白血病,单核细胞,急性

摘要： 目的 探讨miRNA-618(miR-618)对急性单核细胞白血病THP-1细胞增殖和凋亡的影响.方法 采用实时荧光定量聚合酶链反应(PCR)检测miR-618在THP-1细胞和健康人外周血分离的单核细胞中的相对表达量.构建过表达miR-618质粒载体,以空载体作为阴性对照,将二者分别转染THP-1细胞,设定为miR-618过表达组和阴性对照组.采用CCK-8法和流式细胞术分别检测各组THP-1细胞增殖和凋亡情况.采用TargetScan软件预测miR-618靶基因,通过荧光素酶报告基因实验对其进行验证.采用蛋白质印迹法检测miR-618过表达组或阴性对照组的THP-1细胞和健康人外周血单核细胞中预测的miR-618靶基因蛋白表达的水平.结果 PCR结果显示,与健康人外周血分离的单核细胞相比,THP-1细胞中miR-618表达量低(P＜0.05).CCK-8法检测结果显示,与阴性对照组比较,miR-618过表达组THP-1细胞增殖能力降低(转染0、24、48、72 h细胞吸光度值:0.20±0.03比0.20±0.03、0.28±0.02比0.35±0.03、0.34±0.03比0.43±0.04、0.39±0.02比0.53±0.05,均P＜0.05),细胞晚期凋亡率升高[(27.1±0.1)％比(14.9±0.1)％,t=2.13,P=0.03].TargetScan软件预测miR-618靶基因为ARPP19.荧光素酶报告基因实验结果显示,转染野生型ARPP19基因质粒+miR-618基因质粒组的THP-1细胞相对荧光素酶活性均高于空白对照组和转染野生型ARPP19基因质粒+miR-618空载质粒组(0.170±0.003比0.100±0.004、0.100±0.001,均P＜0.05).蛋白质印迹法检测结果显示,miR-618过表达组THP-1细胞ARPP19蛋白表达水平低于阴性对照组,而两组健康人外周血单核细胞中ARPP19蛋白表达水平相近.结论 miR-618可能通过抑制急性单核细胞白血病THP-1细胞ARPP19的表达而抑制细胞增殖、促进细胞凋亡.

摘要： 急性单核细胞白血病是急性髓系白血病中发病率较高的一类疾病,随着中医药研究的不断深入,对其临床疗效和作用机制方面的研究均取得了一定的进展.文章将近年来中医药治疗急性单核细胞白血病的研究进展进行综述.

摘要： 目的 探讨CUEDC1基因对急性单核细胞白血病THP-1细胞基因表达谱的影响.方法 构建CUEDC1基因干扰的THP-1细胞差异表达基因库.基于RNA测序技术比较CUEDC1基因干扰的THP-1细胞与阴性对照THP-1细胞基因表达谱的差异性表达.采用实时荧光定量聚合酶链反应验证差异表达的部分基因.将表达上调和下调的基因分别导入DAVID软件,进行基因本体(GO)功能富集分析.结果 成功构建CUEDC1基因干扰的THP-1细胞差异表达基因库.CUEDC1干扰组与阴性对照组间共检测到161个差异表达基因(P＜0.05),其中显著上调基因85个,显著下调基因76个;与细胞增殖相关的基因9个,与细胞凋亡相关的基因10个,与p53基因有关的基因2个,与转录调控有关的基因3个,与泛素化有关的基因8个;其中SMAD5、SG15、CBLL1、FANCF等基因与急性白血病的发生发展密切相关.结论 CUEDC1基因可能影响SMAD5、SG15、CBLL1、FANCF等基因的表达,进而参与了急性单核细胞白血病的发生发展.

