急性早幼粒细胞白血病全反式维甲酸治疗时IL-8及其受体表达的观察

目的：探讨白细胞介素８（ＩＬ８）及其Ａ型受体（ＩＬ８ＲＡ）的表达在全反式维甲酸（ＡＴＲＡ）诱导治疗急性早幼粒细胞白血病（ＡＰＬ）中的临床意义。方法：动态检测ＡＰＬ患者１８例ＡＴＲＡ治疗中血浆ＩＬ８水平（ＥＬＩＳＡ法），取３例骨髓单个核细胞（ＭＮＣ）加ＡＴＲＡ（１０－６ｍｍｏｌ／Ｌ）体外诱导，流式细胞仪动态检测ＭＮＣ膜ＩＬ８ＲＡ的表达。结果：ＭＮＣ加ＡＴＲＡ诱导７２小时，上清ＩＬ８水平明显下降，ＭＮＣ膜表达ＩＬ８ＲＡ增高；维甲酸综合征（ＲＡＳ）发生前血浆ＩＬ８异常升高（达１０１０～２０００ｎｇ／Ｌ），较体温及白细胞数量变化更敏感；感染时血浆ＩＬ６、ＩＬ８水平均明显升高［分别为（１１２．３４±５７．３１）×１０３Ｕ／Ｌ，２３４．１６±７２１８ｎｇ／Ｌ］；弥散性血管内凝血（ＤＩＣ）恶化时ＩＬ８与Ｄ二聚体异常同步上升。结论：ＡＴＲＡ抑制ＡＰＬ细胞分泌ＩＬ８，加强ＩＬ８ＲＡ的表达；监测ＩＬ８水平可预测ＲＡＳ及感染发生；ＩＬ８与Ｄ二聚体异常同步上升提示ＤＩＣ恶化趋势。     

白细胞介素8及其受体在急性白血病的表达及其意义

目的探讨白细胞介素８（ＩＬ８）及其Ａ、Ｂ受体（ＩＬ８ＲＡ、ＩＬ８ＲＢ）的表达与急性白血病（ＡＬ）的分型、疗效及并发症的关系。方法用酶联免疫夹心法检测７７例初诊ＡＬ患者外周血ＩＬ８含量,用间接免疫荧光及流式细胞术检测骨髓单个核细胞（ＭＮＣｓ）表达ＩＬ８Ｒ,并检测了１５例ＡＬ完全缓解（ＣＲ）期脑脊液（ＣＳＦ）中ＩＬ８水平。结果ＡＬ患者外周血ＩＬ８水平高于正常人,其中急性髓系白血病（ＡＭＬ）高于急性淋巴细胞白血病（ＡＬＬ）,Ｍ４、Ｍ５高于Ｍ１～Ｍ３,ＢＡＬＬ高于ＴＡＬＬ（Ｐ＜０．０５）。ＡＬＬ中ＩＬ８＞１００ｎｇ／Ｌ组比≤１００ｎｇ／Ｌ组疗效差（Ｐ＜０．０５）;约３６．３６％的ＡＬ患者ＩＬ８Ｒ（＋）,ＩＬ８Ｒ（＋）者的外周血白细胞计数及幼稚细胞比例显著高于ＩＬ８Ｒ（－）者（Ｐ＜０．０５）;ＣＲ期患者ＣＳＦ中ＩＬ８水平与治疗前比较,差异无显著性（Ｐ＞０．０５）,合并中枢神经系统白血病（ＣＮＳＬ）时明显升高。结论外周血和ＣＳＦ中ＩＬ８水平的检测及检测骨髓ＭＮＣｓ膜ＩＬ８Ｒ的表达有助于ＡＬ各亚型的鉴别及预后判断;ＣＮＳＬ发生时ＣＳＦ中ＩＬ８增高。     

灵芝多糖对人脐血LAK细胞增殖活性的影响

本研究表明，灵芝多糖（ＧＬＰ）能直接刺激人脐血单个核细胞（ＣＢＭＣ）增殖，并能协同ＰＨＡ刺激ＣＢＭＣ增殖在ｒＩＬ－２诱导人脐血ＬＡＫ细胞（简称ＣＢ－ＬＡＫ）早期加入ＧＬＰ，能明显增强ＣＢ－ＬＡＫ细胞增殖活性，最佳浓度１０μ／ｍｌ；ＧＰＬ本身不能诱导ＣＢＭＣＩＬ－２Ｒ的表达，但能协同ｒＩＬ－２提高ＣＢ－ＬＡＫ细胞表达ＩＬ－２Ｒ的表达。     

儿童急性早幼粒细胞白血病PML－RARa基因的检测及意义

作者应用筑巢式逆转录／多聚酶链反应（ＲＴ－ＰＣＲ）对３４例儿童急性早幼粒细胞白血病（ＡＰＬ，Ｍ３）患者进行ＰＭＬ－ＲＡＲａ融合基因的检测，发现１８例初发患者标本中均有融合基因转录本；１３例经全反式维甲酸（ＡＴＲＡ）诱导缓解（ＣＲ）后的患者中，１２例仍可检测到融合基因的表达；同时对１６例巩固化疗后的患者进行微量残留病（ＭＲＤ）的检测：８例融合基因持续阴性或未次阴性的患者，除ｌ例不久复发外，余均处于良好的ＣＲ状态；而８例融合基因持续阳性或未次阳性的患者，７例已复发，其中３例分别是在ＰＣＲ阳性结果后３，３及４个月复发的。以上结果表明ＰＭＬ－ＲＡＲａ基因检测在儿童ＡＰＬ的诊断，疗效评价及ＭＲＤ监测中同样是一个快速、准确且灵敏的方法。     

白介素—2及其受体与急性髓细胞白血病

白介素－２（ＩＬ－２）活化的Ｔ淋巴细胞有ＩＬ－２受体（ＩＬ－２Ｒ）表达，除ＮＫ细胞外，休止期的Ｔ淋巴细胞无ＩＬ－２Ｒ表达，近年来的研究发现，急性髓细胞白血病（ＡＭＬ）细胞有ＩＬ－２Ｒ的表达，本文就ＡＭＬ细胞ＩＬ－２Ｒ表达、ＩＬ－２对这些细胞的影响及其在ＡＭＬ治疗中的应用等作一综述。     

再生障碍性贫血患者细胞免疫功能与造血细胞因子的研究

目的：进一步探讨再生障碍性贫血（再障）的免疫发病机制，阐明细胞免疫、造血细胞因子在再障患者中发生变化的基础与临床意义。方法：用单抗试剂盒，采用改良ＡＰＡＡＰ法及酶联免疫试剂盒，采用ＥＬＩＳＡ法对３８例再障患者及２０名正常人外周血Ｔ细胞亚群，ＨＬＡ－ＤＲ抗原表达以及外周血单个核细胞（ＰＢＭＮＣ）培养上清诱生Ｇ－ＣＳＦ、ＩＬ－６、ＴＮＦα、ＩＦＮα及ＩＬ－８水平进行测定。结果：再障患者外周血ＣＤ４细胞减低、ＣＤ８细胞增高、ＣＤ４／ＣＤ８降低或倒置，ＨＬＡ－ＤＲ抗原表达率增高。再障患者ＰＢＭＮＣ培养上清中Ｇ－ＣＳＦ阳性率减低，ＩＬ－６、ＴＮＦα、ＩＦＮα及ＩＬ－８水平增高。相关分析发现Ｇ－ＣＳＦ与ＣＤ４细胞及ＣＤ４／ＣＤ８呈正相关，而与ＩＦＮα呈负相关；ＩＬ－６与白细胞数及ＣＤ４细胞呈负相关；ＴＮＦα与ＣＤ８细胞呈正相关而与ＣＤ４／ＣＤ８呈负相关；ＩＬ－８与ＣＤ８细胞及ＨＬＡ－ＤＲ呈正相关。结论：细胞免疫功能异常及细胞因子网络失调在再障发病中起一定的作用。     

中期荧光原位杂交在急性早幼粒细胞白血病诊断和微小残？…

为研究中期荧光原位杂交（Ｍ－ＦＩＳＨ）在急性早幼粒细胞白血病（ＡＰＬ）诊断及其微小残留病（ＭＲＤ）检测中的价值，应用１７号全染色体彩涂探针对１０例初诊时按细胞形态学诊断为急性髓细胞白血病（ＡＭＬ）的未治疗患（初治ＡＰＬ５例，复发ＡＰＬ３例，ＡＭＬ－Ｍ１和ＡＭＬ－Ｍ５各１例）和１０例治疗后获完全缓解（ＣＲ）的ＡＰＬ患作耻Ｍ－ＦＩＳＨ检测，并与常规细胞遗传学和逆转录－聚合酶链反应（ＲＴ－ＰＣＲ）结     

