allo-stimulatory capacity for CD4⁺ and CD8⁺ cells compared to non-cultured PBMC in mixed lymphocyte reaction (MLR). Only DCs obtained from CML patients at diagnosis exhibited bcr/abl fusion gene when tested by fluorescentin situ hybridization (FISH). CD34-selection on leukapheresis products from diagnosis (7 patients) resulted in later maturation of DCs (after 14–15 d), compared to the non-selected PBMC. CD34-selection significantly increased the DC growth, and improved the allo-stimulatory capacity in MLR (on average on day 14, 3.5- and 2.3-fold, respectively). Large differences were observed between individual patients and different leukapheresis products from the same patient. Our report demonstrates the possibility to generateex vivo autologous functionally active DC in CML in a way that allows their clinical application as immunotherapeutic agents.     

ST1926, an orally active synthetic retinoid,induces apoptosis in chronic myeloid leukemia cells and prolongs survival in a murine model

The tyrosine kinase inhibitor, imatinib, is the first line of treatment for chronic myeloid leukemia (CML) patients. Unfortunately, patients develop resistance and relapse due to bcr‐abl point mutations and the persistence of leukemia initiating cells (LIC). Retinoids regulate vital biological processes such as cellular proliferation, apoptosis, and differentiation, in particular of hematopoietic progenitor cells. The clinical usage of natural retinoids is hindered by acquired resistance and undesirable side effects. However, bioavailable and less toxic synthetic retinoids, such as the atypical adamantyl retinoid ST1926, have been developed and tested in cancer clinical trials. We investigated the preclinical efficacy of the synthetic retinoid ST1926 using human CML cell lines and the murine bone marrow transduction/transplantation CML model. In vitro, ST1926 induced irreversible growth inhibition, cell cycle arrest and apoptosis through the dissipation of the mitochondrial membrane potential and caspase activation. Furthermore, ST1926 induced DNA damage and downregulated BCR‐ABL. Most importantly, oral treatment with ST1926 significantly prolonged the longevity of primary CML mice, and reduced tumor burden. However, ST1926 did not eradicate LIC, evident by the ability of splenocytes isolated from treated primary mice to develop CML in untreated secondary recipients. These results support a potential therapeutic use of ST1926 in CML targeted therapy.     

人骨髓间充质干细胞对慢性粒细胞白血病细胞增殖的影响及其机制探讨

背景与目的：我们先前的实验证明,在适宜的刺激下骨髓间充质干细胞（mesenchymal stem cells,MSCs）可分泌可溶性的细胞因子。本实验旨在研究MSCs对慢性粒细胞白血病（chronic myeloid leukemia,CML）细胞增殖的影响．并检测上清液中MSCs分泌的细胞因子。方法：采集健康供者骨髓培养MSCs,流式细胞仪检测第三代MSCs表面标记。将MSCs与不同浓度的CML患者的骨髓单个核细胞（chronic myeloid leukemia mononuclear cells,CML—MNC）共培养;每天收集各组CML—MNC计数取均值,绘制生长曲线。于实验的第3天和第6天收集各培养组的上清液,ELISA法测IFN-α。结果：原代和传代培养的细胞呈大的长梭形,增殖旺盛：细胞表面标记：CD44阳性,而CD45阴性。生长曲线示：与MSCs培养的CML—MNC增殖受抑。ELISA法检测结果示：对照组CML细胞生成IFN-α极低,显著低于各实验组,差异有统计学意义（P〈0．001）。MSCs与CML细胞共培养时可以分泌大量的IFN-α,且随着MSCs浓度的增加和共培养时间的延长,生成的IFN-α量增多。结论：MSCs与CML细胞共培养时能产生大量IFN-α抑制CML细胞增殖。     