摘要： 目的 依据治疗方案及危险度分层,对老年急性单核细胞白血病(M5)患者预后进行综合评价,指导个体化治疗.方法 回顾性分析79例年龄≥60岁初发M5患者的临床资料,其中65例患者接受诱导缓解治疗并评估疗效,依据治疗方案分为标准剂量化疗方案组、低强度化疗方案组,依据细胞遗传学或分子生物学指标分为低危、中危及高危组,分析其与临床预后的关系.结果 65例患者完全缓解(CR)率61.5％(40/65),中位生存时间355 d,1年总生存(OS)率64.0％,2年OS率为36.5％,1年无病生存(DFS)率51.2％,2年DFS率为14.1％.标准剂量化疗方案组CR率为69.2％(27/39),2年OS率为46.4％、2年DFS率为11.7％,与低强度化疗方案组的50％(13/26)、23.3％、17.5％,均差异无统计学意义(P>0.05),两组不良反应发生率相当(P>0.05).低危组患者CR率87.5％(14/16),中危组CR率61.5％(16/26),高危组CR率43.5％(10/23),差异无统计学意义(P>0.05).此外,低危组1年OS率、1年DFS率,2年OS率,2年DFS率,均优于中危及高危组.危险度分层内标准剂量化疗方案组与低强度化疗方案组相比:中危患者前组2年OS率优于后组(P0.05).结论 老年AML-M5患者中危组可从标准剂量化疗方案诱导化疗方案中受益,延长生存时间,低危组及高危组需结合患者综合情况制定个体化治疗方案.

摘要： Objective To screen the optimal RNA interference sequence of acute monocytic leukemia associated antigen 22 (MLAA-22) gene in order to study gene function of it. Methods MLAA-22 coding sequence (CDS) was cloned by reverse transcription polymerase chain reaction (RT-PCR) and the CDS was inserted in to pEGFP-N1-3FLAG vector to construct eukaryotic expression vector of MLAA-22. At the same time, four RNA interference sequences were designed and cloned to the vector. Expression vector and RNA interference vector were co-transfected into 293T cells, and the optimal RNA interference sequence was screened by fluorescence and Western blot analyses. Results MLAA-22 eukaryotic expression vector pEGFP-N1-3FLAG and four RNA interference vectors were successfully constructed. After co-transfected 293T cells, KD2 was selected as the optimal interference sequence of MLAA-22. Conclusion KD2 is an optimal interference sequence for targeting MLAA-22 antigen gene.%目的 筛选获得急性单核细胞白血病相关抗原22(MLAA-22)最佳RNA干扰序列,为后期MLAA-22功能研究奠定基础.方法 采用反转录聚合酶链反应(RT-PCR)克隆MLAA-22蛋白质编码区序列(CDS),将测序正确的MLAA-22 CDS插入pEGFP-N1-3FLAG载体,构建真核pEGFP-N1-3FLAG表达载体,同时构建4个MLAA-22靶向RNA干扰载体,共转染293T细胞后通过细胞荧光强度分析及蛋白印迹法筛选最佳MLAA-22 RNA干扰序列.结果成功构建了MLAA-22真核pEGFP-N1-3FLAG表达载体,同时构建了4个RNA干扰载体,共转染293T细胞后筛选获得KD2为最佳干扰序列.结论 KD2是靶向MLAA-22抗原基因的最佳RNA干扰序列.

摘要： 目的 检测寻常痤疮患者囊肿皮损中白介素6(IL-6)的表达,并观察痤疮丙酸杆菌体外对人急性单核细胞白血病细胞系THP-1信号分子p38MAPK及白介素6水平的影响.方法 实时荧光定量PCR检测6例痤疮患者囊肿皮损和6例健康人皮肤组织中IL-6 mRNA表达水平.用2× 106、2×107、2×1o8 CFU/ml灭活痤疮丙酸杆菌菌悬液或脂多糖(100 μg/L)刺激THP-1细胞,同时设培养基对照组和p38MAPK抑制剂SB203580组(先用20 μmol/LSB203580处理,再用2×108 CFU/ml痤疮丙酸杆菌刺激),作用不同时间(1～6 h)后,实时荧光定量PCR检测IL-6 mRNA表达水平,酶联免疫吸附试验检测上清液中IL-6含量.2×108 CFU/ml灭活痤疮丙酸杆菌菌悬液刺激THP-1细胞15、30、60 min或脂多糖(100 μg/L)刺激30 min后,Western印迹法检测p38MAPK和磷酸化p38MAPK表达水平.结果 痤疮囊肿皮损和健康对照皮肤IL-6 mRNA水平分别为3.680±0.790、1.155±0.250,两组比较差异有统计学意义(t=3.047,P＜0.05).双因素方差分析显示,不同浓度痤疮丙酸杆菌组、脂多糖组、培养基对照组IL-6 mRNA表达水平差异有统计学意义(F=532.3,P＜0.001,v=4),痤疮丙酸杆菌刺激1、3、6h之间差异也有统计学意义(F=526.6,P＜0.001,v=2).2×1o8 CFU/ml痤疮丙酸杆菌组、脂多糖组、培养基对照组上清液中IL-6浓度分别为(1 618.22±32.23)、(3 212.06±353.00)、(147.10±0.53) ng/L,3组间差异有统计学意义(v=2,F=102.35,P＜0.01).2×108 CFU/ml痤疮丙酸杆菌作用于THP-1细胞15、30、60 min后磷酸化p38MAPK蛋白水平升高.SB203580组THP-1细胞IL-6 mRNA水平与未抑制组比较明显降低(t=15.91,P=0.004).结论 寻常痤疮患者囊肿中IL-6mRNA水平显著升高.痤疮丙酸杆菌体外可激活人THP-1细胞信号分子p38MAPK,促进其分泌IL-6.%Objective To determine the expression of interleukin-6 (IL-6) in cystic lesions of patients with acne vulgaris,and to evaluate the in vitro effect of Propionibacterium acnes (P.acnes) on the production of IL-6 and activation of p38 mitogen-activated protein kinase (p38MAPK) in the human acute monocytic leukemia cell line THP-1.Methods Real-time fluorescence-based quantitative PCR was performed to determine the mRNA expression of IL-6 in cystic lesions of 6 patients with acne vulgaris,as well as in skin tissues of 6 healthy persons.Some cultured THP-1 cells were divided into 5 groups to be treated with 2 × 106 CFU/ml,2 × 107 CFU/ml and 2 × 108 CFU/ml heat-killed P.acnes suspensions (P.acnes groups),100 μμtg/L lipopolysaccharide (LPS group) and RPMI 1640 medium (control group) respectively.After 1-,3-and 6-hour treatment,real-time fluorescence-based quantitative PCR was conducted to determine the mRNA expression of IL-6 in the above groups.Enzyme-linked immunosorbent assay (ELISA) was performed to detect the level of IL-6 in the culture supernatant of cells in the 2 × 108-CFU/ml P.acnes group,LPS group and control group at 24 hours after the treatment.Western blot analysis was conducted to determine the protein expression of p38MAPK and phosphorylated p38MAPK in the 2 × 108-CFU/ml P.acnes group after 15-,30-and 60-minute treatment,as well as in the LPS group after 30-minute treatment and in the control group.Some other THP-1 cells were divided into 3 groups:2 × 108-CFU/ml P.acnes group treated with 2 × 108 CFU/ml P.acnes suspensions,SB203580 (an inhibitor of p38MAPK) group treated with 20 μmol/L SB203580 for 30 minutes followed by the treatment with 2 × 108 CFU/ml P.acnes suspensions,and control group treated with RPMI 1640 medium alone.After 6-hour treatment,the mRNA expression of IL-6 in the above 3 groups was measured by real-time fluorescencebased quantitative PCR.Results The mRNA expression of IL-6 was significantly higher in the cystic lesions of acne vulgaris than in the normal skin tissues (3.680:±:0.790 vs.1.155 ± 0.250,t =3.047,P ＜0.05).Two-way analysis of variance showed that there were significant difference in the mRNA expression of IL-6 among the 2 × 106-CFU/ml,2 × 107-CFU/ml and 2 × 108-CFU/ml p.acnes groups,LPS group and control group (F =532.3,P ＜ 0.001,v =4),and the mRNA expression of IL-6 significantly differed among different time points (F =526.6,P ＜ 0.001,v =2).There were also significant differences in the IL-6 level in the culture supernatant of cells among the 2 × 108-CFU/ml p.acnes group ([1 618.22 ± 32.23] ng/L),LPS group ([3 212.06 ± 353.00] ng/L) and control group ([147.10 ± 0.53] ng/L;v =2,F =102.35,P ＜0.01).After 15-,30-and 60-minute treatment with 2 × 108 CFU/ml P.acnes suspensions,the protein expression of phosphorylated p38MAPK obviously increased.The mRNA expression of IL-6 in THP-1 cells was significantly lower in the SB203580 group than in the 2 × 108-CFU/ml p.acnes group (t =15.91,P =0.004).Conclusions The mRNA expression of IL-6 evidently increases in the cystic lesions of patients with acne vulgaris.P.acnes can activate the signaling molecule p38MAPK in THP-1 cells,and promote the production of IL-6 by THP-1 cells.

摘要： Objective To investigate the roles of Dectin-1 in phagocytosis of Candida albicans (C.albicans) by macrophage-like cells derived from a human acute monocytic leukemia cell line THP-1.Methods THP-1 macrophage-like cells served as the target cells,and were transfected with small interfering RNA (siRNA) targeting Dectin-1 to down-regulate the expression of Dectin-1 receptor (siRNA-Dectin-1 group).THP-1 macrophage-like cells transfected with nonsense siRNA (siRNA-NC) served as a negative control group.After transfection,the THP-1 macrophage-like cells in the above 2 groups were cocultured with heat-killed C.albicans separately.And then,fluorescence microscopy was performed to count THP-1 macrophage-like cells phagocytosing C.albicans,and flow cytometry was used to determine the mean fluorescence intensity (MFI) of dihydrorhodamine (DHR)-123 fluorescent cells.Statistical analysis was done by one-way analysis of variance (ANOVA) and t test with the SPSS19.0 software.Results After transfection with siRNA-Dectin-1,the mRNA and protein expression of Dectin-1 significantly decreased in THP-1 macrophage-like cells (t =26.163,P ＜ 0.001).After 1-,2-,4-hour co-culture of THP-1 macrophagelike cells with C.albicans,fluorescence microscopy showed that the phagocytosis rates of C.albicans by THP -1 macrophage-like cells were significantly lower in the siRNA-Dectin-1 group than in the negative control group (17.5％ vs.22.1％,18.6％ vs.24.3％,39.2％ vs.59.1％,respectively,all P ＜ 0.05),so were the percentage of THP-1 macrophage-like cells phagocytosing more than 3 C.albicans cells (2.2％ vs.4.7％,2.5％ vs.5.4％,5.1％ vs.8.3％,respectively,all P ＜ 0.05).After 30-minute,1-,2-and 4-hour co-culture of THP-1 macrophage-like cells with DHR-123-labelled C.albicans,flow cytometry showed that the MFI of C.albicans-phagocytosing cells was significantly lower in the siRNA-Dectin-1 group than in the negative control group (36.8 vs.45.7,54.3 vs.62.4,72.1 vs.84.9,93.6 vs.116.7,respectively,all P ＜ 0.05).Conclusion Dectin-1 receptor plays an important role in the phagocytosis of C.albicans by macrophages.%目的 探讨Dectin-1受体在源于人急性单核细胞白血病细胞(THP-1)的巨噬细胞样细胞吞噬白念珠菌中的作用.方法 以THP-1巨噬细胞样细胞为靶细胞,siRNA靶向下调Dectin-1受体表达,并与热灭活白念珠菌共培养,通过荧光显微镜计数、流式细胞仪检测其对白念珠菌的吞噬作用.应用SPSS19.0统计软件,采用单因素方差分析及t检验进行统计分析.结果 细胞转染siRNA-Dectin-1后,Dectin-1 mRNA相对表达量及蛋白表达水平明显降低(t=26.163,P＜0.001).显微镜观察转染siRNA-Dectin-1和siRNA无义片段(NC)的THP-1巨噬细胞样细胞与白念珠菌共培养1、2、4h吞噬率分别为17.5％和22.1％、18.6％和24.3％、39.2％和59.1％,两两比较差异均有统计学意义(P＜0.05);吞噬≥3个菌的细胞百分比分别为2.2％比4.7％、2.5％比5.4％、5.1％比8.3％,两两比较差异均有统计学意义(P＜0.05).流式细胞仪检测显示,THP-1巨噬细胞样细胞与带有荧光的白念珠菌共培养30 min、1h、2h、4h后,转染siRNA-Dectin-1组较转染siRNA-NC组平均荧光强度明显降低,分别为36.8和45.7、54.3和62.4、72.1和84.9、93.6和116.7,两两比较差异均有统计学意义(P＜0.05).结论 Dectin-1受体在巨噬细胞吞噬白念珠菌的效应中发挥重要作用.