白血病患者血清IL-8的测定

目的：探讨血清白细胞介素８（ＩＬ－８）变化在白血病中的意义。方法：采用平似酶联免疫吸附法测定了１０例急性淋巴细胞白血病（ＡＬＬ）,２５例急性非淋巴细胞白血病（ＡＮＬＬ）,１１例慢性粒细胞白血病（ＣＭＬ）慢性期血清ＩＬ－８浓度。结果：ＡＬＬ、ＡＮＬＬ和ＣＭＬ患者血清ＩＬ－８水平显著高于正常对照组,ＡＬＬ与ＡＮＬＬ患者无显著性差异,急性单细胞白血病组水平显著高于急粒白细胞病（Ｍ１￣Ｍ３）组,治疗有铲的     

急性早幼粒细胞白血病基因分析

目的：分析急性早幼粒细胞白血病（ＡＰＬ）患者经全反式维甲酸（ＡＴＲＡ）联合细胞毒药物及异基因骨髓移植（ａｌｏ－ＢＭＴ）治疗后融合基因的变化。方法：采用逆转录－多聚酶链反应（ＲＴ－ＰＣＲ）对２２例ＡＰＬ患者治疗前后ＲＡＲα／ＰＭＬ融合基因进行检测。其中１２例患者为单纯化疗，１０例接受了ａｌｏ－ＢＭＴ，９例患者于第１次完全缓解（ＣＲ１）期、１例于第１次复发（ＲＲ１）期接受了ａｌｏ－ＢＭＴ。结果：单纯维甲酸诱导完全缓解时，７５％ＡＰＬ患者融合基因仍然阳性；继用强化疗后８３％患者融合基因转为阴性，ＲＴ－ＰＣＲ转阴时间为发病后１～３９个月；ａｌｏ－ＢＭＴ后４个月内及４个月后，分别有６２．５％及８５．７％患者融合基因转阴。结论：化疗及ＢＭＴ均可使患者融合基因转阴，ａｌｏ－ＢＭＴ似乎能更快地清除体内白血病细胞     

35例急性白血病细胞IL—2受体α的基因表达的检测分析

为研究ＩＬ－２受体α链基因在急性白血病（ＡＬ）细胞的表达，对１９例ＡＬＬ和１６例ＡＭＬ患者治前白血病细胞用逆转录＝聚合酶链反应（ＲＴ－ＰＣＲ）及芝光素标记单抗ＩＬ－２Ｒ１流式细胞分析，分别进行了ＩＬ－２Ｒα基因ｍＲＮＡ和蛋白质水平表达的检测。３５例ＡＬ患者白血病细胞ＩＬ－２ＲαｍＲＮＡ和Ｐ阳性表达者分别为５例和１４例，前者阳性表达明显高于后者，１４例ＡＬ患者白血病细胞ＩＬ－２ＲαｍＲＮＡ表达阳性，     

急性早幼粒细胞白血病患者纤溶活性的临床研究

目的 研究急性早幼粒细胞白血病(APL)患者纤溶活性在诱导治疗缓解前后的改变及其机制,观察全反式维甲酸(ATRA)或ATRA+三氧化二砷(ATO)诱导治疗对APL患者纤溶活性的影响.方法 选择初治APL患者26例,在诱导治疗过程中分别用发色底物法和ELISA法检测患者血浆纤溶酶原和纤维蛋白(原)降解产物(FDP),用全自动血凝仪检测纤维蛋白原和D-二聚体,在治疗前和完全缓解后用流式细胞术检测细胞表面膜联蛋白Ⅱ(Annexin Ⅱ)和尿激酶型纤溶酶原激活剂受体(u-PAR)的表达,实时定量PCR检测AnnexinⅡ和u-PAR的mRNA表达水平.结果 APL患者存在原发性纤溶亢进,APL细胞表面Annexin Ⅱ和u-PAR蛋白的表达率和mRNA水平均高于正常对照,经以ATRA或ATRA+ATO为基础的诱导缓解方案治疗达到完全缓解后血浆纤维蛋白原、纤溶酶原、FDP及D-二聚体恢复正常,Annexin Ⅱ和u-PAR表达水平相应下降,但仍高于正常对照水平.结论 APL细胞表面Annexin Ⅱ和u-PAR高表达可促使APL纤溶酶生成增多,导致APL患者纤溶亢进.ATRA或ATRA+ATO可通过下调APL细胞Annexin Ⅱ和u-PAR表达纠正APL纤溶异常,这可能是减少APL出血的机制之一.     

