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第二届全国中毒与急诊救治学术研讨会

作者：董群生第二军医大学长海医院外诊部

原始细胞危象是指急性白血病患者白血病细胞负荷极度增高并极易造成体内重要器官出血和功能衰竭的一种状态。是血液科常见的危急情况,处理不合理, 合并症多,病死率高。我科1985年至2000年共收治该类患者19例,经抢救成功16例,死亡3例,主... 详细信息

原始细胞危象是指急性白血病患者白血病细胞负荷极度增高并极易造成体内重要器官出血和功能衰竭的一种状态。是血液科常见的危急情况,处理不合理, 合并症多,病死率高。我科1985年至2000年共收治该类患者19例,经抢救成功16例,死亡3例,主要体会是:(1)及时进行细胞分离;(2)小剂量化疗;(3)及时进行"水化”、"碱化”治疗。现报告如下: 一、临床资料1.一般情况:19例均为急性白血病患者,其中男性14例,女性5例。白血病类型AML(M16例,M28例, M35例)。明确诊断时白细胞总数为(40.0～120.0)×

关键词：原始细胞危象白血病细胞急性白血病抢救体会

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Stem cell regulation and the development of blast crisis in chronic myeloid leukemia: Implications for the outcome of Imatinib treatment and discontinuation

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MEDICAL HYPOTHESES 2008年第1期70卷 128-136页

作者： Wodarz, Dominik Univ Calif Irvine Dept Ecol & Evolutionary Biol Irvine CA 92697 USA

Chronic myeloid leukemia (CML) is a cancer of the hematopoietic system that is initiated by a single genetic alteration (the BCR-ABL fusion gene or Philadelphia chromosome) and progresses in several phases: during the chronic phase the number of cells grows slowly and the fraction of immature cells is low. During the accelerated phase and blast crisis, the population of CML cells and the fraction of immature cells rises sharply. The mechanisms that drive the transition from the chronic phase to blast crisis are not understood, and the requirement of genetic instability and further mutations has been suggested. Using mathematical models, I describe a theory that can account for the transition from the chronic phase to blast crisis without the need to invoke further mutations. The transition to blast crisis can be explained solely by feedback mechanisms that regulate the patterns of stem cell division, in particular the occurrence of symmetric versus asymmetric cell division. The model also has implications for the outcome of Imatinib treatment. According to the model, treatment can lead to the low level persistence of CML stem cells without assuming that these cells are less susceptible to drug-mediated activity, and this might explain why disease tends to relapse after treatment discontinuation even in the absence of acquired drug resistance. Further, the model defines conditions when Imatinib treatment might lead to the eradication of CML, which is relevant in the context of recent data that show absence of relapse as tong as two years after treatment cessation. (c) 2007 Elsevier Ltd. All rights reserved.

关键词： therapeutic aspects Blast Crisis BCR Gene Stem Cells Chronic 原始细胞危象干细胞 Stem Cells Crisis BCR gene Imatinib Blast Phase

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衍生9号染色体缺失对慢性髓细胞白血病的预后价值

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中华内科杂志 2007年第5期46卷 386-388页

作者：吴炜李建勇沈云峰曹祥山仇海荣徐卫南京医科大学第一附属医院江苏省人民医院血液科210029 南京医科大学附属无锡医院血液科苏州大学附属常州医院血液科

目的研究慢性髓细胞白血病(CML)中衍生9号染色体[der(9)]缺失的发生率及预后意义。方法随机选取48例 CML-急变期(BC)患者,以 BCR-ABL 双色双融合荧光原位杂交(FISH)技术检测其染色体标本。对于 FISH 技术检测到的间期细胞中只有单个融... 详细信息

目的研究慢性髓细胞白血病(CML)中衍生9号染色体[der(9)]缺失的发生率及预后意义。方法随机选取48例 CML-急变期(BC)患者,以 BCR-ABL 双色双融合荧光原位杂交(FISH)技术检测其染色体标本。对于 FISH 技术检测到的间期细胞中只有单个融合信号的标本,则观察其中期细胞,以明确是否为 der(9)缺失。对于 der(9)缺失患者,以相同方法检测其初诊时的染色体标本,以明确 der(9)缺失是否和 Ph 易位同时发生。患者慢性期以羟基脲治疗。结果 48例CML-BC 患者中有8例(16.7%)der(9)缺失,其初诊时的染色体标本 der(9)也缺失。der(9)缺失组慢性期及总生存期分别平均为20.9和36.4个月,明显短于未缺失组(55.1和70.3个月)(P<0.05)。CML-BC 急淋变与急非淋变患者中 der(9)缺失概率无统计学意义(P>0.05)。结论 FISH技术可有效检测 der(9)缺失。der(9)缺失与 Ph 易位同时发生。具有 der(9)缺失的 CML 疾病进展较快,预后较差。羟基脲不具有逆转 CML 中 der(9)缺失的不良预后的作用。der(9)缺失不导致CML 向某一特定类型转化。

