骨髓增生异常综合征患者体外CFU-GM、CFU-L培养和细胞遗传学研究

研究了４２例骨髓增生异常综合征患者体外ＣＦＵ－ＧＭ、ＣＦＵ－Ｌ培养和细胞遗传学改变。结果显示，患者ＣＦＵ－ＧＭ明显低于正常对照组（Ｐ＜０．０１），但高于再生障碍性贫血（ＡＡ）（Ｐ＜０．０１），ＣＦＵ－Ｌ高于正常对照组和ＡＡ组（Ｐ＜０．０１）。患者５２．４％存在染色体异常，常见为：＋８、－２２、－Ｘ、－Ｙ、－２０、－７／７ｑ－。ＣＦＵ－ＧＭ减低、ＣＦＵ－Ｌ增高和染色体异常者疗效较正常者差。表明ＣＦＵ－ＧＭ、ＣＦＵ－Ｌ体外培养和细胞遗传学检查可作为ＭＤＳ协助诊断和预测疗效的指标之一。     

骨髓增生异常综合征患者体外CFU—GM,CFU—L培养和细胞遗传学研究

研究了４２例骨髓增生异常综合征患者体外ＣＦＵ－ＧＭ、ＣＦＵ－Ｌ培养和细胞遗传学改变。结果显示，患者ＣＦＵ－ＧＭ明显低于正常对照组（Ｐ〈０．０１），但高于再生障碍性贫血（ＡＡ）（Ｐ〈０．０１），ＣＦＵ－Ｌ高于正常对照组和ＡＡ组（Ｐ〈０．０１）。患者５２．４％存在染色体异常，常见为：＋８、－２２、－Ｘ、－Ｙ、－２０、－７／７ｑ＾－。ＣＦＵ－ＧＭ减低、ＣＦＵ－Ｌ增高和染色体异常者疗效较正常者差。表明ＣＦ     

ADMV方案治疗中晚期非小细胞肺癌62例近期疗效分析

采用ＡＤＭＶ（ＡＤＭ＋ＤＤＰ＋ＭＭＣ＋ＭＭＣ＋ＶＰ－１６）方案联合化疗，对６２例中晚期非小细胞肺癌近期疗效观察，ＣＲ２例，ＰＲ１８例，ＮＲ３２例，ＰＤ１０例，总有效率（ＣＲ＋ＰＲ）３２．２６％（２０／６２）。化疗毒副反应主要是消化道反应（５９．６８％）及骨髓抑制（白细胞下降占６１．２９％）。     

ADMV方案治疗中晚期非小细胞肺癌62例近期疗效分析

采用ＡＤＭＶ（ＡＤＭ＋ＤＤＰ＋ＭＭＰ＋ＭＭＣ＋ＶＰ－１６）方案联合化疗，对６２例中晚期非小细胞肺癌近期疗效观察，ＣＲ２例，ＰＲ１８例，ＮＲ３２例，ＰＤ１０例， 效率（ＣＲ＋ＰＲ）３２．２６％）２０／６２），化疗毒副反庆主要是消化道反 （５９．６８％）及骨髓抑制（白细胞下降占６１．２９％）．     

成人急性白血病强化治疗67例预后分析

目的：观察成人急性白血病（ＡