查询词典 leukemic

PCR requires a specific DNA abnormality or marker, like an oncogene, in the leukemic or lymphomatous cells in order to identify residual abnormal cells.

为了识别残存的异常细胞，聚合酶链式反应需要一个特殊的DNA或RNA的畸形或标记物，在白血病细胞或淋巴瘤细胞中，如同致癌基因一样。

PCR requires a specific DNA abnormality or marker, like an oncogene, in the leukemic or lymphomatous cells in order to identify residual abnormal cells.

为了识别残存的异常细胞，聚合酶链反应需要在白血病细胞或淋巴瘤细胞中找到一个特定的DNA或RNA的异常点或标记物，如致癌基因。

PCR requires a specific DNA abnormality or marker, like an oncogene, in the leukemic or lymphomatous cells in order to identify residual abnormal cells.

为了识别残留的异常细胞，聚合酶链式反应需要一个特殊的DNA或RNA的畸形或标记物，在白血病细胞或淋巴瘤细胞中，如同致癌基因一样。

PCR requires a specific DNA abnormality or marker, like an oncogene, in the leukemic or lymphomatous cells in order to identify residual abnormal cells.

聚合酶链反应通过发现白血病细胞或淋巴瘤细胞中特定的DNA或RNA的异常点或标记物如致癌基因来识别残存的异常细胞。

In the past two decades immence amount of data have demonstrated to behigh levels of sFR in serum of megaloblastic anemia and leukemia,andshown to be two kind FBPs of FR and RFC on leukemic cells,but thesignificance of RFC are unknown completely.

经过近20年研究已证实，在巨幼细胞贫血、白血病等患者血清中sFR水平升高，同时也发现在白血病细胞膜上存在有两种FBP，即FR和RFC，其意义不完全清楚。

This study was aimed to explore the effect of bortezomib on proliferation and apoptosis of acute monocytic leukemic cells SHI-1 and the function of Bcl-2 gene family including Bcl2l12, Bcl-2 and Bax in its apoptosis.

本研究探讨蛋白酶抑制剂硼替佐米对急性单核细胞白血病细胞株SHI-1增殖和凋亡的影响及Bcl2l12、Bcl-2和Bax基因在其中的作用。

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。

Objective: To investigate the expression of Id1 gene in leukemic leukocyte,and determine its relationship with the pathogenesis of acute non-lymphocytic leukemia and chronic myelocytic leukemia,so as to provide some clues to their diagnosis, treatment and prognosis.

目的：研究分化抑制因子-1（inhibitors of differentiation，Id1）在白血病白细胞中的表达，探讨其与急性非淋巴细胞和慢性粒细胞白血病发病的相关性，为白血病的诊断、治疗提供参考。

Skin manifestations of leukemia are varied and include leukemia cutis (direct cutaneous infiltration by leukemic cells), Sweet's syndrome, erythema multiforme, erythema nodosum, pyoderma gangrenosum, and bullous pemphigoid.

白血病的皮肤表现比较多样，包括皮肤白血病（白血病细胞直接渗入皮下）、斯威特氏综合征、多形性红斑、结节性红斑、坏疽性脓皮症以及大疱性类天疱疮。

But we don't care about Battlegrounds.

但我们并不在乎沙场中的显露。

Ah! don't mention it, the butcher's shop is a horror.

啊！不用提了。提到肉，真是糟透了。