急性白血病骨髓间充质干细胞调控免疫的功能及机制

目的 探讨急性白血病患者骨髓间充质干细胞(MSC)的免疫原性及抑制异体T淋巴细胞增殖的功能和机制.方法 采用细胞贴壁法获取急性髓细胞白血病(AML)和急性淋巴细胞白血病(ALL)骨髓MSC,在低血清培养液中培养和扩增.采用流式细胞仪和免疫组化方法检测免疫表型,应用酶联免疫吸附实验检测MSC培养上清液中细胞因子的分泌水平,Transwell检测骨髓MSC抑制T淋巴细胞增殖的能力,混合淋巴细胞反应检测骨髓MSC抑制异体T淋巴细胞增殖的能力.结果 ALL骨髓MSC在倒置显微镜下为梭形,CD29、CD44和CD105的表达阳性率分别为98.81%、99.25%和90.52%,而CD31、CD34和CD45均为阴性.AML骨髓MSC表达CD29和CD44.ALL和AML骨髓MSC不表达人白细胞DR抗原(HLA-DR)和共刺激分子CD80、CD86和CD40.ALL骨髓MSC和AML骨髓MSC均具有分泌TGF-β1(567.58±52.64和357.15±33.52)、HGF(647.27±102.54和219.67±62.37)、IL-6(59.67±15.69和54.35±12.31)和IL-11(102.58±23.54和78.21±9.67)的功能,但是AML骨髓MSC的TGF-β1和HGF分泌水平明显低于ALL骨髓MSC(均P＜0.05).在MSC数量分别为0.5×104、1×104、2×104和5×104个时,加入AML骨髓MSC的CD3+T淋巴细胞3H-TdT掺入的CPM值分别为(3.58±0.54)×104、(2.87±0.33)×104、(1.78±0.51)×104和(1.15±0.15)×104,加入ALL骨髓MSC相应的CD3+T淋巴细胞3H-TdT掺入的CPM值分别为(1.96±0.31)×104、(1.57±0.28)×104、(0.91±0.41)×104和(0.22±0.11)×104,而未加入MSC的CD3+T淋巴细胞3H-TdT掺入的CPM值为(4.01±0.72)×104,AML和ALL骨髓MSC抑制T淋巴细胞的增殖存在明显差异.ALL骨髓MSC抑制T淋巴细胞增殖的能力可以被抗TGF-β1和HGF抗体逆转.结论 ALL骨髓MSC具有低免疫原性及体外调节免疫的功能,该免疫调节功能与其分泌细胞因子有关.AML骨髓MSC调控免疫的能力存在病理改变.

Abstract：

Objective To study the immunomodulatory effects and mechanisms of mesenchymal stem cells(MSC) derived from the bone marrow in acute leukemia patients in vitro. Methods Bone marrow mononuclear cells from acute myeloid leukemia(AML) and acute lymphoblastic leukemia(ALL)were obtained and cultured in low serum medium.The immunophenotypes were assessed by FACS and immunol histochemistry.The levels of cytokines were evaluated by enzyme linked immunosorbant assay (ELISA).T-cell suppression ability was evaluated by Transwell chamber assay.Moreover,the immunoregulatory ability of AML-and ALL-derived MSC was detected by mixed lymphocyte culture assay. Results ALL-derived MSC showed a typical fibroblast-like morphology.They were positive for CD29,CD44 and CD105,the positive rate were 98.81%,99.25% and 90.52%,respectively,while negative for CD31,CD45 and CD34.Moreover,ALL-and AML-derived MSC didn't express HLA-DR and costirnulatory molecules(CD40,CD80 and CD86ALL and AML derived MSC could secret several cytokines,such as TGF-β1(567.58 ±52.64 and 357.15 ±33.52),HGF(647.27 ± 102.54 and 219.67 ±62.37),IL-6(59.67 ± 15.69 and 54.35 ±12.31) and IL-11(102.58 ±23.54 and 78.21 ±9.67),the level of secretion of TGF-β1 and HGF were higher in ALL bone marrow derived MSC than that of in AML bone marrow derived MSC.ALL and AML derived MSC significantly suppressed T lymphocyte proliferation in a dose-dependent manner,the counts per minute(CPM) were(3.58 ± 0.54) × 104,(2.87 ± 0.33) ×104,(1.78 ±0.51) × 104 and(1.15 ± 0.15) × 104 for AML derived MSC,and CPM were(1.96 ± 0.31)×104,(1.57 ±0.28) ×104,(0.91 ±0.41) ×104 and(0.22 ±0.11) ×104 for ALL derived MSC when MSCwere0.5×104,1×104,2×104 and5×104.In addition,the CPM was(4.01 ±0.72) ×104 in control group.The immunosuppressive ability was different between MSCs derived from AML and ALL.The immunosuppressive effect of ALL derived MSC could be reversed by anti-TGF-βl and anti-HGF antibody.Conclusion ALL-derived MSC show immunoregulatory effect in vitro and this effect is achieved through cytokines.But MSCs derived from AML display abnormal changes in T-cell suppression ability.