Effects of all-trans retinoic acid or chemotherapy on the molecular regulation of systemic blood coagulation and fibrinolysis in patients with acute promyelocytic leukemia.

We studied the pathogenesis of the bleeding disorder in acute promyelocytic leukemia by measuring procoagulant, profibrinolytic, and proinflammatory mediators in peripheral blood and bone marrow cells from 25 previously untreated patients. Patients were induced with either all-trans retinoic acid (ATRA) or chemotherapy. Plasma levels of fibrinopeptide A (FPA), fibrin d-dimer, thrombin antithrombin (TAT) complex, prothrombin fragment 1.2 (F1.2), urokinase-type plasminogen activator (uPA), tissue-type plasminogen activator (t-PA) and plasminogen activator-inhibitor 1 (PAI-1) were measured before and after therapy, as was the cellular expression of the genes for tissue factor (TF) and interleukin-1 beta (IL-1 beta). The mean plasma levels of fibrin d-dimer, F1.2, TAT and FPA were markedly elevated prior to therapy and declined during the first 30 days of treatment with either ATRA or chemotherapy, but more rapidly and to a greater extent in patients treated with ATRA. ATRA treatment was associated with a significant decrease in TF gene expression in bone marrow cells during the first 30 days of treatment, whereas IL-1 beta gene expression, which decreased in the cells of six patients treated with either chemotherapy or ATRA, actually increased in the remaining six patients treated with either chemotherapy or ATRA. In patients with APL, treatment with either chemotherapy or ATRA rapidly ameliorates the coagulopathy, as indicated by an abrupt decline in markers of clotting activation. An increase in cytokine gene expression (e.g. IL-1 beta) may provide an explanation for the persistent hypercoagulability observed in some patients with APL, regardless of therapeutic approach. Our data confirms and extends earlier observations by others that ATRA is more effective than chemotherapy alone in rapidly reducing the procoagulant burden of APL tumor cells. However, our data also suggests that cytokine expression in some patients may be accelerated by either chemotherapy or ATRA. The implications of this observation for understanding the retinoic acid syndrome will require further studies.     

The differentiating effect of retinoic acid and vincristine on acute myeloid leukemia.

We have shown previously that granulocytic maturation and differentiation occurred when HL-60 cells and leukemia cells from a patient with acute promyelocytic leukemia (APL) were exposed to all-trans retinoic acid (ATRA) after treatment with a noncytotoxic concentration of vincristine (VCR), suggesting that VCR might have synergistic action with ATRA in the treatment of APL. Leukemic cells obtained from 24 patients with AML were exposed to 20 nM VCR for 1 h, followed by 1 microM ATRA for 6 days. Changes in the expression of myeloid leukocyte antigens were observed using flow cytometry. Differentiation phenotype as determined by the decrease or increase in maturation cell marker was observed in three samples treated with VCR alone, four samples treated with RA alone, and two samples treated with the combination of VCR and RA. The results suggest that treatment using VCR and ATRA may be effective in the differentiation therapy of AML.     

全反式维甲酸诱导急性早幼粒细胞白血病细胞分化为树突状细胞的实验研究

全反式维甲酸（ATRA）诱导APL细胞分化为成熟树突状细胞（dendritic cell，DC），目前国内外鲜见报道。本研究探讨全反式维甲酸与经典细胞因子共同作用诱导急性早幼粒细胞白血病（APL）细胞分化为DC的可能性，为研制APL-DC疫苗提供新的方法。对初治APL患者骨髓单个核细胞及HL-60细胞株分别在完全培养液中培养，用经典细胞因子组合（GM—CSF、IL-4、TNF-α）共处理，ATRA只在实验组加用。观测细胞形态，检测DC免疫表型，测定上清液IL-12水平，观察MLR反应及CTL效应。结果表明：实验组所得细胞有较明显树突状突起，有APL遗传学特征，其CD1a、CD83、CD80、CD86、HLA—DR和CD1d表达及IL-12分泌水平明显增高，并具有明显的MLR反应及CTL效应，但在HL60-DC中，CD1a增加无统计学差异。结论：利用ATRA可以成功诱导APL细胞为成熟功能性DC，其介导的MLR及CTL效应明显。经ATRA组合诱导的树突状细胞CD1d表达明显增高，推测可能参与NKT细胞激活，具体机制需进一步研究。     