关键词：白血病,慢性,粒细胞性原始细胞危象染色体缺失原位杂交,荧光

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中西医结合治疗急性白血病原始细胞危象18例

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山东中医杂志 2003年第9期22卷 550-551页

作者：张新华唐由君山东省中医药研究院山东济南250014 山东中医药大学附属医院山东济南250011

在血液病临床,少数急性白血病患者外周血液中白细胞＞100×109/L,即为高白细胞白血病;原始细胞绝对值＞100×109/L,且伴有颅内出血和/或中枢神经系统浸润、呼吸窘迫综合征等临床危险症候者,可称急性白血病原始细胞危象.我院自1... 详细信息

在血液病临床,少数急性白血病患者外周血液中白细胞＞100×109/L,即为高白细胞白血病;原始细胞绝对值＞100×109/L,且伴有颅内出血和/或中枢神经系统浸润、呼吸窘迫综合征等临床危险症候者,可称急性白血病原始细胞危象.我院自1970～1990年以中西医结合疗法治疗18例,报告如下.

关键词：急性白血病原始细胞危象中西医结合疗法

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Combination of the histone deacetylase inhibitor LBH589 and the hsp90 inhibitor 17-AAG is highly active against human CML-BC cells and AML cells with activating mutation of FLT-3

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BLOOD 2005年第4期105卷 1768-1776页

作者： George, P Bali, P Annavarapu, S Scuto, A Fiskus, W Guo, F Sigua, C Sondarva, G Moscinski, L Atadja, P Bhalla, K H Lee Moffitt Canc Ctr & Res Inst Dept Interdisciplinary Oncol Tampa FL USA Novartis Pharmaceut Inc Cambridge MA USA

Present studies show that LBH589, a novel cinnamic hydroxamic acid analog histone deacetylase inhibitor, induces acetylation of histone H3 and H4 and of heat shock protein 90 (hsp90), increases p21 levels, as well as induces cell-cycle G(1) phase accumulation and apoptosis of the human chronic myeloid leukemia blast crisis (CML-BC) K562 cells and acute leukemia MV4-11 cells with the activating length mutation of FLT-3. In MV4-11 cells, this was associated with marked attenuation of the protein levels of p-FLT-3, FLT-3, p-AKT, and p-ERK1/2. In K562 cells, exposure to LBH589 attenuated Bcr-Abl, p-, AKT, and p-ERK1/2. Treatment with LBH589 inhibited the DNA binding activity of signal transducers and activators of transcription 5 (STAT5) in both K562 and MV4-11 cells. The hsp90 inhibitor 17-allyl-amino-demethoxy geldanamycin (17-AAG) also induced polyubiquitylation and proteasomal degradation of FLT-3 and Bcr-Abl by reducing their chaperone association with hsp90. Cotreatment with LBH589 and 17-AAG exerted synergistic apoptosis of MV4-11 and K562 cells. In the imatinib mesylate (IM)-refractory leukemia cells expressing Bcr-AbI with the T3151 mutation, treatment with the combination attenuated the levels of the mutant Bcr-Abl and induced apoptosis. Finally, cotreatment with LBH589 and 17-AAG also induced more apoptosis of IM-resistant primary CML-BC and acute myeloid leukemia (AML) cells (with activating mutation of FLT-3) than treatment with either agent alone. (C) 2005 by The American Society of Hematology.

关键词： Blast Crisis Enzyme Inhibitors Heat-Shock Proteins 90 HistoneDeacetylases 原始细胞危象酶抑制剂热休克蛋白质类90 羟肟酸类白血病髓样原癌基因蛋白质类

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白细胞去除术治疗慢性粒细胞白血病原始细胞危象2例

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内科急危重症杂志 2000年第3期6卷 165-165页

作者：史克倩云南省第一人民医院昆明650032

慢性粒细胞白血病(CML)患者60%以上最终发生急性变,其中称之为'原始细胞危象”,病情进展迅速,治疗常无效,多于6周内死亡.[1]我科1997年10月至1998年5月采用白细胞去除术治疗慢粒原始细胞危象2例取得良好效果,现报道如下:

关键词：白细胞去除术治疗慢性白血病原始细胞危象

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无血缘关系骨髓移植治疗慢性粒细胞性白血病原始细胞危象1例

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白血病 1999年第3期8卷 168-168页

作者：杜欣林伟黄梓伦陆泽生翁建宇广东省人民医院

我们于１９９７年１１月对１例慢性粒细胞性白血病原始细胞危象患者进行了无关供者骨髓移植（ＵＤ－ＢＭＴ），现报告如下。１病例资料患者，男，１４岁，因咽痛１０ｄ于１９９６年４月入院，白细胞２５０×１０９／Ｌ，脾肋缘下４... 详细信息

我们于１９９７年１１月对１例慢性粒细胞性白血病原始细胞危象患者进行了无关供者骨髓移植（ＵＤ－ＢＭＴ），现报告如下。１病例资料患者，男，１４岁，因咽痛１０ｄ于１９９６年４月入院，白细胞２５０×１０９／Ｌ，脾肋缘下４指，骨髓象示慢粒慢性期，Ｐｈ（＋），予...

