查询词典 leukemia

Background and objective Although marked progress has been made in the treatment of acute myeloid leukemia,about 20%～40% patients with AML failed to get complete remission after standard induction chemotherapy. Furthmore, approximate 70% patients in CR will die because of relapse or refractory to therapy during post remission chemotherapy.

研究背景及目的：尽管目前急性髓系白血病(acute myeloid leukemia，AML)的治疗取得了显著的进步，但仍有20％～40％的患者经标准诱导治疗未能达到完全缓解(complete remission，CR)，即使获得CR的患者，在巩固化疗后仍有70％左右复发或发展为难治性急性髓系白血病而治疗无效死亡。

BMI-1(B-cell-specific Moloney murine leukemia virus integration site 1), a Polycomb group repressor, is always present as a PcG complex combined with RING1, HPC2, Mph2, et al. BMI-1 prolongs cells'capacity to proliferate and represses their senescence by repressing the transcription of CDKN2A through acetylhydrolasing or deacetylhydrolasing the Polycomb response elements in chromosome.

BMI-1 (B-cell-specific Moloney murine leukemia virus integration site 1)属于PcG家族，它与该家族其他成员如RING1，HPC2，Mph2等结合形成蛋白复合体，作用于染色质PREs位点，通过对组蛋白进行乙酰化和去乙酰化修饰，从而稳定抑制CDKN2A转录，最终促进细胞的增殖并抑制细胞凋亡。

The mouse embryonic stem cells cDNA library was screened by yeast two-hybrid assay,some candidate molecules were get,including DDX39 DEAD (Asp-Glu-Ala-Asp box polypeptide 39, BAT1A(HLA-B-associated transcript 1A), NAC1 ( nucleus accumbens-1 ), BicD2 (bicaudal D homolog 2)、MLL3 (myeloid/lymphoid or mixed-lineage leukemia 3). NAC1 and MLL3 were associated with regulation of gene transcription. DDX39 andBAT1A were associated with pre-mRNA processing and mRNA export from nucleus to cytoplasm. BicD2 was associated with the regulation of Golgi body.

通过利用酵母双杂交方法，以小鼠全长Plk1作为诱饵蛋白筛选小鼠胚胎干细胞cDNA文库中与其相互作用的蛋白，获得了DDX39DEAD(Asp-Glu-Ala-Aspbox polypeptide 39、BAT1A(HLA-B-associated transcript 1A)、NAC1(nucleus accumbens-1)、BicD2(bicaudal D homolog 2)、MLL3(myeloid／lymphoid or mixed-lineage leukemia 3)等几个候选蛋白，其中NAC1、MLL3与基因的转录调控有关，DDX39、BAT1A与mRNA前体的剪切、加工及mRNA从细胞核转运到细胞质紧密相关，而BicD2与高尔基体的调控紧密相关，提示我们Plk1与基因转录、mRNA前体的剪切、加工、mRNA的运输及胞质分裂中高尔基体的调控有关。

To explore the expressions of the intercellular adhesion molecule3（ICAM3） in acute leukemia and to investigate its role in clinical therapeutic efficacy and extramedullary infiltration.

目的 探讨细胞间粘附分子3(intercellular adhesion molecule3，ICAM3)在急性白血病（acute leukemia，AL）中的表达及其在临床疗效、髓外浸润中的意义。

Objective To explore the expressions of the inter-cellular adhesion molecule-3 (ICAM-3) in acute leukemia and to investigate its role in clinical therapeutic efficacy and extramedullary infiltration.

目的 探讨细胞间粘附分子－3(inter-cellular adhesion molecule-3， ICAM-3)在急性白血病(acute leukemia， AL)中的表达及其在临床疗效、髓外浸润中的意义。

To explore the expressions of the intercellular adhesion molecule-3（ICAM-3） in acute leukemia and to investigate its role in clinical therapeutic efficacy and extramedullary infiltration.

目的探讨细胞间粘附分子-3(intercellular adhesion molecule-3，ICAM-3)在急性白血病（acute leukemia，AL）中的表达及其在临床疗效、髓外浸润中的意义。

Results Among the 104 primary acute leukemia patients, the number of patients with T lymphocyte leukemia,B lymphocyte leukemia,acute myeloblastic leukemia,mixed phenotype acute leukemia and umclassified leukemia were 4(3.8％),38(36.5％),58(55.8％),2(1.9％),and 2(1.9％),respectively.