摘要： 目的 构建pIRES2-MLAA34-HSP70重组质粒,并检测其免疫效果.方法 采用逆转录PCR(RT-PCR)的方法提取急性单核细胞白血病相关抗原基因MLAA-34和热休克蛋白(HSP) 70基因,设计特异性重叠引物,以重叠延伸PCR(SOE-PCR)技术扩增MLAA34-HSP70融合基因,构建核酸疫苗pIRES2-MLAA34-HSP70.将核酸疫苗免疫BALB/c小鼠,检测小鼠脾淋巴细胞对U937细胞的杀伤作用及小鼠脾细胞悬液中白细胞介素(IL)-2、IL-4和γ干扰素(IFN-γ)水平.结果 扩增出MLAA34-HSP70融合基因2 956 bp,成功构建了核酸疫苗pIRES2-MLAA34-HSP70,经鉴定与预期结果一致;脾淋巴细胞杀伤活性结果显示,核酸疫苗pIRES2-MLAA34-HSP70对U937细胞的杀伤效率明显高于其他实验组及对照组(P＜0.01);核酸疫苗pIRES2-MLAA34-HSP70组细胞因子IL-2、IL-4和IFN-γ水平亦明显高于其他实验组及对照组(P＜0.01).结论 成功构建了pIRES2-MLAA34-HSP70核酸疫苗,该核酸疫苗能诱发强烈的体液免疫,增强机体对肿瘤细胞的免疫应答,对MLAA34阳性细胞具有特异性杀伤作用.%Objective To construct the DNA vaccine pIRES2-MLAA34-HSP70,and to detect its immune effect.Methods The acute monocytic leukemia associated antigen gene MLAA-34 and heat-shock protein (HSP)70 gene were extracted by using RT-PCR.The specific overlapping primer was designed,and the fusion gene MLAA34-HSP70 was amplified by using SOE-PCR technique.Then the DNA vaccine pIRES2-MLAA34-HSP70 was constructed,and BALB/c mice were immunized with this DNA vaccine.The splenic lymphocyte killing activity was detected by using MTT,levels of IL-2,IL-4 and IFN-γ were also detected by using ELISA.Results The MLAA34-HSP70 gene (2 956 bp) and the DNA vaccine pIRES2-MLAA34-HSP70 was amplified and constructed successfully.The killing efficiency of DNA vaccine pIRES2-MLAA34-HSP70 in U937 cells was significantly higher than that in other experimental groups and control group (P＜0.01),and levels of IL-4,IL-2 and IFN-γin DNA vaccine pIRES2-MLAA34-HSP70 group were significantly higher than those in the other experimental groups and control group (P＜0.01).Conclnsion The DNA vaccine pIRES2-MLAA34-HSP70 is constructed successfully.It is shown that the DNA vaccine induces strong humoral immunity,which could enhance immune responses to tumor cells and specificlly kill MLAA34 positive cells.

摘要： Objective To analyze the role of hDOT1L signaling pathway on the proliferation of human acute monocytic leukemia cell line THP-1 cell inhibited by demcitabine, and to explore the other effects except DNA demethylation and the mechanism of hDOT1L signaling pathways involved in leukemia. Methods Methyl thiazolyl tetrazolium (MTT) method was used to detect the influence of decitabine on THP-1 cell proliferation, and trypan blue anti-staining was applied to detect the effect of decitabine on THP-1 cell survival rate, reverse transcriptase polymerase chain reaction (RT-PCR) was used to detect the expression levels of hDOT1L, HOXA9, HOXA10, MLL-AF10 (MLLT10) mRNA, then the methylation level of H3K79 was detected by Western blotting assay. Results Compared with the control group, decitabine inhibited the proliferation of THP-1 cell in a time and dose-dependent manner. The inhibitory effect of 72 h was the highest, and the highest inhibition rate was 56.18%. In addition to 0.5 μmol/L in decitabine treatment group, the other groups were statistically significant (all P<0.05). There were high expressions of hDOT1L, HOXA9, HOXA10, MLLT10 mRNA and H3K79 hypermethylation in the THP-1 cell, meanwhile decitabine reduced the levels of hDOT1L mRNA after 48 h as well as HOXA9, HOXA10, MLLT10 mRNA, and there was a significant difference compared with the control group (all P < 0.01). Decitabine reduced obviously the methylation of H3K79 in cell after 48 h, especially the expression levels of bis and three methyl protein, and these differences were significant compared with the control group (all P< 0.01). Conclusion Decitabine plays its inhibitory effect on the proliferation of THP-1 cells probably through reducing the expression level of hDOT1L and H3K79 methylation level and decreasing the expression levels of key molecules, HOXA9, MLL-AF10, HOXA10, MLLT10 in the hDOT1L signal pathway.%目的 分析人类DOT1L(hDOT1L)信号途径在地西他滨抑制人单核细胞白血病细胞株THP-1细胞增殖中的作用,探讨其DNA去甲基化以外的可能作用及hDOT1L信号途径参与白血病发生的机制.方法 四甲基偶氮唑盐(MTT)法检测不同浓度地西他滨对THP-1细胞增殖的影响,锥虫蓝拒染法检测地西他滨对THP-1细胞存活率的影响,反转录聚合酶链反应(RT-PCR)检测hDOT1L、HOXA9、HOXA10、MLL-AF10(MLLT10)mRNA表达水平,蛋白印迹法检测甲基化H3K79蛋白水平.结果 与阴性对照组相比,各浓度地西他滨明显抑制THP-1细胞增殖,72 h抑制作用最明显,最高抑制率达56.18%,呈时间和浓度依赖性.与阴性对照组相比,除0.5μmol/L地西他滨处理组外,其余各浓度地西他滨对THP-1细胞抑制率差异均有统计学意义(均P<0.05).THP-1细胞内hDOT1L及HOXA9、HOXA10、MLLT10 mRNA水平高H3K79过甲基化,各浓度地西他滨处理48 h后均可降低细胞内hDOT1L mRNA水平,并下调细胞内HOXA9、HOXA10、MLLT10 mRNA水平,与阴性对照组比较差异均有统计学意义(均P<0.01).各浓度地西他滨处理48 h后细胞内H3K79甲基化水平明显降低,以双甲基化和三甲基化H3K79蛋白表达水平下降最明显,与阴性对照组比较差异均有统计学意义(均P<0.01).结论 地西他滨可能通过某种机制减少hDOT1L表达水平,降低H3K79甲基化水平,并可能抑制其信号途径中的关键分子HOXA9、HOXA10、MLLT10的表达,发挥其抑制THP-1细胞增殖的作用.