Role of interleukin-8 and growth-regulated oncogene-alpha in the chemotactic migration of all-trans retinoic acid-treated promyelocytic leukemic cells toward alveolar epithelial cells

OBJECTIVE: Although all-trans retinoic acid (ATRA) can treat acute promyelocytic leukemia (APL), it also causes retinoic acid syndrome with presentations similar to acute respiratory distress syndrome. We investigated the role of interleukin (IL)-8 and growth-regulated oncogene (GRO)-alpha in the chemotactic transmigration of ATRA-treated NB4 (ATRA-NB4) APL cells toward A549 alveolar epithelial cells. DESIGN: An in vitro human cell culture study. SETTING: University hospital research laboratories. SUBJECTS: NB4 and A549 cells. INTERVENTIONS: NB4 and A549 cells were separately cultured with ATRA and/or dexamethasone for 1-3 days. NB4 or ATRA-NB4 cells were then placed in an upper insert and co-incubated with A549 cells or their conditioned medium located in a lower plate. MEASUREMENTS AND MAIN RESULTS: ATRA stimulated NB4 cells to transmigrate toward the A549 cells in a time- and dose-dependent manner. Replacement of A459 condition medium by its original medium abrogated this transmigration. Only A549 cells constitutively secreted GRO-alpha, and both A549 and NB4 cells constitutively secreted IL-8, which was enhanced by ATRA. Exogenous administration of IL-8 or GRO-alpha also promoted the ATRA-NB4 transmigration. The binding assay demonstrated that ATRA-NB4 cells bound IL-8, but not GRO-alpha, more avidly. Pretreatment with antibodies directed against IL-8 and GRO-alpha receptors reduced ATRA-NB4 transmigration by about 60%. Dexamethasone did not suppress their IL-8 secretion and transmigration in ATRA-NB4 cells, but when applied to A549 cells, IL-8 secretion was suppressed but not GRO-alpha secretion, and there was attenuation of ATRA-NB4 transmigration. CONCLUSIONS: IL-8 and GRO-alpha secreted from alveolar epithelial cells play an important role in the cell-cell interaction involved in the chemotactic transmigration of ATRA-treated APL cells toward alveolar epithelial cells.     

急性早幼粒细胞白血病患者血清及NB4细胞上清对正常粒系造血？…

OBJECTIVE: To explore the inhibitory activity of sera from acute promyelocytic leukemia(APL) patients on the growth of granular-macrophage progenitors(CFU-GM) and factors affecting the inhibitory activity. METHODS: Sera of 24 APL patients on the all-trans retinoic acid(ATRA) therapy course were kinetically obtained for cellular culture assay. Meanwhile, granulocyte-colony-stimulating-factor(G-CSF), interferon gamma and tumor necrosis factor(TNF) activities in the patient serum and supernate of NB4 cell culture were detected. RESULTS: Before treatment, there was an inhibitory activity on CFU-GM growth in the sera of APL patients and it was statistically higher than that in remission patients and controls(P < 0.01). As the treatment going on the activity was gradually increased, reached its maximum 3-6 days prior to the peak of white blood cell(WBC) and declined to normal when bone marrow remission was obtained. It was positively correlated with the number of CFU-L and the percentage of promyelocyte in bone marrow, negatively with the number of CFU-GM but not with serum G-CSF and TNF activity. Serum G-CSF level was positively correlated with the number of WBC (P < 0.05). No serum IFN-gamma activity was detected in the sera. CONCLUSIONS: 1. One of the therapeutic mechanisms of ATRA on APL is that ATRA induces APL cell maturation thus reduces the serum inhibitory activity on normal hematopoiesis. 2. The inhibitory activity of APL patient serum on normal hemopoiesis consists of complicated factors.     