关键词：慢性白血病骨髓移植治疗原始细胞危象

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Telomere length shortening in chronic myelogenous leukemia is associated with reduced time to accelerated phase

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BLOOD 2000年第1期96卷 358-361页

作者： Boultwood, J Peniket, A Watkins, F Shepherd, P McGale, P Richards, S Fidler, C Littlewood, TJ Wainscoat, JS John Radcliffe Hosp Dept Cellular Sci Leukaemia Res Fund Mol Haematol Unit Oxford OX3 9DU England Western Gen Hosp MRC CML Trials Unit Edinburgh EH4 2XU Midlothian Scotland Radcliffe Infirm Clin Trial Serv Unit Oxford OX2 6HE England

Telomere shortening is associated with disease evolution in chronic myelogenous leukemia (CML). We have examined the relationship between diagnostic telomere length and outcome in 59 patients with CML who entered into the MRC CMLIII Trial by Southern blot hybridization using the (TTAGGG)(4) probe. Age-adjusted telomere repeat array (TRA) reduction was found to significantly correlate with time from diagnosis to acceleration, such that patients with a larger TRA reduction entered the accelerated phase more rapidly (r = -0.50;P = .008). Cox-regression analysis for this group was suggestive of a relationship between a greater TRA-reduction and a shorter time to acceleration (P = .054). Age-adjusted TRA reduction did not significantly affect either the time to blast crisis or overall survival. Our results show that telomere shortening observed at the time of diagnosis in CML significantly influences the time to progress to the accelerated phase. The measurement of diagnostic TRA may prove to be clinically important in the selection of patients at high risk of disease transformation in CML. (Blood. 2000;96:358-361) (C) 2000 by The American Society of Hematology.

关键词：年龄因素抗肿瘤药/治疗应用原始细胞危象印迹法 DNA 干扰素α/治疗应用寡核苷酸探针血小板计数回归分析脾/病理学存活率端粒/超微结构肿瘤标记生物学人类

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Quantitative measure of c-abl and p15 methylation in chronic myelogenous leukemia:: biological implications

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BLOOD 2000年第9期95卷 2990-2992页

作者： Nguyen, TT Mohrbacher, AF Tsai, YC Groffen, J Heisterkamp, N Nichols, PW Yu, MC Lübbert, M Jones, PA Univ So Calif Kenneth Norris Jr Comprehens Canc Ctr Dept Biochem & Mol Biol Los Angeles CA 90033 USA Univ So Calif Kenneth Norris Jr Comprehens Canc Ctr Dept Hematol Oncol Los Angeles CA 90033 USA Univ So Calif Kenneth Norris Jr Comprehens Canc Ctr Dept Pathol Los Angeles CA 90033 USA Univ So Calif Kenneth Norris Jr Comprehens Canc Ctr Dept Prevent Med Los Angeles CA 90033 USA Childrens Hosp Div Hematol Oncol Los Angeles CA 90027 USA Univ Freiburg Med Ctr Div Hematol Oncol D-7800 Freiburg Germany

We used a sensitive, quantitative bisulfite PCR assay, methylation sensitive single nucleotide primer extension (Ms-SNuPE), to measure methylation of the 5' CpG islands of c-abl and p15 in chronic myelogenous leukemia (CML) patients during progression. We found that the Pa promoter of c-abl was methylated in 81% (17/21) of the white blood cells (WBCs) of CML patients, which correlates with previous reports. In contrast, WBCs from healthy donors, acute myelogenous leukemias, acute lymphocytic leukemias, and myelodysplastic syndromes were unmethylated at the c-abl Pa promoter locus. We also observed p15 hypermethylation in 24% (8/34) of CML cases. Methylation of the p15 but not c-abl Pa promoters was associated with CML progression (P = 0.047 vs 0.46), and the two events were independently acquired. We conclude that de novo methylation of c-abl and p15 both occur in CML, and analysis of DNA methylation changes using the bisulfite-based MS-SNuPE assay allows both a sensitive and quantitative assessment of these molecular events compared to other methods currently utilized. (Blood, 2000;95:2990-2992) (C) 2000 by The American Society of Hematology.

关键词：原始细胞危象载体蛋白质类/遗传学细胞周期蛋白质类周期素依赖激酶抑制剂p15 周期素依赖激酶抑制剂p16 DNA甲基化基因肿瘤抑制基因 abl 启动区(遗传学) 原癌基因蛋白质c-abl/遗传学肿瘤抑制蛋白质类人类

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Nonclonal abnormalities in leukemia

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CANCER GENETICS AND CYTOGENETICS 2000年第1期118卷 85-86页

作者： Vázquez-Mazariego, Y Ramiro, S Steegman, JL García-Sagredo, JM Sánchez-Hombre, MC Ferro, MT Univ Hosp Ramon & Cajal Dept Med Genet Madrid Spain

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