结果 104例初发急性白血病中，T淋巴细胞白血病4例(3.8％)，B淋巴细胞白血病38例(36.5％)，急性髓细胞白血病58例(55.8％)，急性混合性白血病2例(1.9％)，未行明确分类的2例(1.9％)。

Results among the 104 primary acute leukemia patients, the number of patients with t lymphocyte leukemia,b lymphocyte leukemia,acute myeloblastic leukemia,mixed phenotype acute leukemia and umclassified leukemia were 4(3.8％),38(36.5％),58(55.8％),2(1.9％),and 2(1.9％),respectively.conclusion detecting immune marker on leukemic cell by abc-ap two step immune method is very simple which can be finished with a light microscope,and it can provide a reliable basis for the diagnosis and classification of leukemia and even the targeting therapy for leukemia.

结果 104例初发急性白血病中，t淋巴细胞白血病4例(3.8％)，b淋巴细胞白血病38例(36.5％)，急性髓细胞白血病58例(55.8％)，急性混合性白血病2例(1.9％)，未行明确分类的2例(1.9％)。结论 abc-ap免疫二步法检测白血病细胞免疫标记方法简单，只须普通光学显微镜就能开展实验，可为白血病的诊断、分型、分类乃至白血病靶向治疗提供可靠依据。

Majority of acute leukemias in infant, either acute lymphoblastic leukemia or acute myeloblastic leukemia, posses a chromosomal translocation affecting the 11q23 chromosome region which specifically inoles the mixed-lineage leukemia gene.1-3 Most pediatric leukemias with MLL rearrangement clearly hae a remarkably short latency.1,4 MLL gene rearrangement is also associated with secondary leukemias of patients preiously treated with the topoisomerase II inhibitors.4 The latency of these secondary leukemias is similarly ery short.4 Of note, the concordance rate of leukemia with MLL rearrangement in infant monozygotic twins approximates to 100%,1,4 and identical breakpoint in the MLL gene was shared in these pairs of identical twin infants with concordant ALL.1,4 Moreoer, the unique and clonotypic MLL fusion gene was detectable in neonatal blood spots for Guthrie cards from non-twined indiiduals who subsequently deeloped ALL.1,4 These obserations indicate not only that MLL fusion is generated in utero but also that MLL fusion proteins could be capable of inducing leukemic transformation with few, if any, secondary mutations.2,3,4 Greaes et al speculate that an MLL fusion protein somehow promotes rapid transition to full-blown disease in patients ia ery rapid clonal expansion, genetic instability, or inhibition of DNA damage repair.4 In general, for clonal expansion of malignancies, tumor cells often hae acquired strategies that escape immune sureillance of the hosts.5,6 Immune escape mechanisms also contribute to the failure of graft-ersus-leukemia effect after allogeneic hematopoietic stem cell transplantation.7 Therefore, leukemia cells could acquire some immune escape mechanisms during leukemogenesis.

绪论 绝大多数的婴儿白血病，不管是急性淋巴性白血病或是急性骨髓性白血病，在染色体11q23部位有染色体易位的情况；这个部位的染色体易位牵连了混合谱系白血病基因。大多数具有MLL基因重排的儿童白血病潜伏期明显短很多。MLL基因重排也和经拓扑异构酶II抑制剂治疗后的继发性白血病有关。这些继发性白血病的潜伏期类似地都非常的短。很重要的是，单卵双胞胎婴儿同时患有或同时免于MLL基因重排阳性的白血病的一致性接近100%；并且同样患有ALL的同卵双胞胎的MLL基因的断裂点是一致的。而且，这种独特的克隆特异性的MLL融合基因能够从那些得ALL的非双生个体出生时的血斑标本中检测到。这些发现表明MLL融合基因产生在胎儿还在子宫的是后，而且MLL融合蛋白能过和其他的基因突变一起诱导白血病的产生。Greaes 等推测MLL融合蛋白在某种情况下同过快速克隆增殖，遗传的不稳定性或是DNA损伤修复的抑制促使疾病迅速地全面爆发。恶性肿瘤细胞的克隆增殖通常已经获得了逃避机体免疫监视的能力。免疫逃避机制也归因于异体外周血干细胞移植后移植物抗白血病作用的失效。所以，白血病细胞在白血病的产生过程中可能获得了某些免疫逃脱机制。

The condition was attributed presumptively to infection with Abelson's murine leukemia virus.

此状况推测乃由於 Abelson 小鼠白血病病毒(Abelson's murine leukemia virus)感染所致。

The split between the two groups can hardly be papered over.

这两个团体间的分歧难以掩饰。

This approach not only encourages a greater number of responses, but minimizes the likelihood of stale groupthink.

这种做法不仅鼓励了更多的反应，而且减少跟风的可能性。