维甲酸、砷剂及柔红霉素对NB4细胞组织因子表达的影响

目的　探讨全反式维甲酸（ Ａ Ｔ Ｒ Ａ） 、三氧化二砷（ Ａｓ２ Ｏ３） 及柔红霉素（ Ｄ Ｎ Ｒ） 对急性早幼粒细胞白血病（ Ａ Ｐ Ｌ） 细胞株 Ｎ Ｂ４ 细胞组织因子（ Ｔ Ｆ） 表达的影响。方法　用复钙时间检测 Ｎ Ｂ４ 细胞的促凝活性（ Ｐ Ｃ Ａ） ;用 Ｅ Ｌ Ｉ Ｓ Ａ 方法检测其 Ｔ Ｆ 抗原;用逆转录聚合酶链反应（ Ｒ Ｔ Ｐ Ｃ Ｒ） 检测 Ｔ Ｆｍ Ｒ Ｎ Ａ的转录水平。结果　 Ａ Ｔ Ｒ Ａ 和 Ａｓ２ Ｏ３ 均呈时间依赖的方式下调 Ｎ Ｂ４ 细胞的 Ｐ Ｃ Ａ、 Ｔ Ｆ 抗原水平以及 Ｔ Ｆ ｍ Ｒ Ｎ Ａ的转录;而 Ｄ Ｎ Ｒ 处理 Ｎ Ｂ４ 细胞的 Ｐ Ｃ Ａ及 Ｔ Ｆ 抗原在早期上调,至２４ ～４８ 小时达到最大值。对 Ｐ Ｃ Ｒ 产物测序,发现 Ａ Ｐ Ｌ 细胞 Ｔ Ｆ 第５ 个外显子缺失的转录本。结论　 Ａ Ｔ Ｒ Ａ 和 Ａｓ２ Ｏ３ 均可下调 Ａ Ｐ Ｌ 细胞 Ｔ Ｆ的表达并降低其 Ｐ Ｃ Ａ,改善 Ａ Ｐ Ｌ患者的弥散性血管内凝血（ Ｄ Ｉ Ｃ） 出血症状; Ａｓ２ Ｏ３ 和 Ｄ Ｎ Ｒ 对 Ａ Ｐ Ｌ凝血障碍不同效应的作用机制至少部分与药物对 Ａ Ｐ Ｌ细胞 Ｔ Ｆ 表达和 Ｐ Ｃ Ａ 的不同调节作用有关。     

急性早幼粒细胞白血病维甲酸和砷剂治疗期间组织因子改变的 …

探讨急性早幼粒细胞白血病发病初期和维甲酸及三氧化二砷治疗期间组织因子的表达。方法；采用ＥＬＩＳＡ法测定血浆可溶性纤维蛋白单体复合物，Ｄ－二聚体和细胞裂解液ＴＦ含量；ＲＴ－ＰＣＲ法测定细胞ＴＦ ｍＲＮＡ的转录情况。结果：发病时，患者血浆ＳＦＭＣ和Ｄ－Ｄ水平，骨髓分离的单个核细胞悬液的促凝活性，细胞裂解液的促凝活性，细胞裂解液的ＴＦ水平，ＴＦｍＲＮＡ的转录均显著升高，经ＡＴＲＡ和ＡＳ２Ｏ３治疗后显著降     

全反式维甲酸诱导APL细胞分化过程中钙信号途径基因表达水平的变化

为研究钙信号途径在髓系分化中的作用,采用基因芯片技术检测了钙信号途径相关基因在全反式维甲酸(ATRA)诱导急性早幼粒细胞性白血病(APL)细胞株NB4细胞分化过程中的表达情况,并运用实时定量RT-PCR验证基因芯片部分结果,同时检测这些基因在ATRA和8-CPT-cAMP单独和联合作用于NB4-R1细胞和ATRA诱导APL初诊患者原代细胞分化时的表达情况。结果发现:在ATRA诱导NB4细胞分化过程中,许多能直接调节胞内钙离子浓度的基因发生了变化,同时发现许多钙信号途径下游的效应分子的表达上调,并得到实时定量RT-PCR验证。这些基因在ATRA和8-CPT-cAMP单独作用于NB4-R1细胞时变化不大,而在ATRA和8-CPT-cAMP联合作用于NB4-R1细胞分化时与ATRA诱导NB4细胞分化时的表达变化相似。另外,以上基因在ATRA诱导APL初诊患者原代细胞分化的变化情况与诱导NB4细胞分化时相似。结论:钙信号途径可能参与了ATRA诱导的APL细胞分化。