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淋巴细胞性白血病

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It might provide theoretical basis for a new clinical application of arsenic trioxide.

为临床上砷剂对急性非淋巴细胞性白血病治疗的应用提供了新思路。

Methylation of CpG islands in the promoters induces gene silencing. The multiple tumor suppressor gene P16, located at chromosome 9p21, regulating normal proliferation of cells with a functional unit constituting of p16, cyclin D1 and pRb together. Methylation of P16 gene has been detected in several lymphocytic and plasmacytic malignancies such as lymphoma, acute lymphocytic leukemia and multiple myeloma and shows relationships with the pathogenesis of these diseases. Application of demethylation agents or arsenical to refresh the gene functions will be expected to be a new treatment for hemopoietic malignancies.

基因启动子区CpG岛甲基化常导致基因沉默。P16基因是一定位于9p21的多种肿瘤抑制基因,通过pl6INK4Acyclin D1-PRb通路维持机体细胞的有序增殖。P16基因甲基化在淋巴瘤、急性淋巴细胞性白血病、多发性骨髓瘤等多种淋巴细胞浆细胞肿瘤中被检测到,并与疾病的发生、发展存在一定关系,应用甲基化抑制因子或砷剂去甲基化治疗,恢复基因功能可望成为血液恶性肿瘤治疗的一种新手段。

OBJECTIVE: To study the cellular activity of asparagine synthetase in different types of childhood acute lymphoblastic leukemia.

目的:不同类型急性淋巴细胞性白血病对左旋门冬酰胺酶敏感度不完全相同,由于LAsp活性水平与细胞内门冬酰胺合成酶活性负相关,因此研究不同类型ALL患儿白血病细胞内门冬酰胺合成酶活性水平分布情况,有助于临床治疗中合理使用LAsp。

This study was purposed to investigate the possible side effects of L-asparaginase in the treatment of patients with acute lymphoblastic leukemia and to explore the corelation of these side effects at different therapeutic stages by means of retrospective analysis, so as to reduce the incidence of side effects and improve the safety of chemotherapy and the long-term survival of patients.

本研究采用回顾性方法分析左旋门冬酰胺酶在儿童急性淋巴细胞性白血病治疗过程中可能发生的副作用,以探索L-ASP副作用的发生与患儿所处治疗阶段的关系,以便采用有效的监测手段减少副作用的发生,提高化疗安全性及患儿的长期存活率。

To date,it has been documented after transfusion of unirradiated blood components to at least 87 patients:in patients with severe combined immunodeficiency,thymic hypoplasia,and Wiskott Aldrich syndrome premature newborns and those with erythroblastosis fetalis; patients with hematologic malignancies including Hodgkin\'s and non-Hodgkin\'s lymphomas,acute myelocytic and lymphoblastic leukemias,chronic lymphocytic leukemia,and aplastic patients with solid tumors including neuroblastomas, glioblastoma,rhabdomyosarcoma,cervical carcinoma,small cell lung cancer,and germ cell tumor;patients after cardiac surgery and cholecystectomp-60;and in an apparently healthy 22-year-old woman.

目前为止,输注未辐照血液成分后,至少引起了87例TA-GVHD的发生,主要见于以下病人:严重的免疫缺陷病人、胸腺发育不全、Wiskott Aldrich综合症、早产儿、胎儿红细胞增多症、何杰金与非何杰金氏淋巴瘤等恶性血液病人、急性粒细胞性和淋巴细胞性白血病、慢性淋巴细胞性白血病、成神经细胞瘤等实体瘤病人、横纹肌赘瘤、宫劲癌、小细胞肺癌、微细胞瘤、心脏和胆囊手术病人。

Four of12patients with non-leukemia were heteroploidy,2of4were precancerous lesion.The S%of marrow cell of leukemia was significant lesser than that of control.Three acute lymphocytic leukemia were got CR,and its S%was more than that before therapy.

白血病组骨髓细胞S%明显低于对照组。3例接受治疗的急性淋巴细胞性白血病患儿达到完全缓解后,其S%明显高于治疗前,非白血病组的骨髓细胞周期与正常对照组差异无显著性。

The second is the lymphocyte-forming organ and is a part of the immune system. It is the site where lymphocytic leukemia begins.

其次是一个淋巴细胞生成的器官组成了免疫系统的一部分,是淋巴细胞性白血病的发生部位。

Ph^1 was observed in all 11 cases of chronic myelocytic leukemia and 3 of the 7 cases of acute lymphoblastic leukemia; chimera was found in 1 of the 7 ALL cases and 4 cases demonstrated-22,+Mar, del(11)(q^23) and normal karyotyp or multiploid.

其中11例慢性粒细胞白血病,均可见费城染色体(即Ph^1)。7例急性淋巴细胞性白血病中有3例出现Ph1,其中1例为嵌合体,其余4例急性淋巴细胞白血病中分别出现-22,+MarD?

On the basis of the percentage of GPI-anchored PLAP conversion, the leucocyte GPI-PLD activities of the 96 leukemia patients were measured. Compared with the 96 healthy controls, the leukocyte GPI-PLD activites of ANLL and CLL patients were significantly increased; the activities of ANLL and CLL patients were significantly reduced.

检测96例白血病患者外周血白细胞GPI-PLD活性时发现,急性非淋巴细胞性白血病和慢性淋巴细胞性白血病患者酶活性较正常人显著性增高,急性淋巴细胞性白血病和慢性粒细胞性白血病患者酶活性较正常人显著性降低。

Furthermore, preliminary work also performed to examine whether PI3K/AKT signal transduction pathway was activated in the process of refractory leukemia development. Materials and methods An immortalized human bone marrow stromal cell line, HS-5, was introduced to establish a bi-phase culture system for the cultivation of B-lineage precursor leukemia cells. ELISA and RT-PCR were used to investigate the expression of VEGF and its receptors in the leukemia cell lines and primary childhood leukemia cells in different treated groups. Flow cytometory method and immunofluorescent staining were employed to examine the apoptosis signals both in the VP16 treated and untreated leukemia cells. Western blot was utilized to explore the PI3K/AKT activated status in the drug induced or uninduced leukemia cells and lymphocytes from healthy donors.

材料和方法使用来源于人类骨髓基质细胞的细胞株HS-5作为滋养层细胞进行急性淋巴细胞性白血病细胞的体外培养,通过细胞生物学和免疫学方法评估培养体系并鉴定出难治性白血病细胞克隆;以ELISA和RT-PCR方法检测急性白血病细胞株和患儿白血病细胞VEGF及其受体的表达,了解不同治疗阶段VEGF及其受体的表达状况,并结合临床指标进行分析,明确VEGF及其受体在白血病发生过程中的作用;流式细胞仪和免疫荧光染色法对正常健康儿童、初发白血病患儿、复发白血病患儿及缓解后患儿进行凋亡因子检测和分析,初步阐明难治性白血病抗凋亡形成的原因;蛋白印记分析检测PI3K/AKT信号传导通路在健康儿童、初发白血病和复发白血病患儿的表达,初步了解难治性白血病形成的分子生物学机制。

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