摘要： 本发明提供了一种治疗急性单核细胞白血病的药物及三氧化二砷和双氢青蒿素的应用，属于治疗白血病药物技术领域。治疗急性单核细胞白血病的药物包括双氢青蒿素(DHA)和三氧化二砷(ATO)；所述DHA和ATO的质量比为1～30:1～8。鉴于DHA或ATO单独给药能有效抑制急性单核细胞白血病典型代表株THP‑1细胞的增殖、能显著增加对THP‑1细胞凋亡比例以及影响THP‑1细胞正常细胞周期等药效，DHA或ATO在制备治疗急性单核细胞白血病的药物中的应用。同时DHA和ATO联合给药能进一步发挥治疗作用。因此，本发明还提供了DHA联合ATO在制备治疗急性单核细胞白血病的药物中的应用。

摘要： 本发明公开了一种急性单核细胞白血病相关抗原MLAA‑34表位多肽及其应用，属于生物技术领域。本发明提供的急性单核细胞白血病相关抗原MLAA‑34表位多肽CP701，能够诱导特异性CTL，在体外对同时表达MLAA‑34和HLA‑A*0201的肿瘤细胞及负载肽的T2细胞产生确定的特异性杀伤作用，将该表位多肽为CP701应用于制备针对急性单核细胞白血病的多肽疫苗，MLAA‑34表位肽CP701(236ILDRHNFAI244)、T辅助性表位和弗氏不完全佐剂组成的多肽疫苗能够抑制荷人单核细胞白血病细胞THP‑1的hu‑PBL‑SCID小鼠瘤体增殖，延长其生存，体内可诱导特异性CTL杀伤活性和NK细胞毒活性。

摘要： 本发明公开提供抗单核细胞白血病相关抗原MLAA‑34全人源单克隆单链抗体ScFv，在噬菌体抗体库中筛选并鉴定得到特异性抗MLAA‑34的单克隆单链抗体scFv，首次表达纯化出了MLAA‑34蛋白，为单抗制备提供了抗原蛋白。利于基因工程的方法，在全人源噬菌体抗体库中淘选并鉴定出抗MLAA‑34全人源单抗。获得了特异性结合高表达MLAA‑34的肿瘤细胞株的全人源单克隆单链抗体ScFv。全人源单克隆单链抗体ScFv解决了鼠源抗体的免疫原性问题，单链抗体ScFv由抗体可变区的重链和轻链由linker连接而成，分子量小，穿透力强，更利于应用。

摘要： 本发明提供了雷公藤内酯酮在制备治疗急性单核细胞白血病药物中的应用，属于白血病药物技术领域。雷公藤内酯酮在制备治疗急性单核细胞白血病药物中的应用。本发明以急性单核细胞白血病细胞U937为研究对象，雷公藤内酯酮溶液处理U937细胞，利用MTT法检测U937细胞的细胞活性，结果表明雷公藤内酯酮对U937白血病细胞的增殖抑制作用。采用Annexin Ⅴ/PI双染法检测雷公藤内酯酮对U937细胞凋亡的影响，结果表明雷公藤内酯酮能诱导U937细胞发生凋亡，且随着浓度的增加，凋亡越明显。因此，雷公藤内酯酮通过抑制急性白血病细胞的增殖和诱导细胞凋亡，从而实现治疗急性单核细胞白血病。

摘要： 本发明提供了一种治疗急性单核细胞白血病的药物及三氧化二砷和双氢青蒿素的应用，属于治疗白血病药物技术领域。治疗急性单核细胞白血病的药物包括双氢青蒿素(DHA)和三氧化二砷(ATO)；所述DHA和ATO的质量比为1～30:1～8。鉴于DHA或ATO单独给药能有效抑制急性单核细胞白血病典型代表株THP‑1细胞的增殖、能显著增加对THP‑1细胞凋亡比例以及影响THP‑1细胞正常细胞周期等药效，DHA或ATO在制备治疗急性单核细胞白血病的药物中的应用。同时DHA和ATO联合给药能进一步发挥治疗作用。因此，本发明还提供了DHA联合ATO在制备治疗急性单核细胞白血病的药物中的应用。

摘要： 本发明提供了特异结合急性单核细胞白血病U-937细胞的核酸适配体；提供该核酸适配体的筛选方法以及临床应用。本发明共筛选出4类具有不同序列的核酸适配体，其与急性单核细胞白血病U-937细胞的结合能力不同。筛选方法包括合成随机单链DNA文库和引物、Cell-SELEX筛选、文库扩增、DNA单链文库的制备、重复多轮及消减筛选、筛选后亲和力测定以及核酸适配体的特异性检测。

摘要： 本发明公开了一种急性单核细胞白血病相关抗原MLAA-34表位多肽及其应用，属于生物技术领域。本发明提供的急性单核细胞白血病相关抗原MLAA-34表位多肽CP701，能够诱导特异性CTL，在体外对同时表达MLAA-34和HLA-A*0201的肿瘤细胞及负载肽的T2细胞产生确定的特异性杀伤作用，将该表位多肽为CP701应用于制备针对急性单核细胞白血病的多肽疫苗，MLAA-34表位肽CP701(236ILDRHNFAI244)、T辅助性表位和弗氏不完全佐剂组成的多肽疫苗能够抑制荷人单核细胞白血病细胞THP-1的hu-PBL-SCID小鼠瘤体增殖，延长其生存，体内可诱导特异性CTL杀伤活性和NK细胞毒活性。

摘要： 本发明公开了包含TIM‑3抑制剂的组合疗法。所述组合可用于治疗包括血液癌的癌病况和病症。

摘要： 本发明公开了一种用于评估幼年型粒单核细胞白血病预后的全基因组DNA甲基化检测方法，包括以下步骤：a.文库构建；b.生物信息分析；c.构建全基因组DNA甲基化图谱。本发明通过检测DNA甲基化水平预测JMML预后，JMML患者异常高甲基化水平提示预后不良,本发明建立JMML DNA甲基化检测方法对于JMML预后评估具有重要的意义，去甲基化药物也有望成为高甲基化水平JMML患者治疗的重要药物之一。本发明为JMML预后评估及药物疗效预测奠定了理论基础和试验基础，具有广阔的应用前景。

摘要： 本发明公开提供抗单核细胞白血病相关抗原MLAA?34全人源单克隆单链抗体ScFv，在噬菌体抗体库中筛选并鉴定得到特异性抗MLAA?34的单克隆单链抗体scFv，首次表达纯化出了MLAA?34蛋白，为单抗制备提供了抗原蛋白。利于基因工程的方法，在全人源噬菌体抗体库中淘选并鉴定出抗MLAA?34全人源单抗。获得了特异性结合高表达MLAA?34的肿瘤细胞株的全人源单克隆单链抗体ScFv。全人源单克隆单链抗体ScFv解决了鼠源抗体的免疫原性问题，单链抗体ScFv由抗体可变区的重链和轻链由linker连接而成，分子量小，穿透力强，更利于应用。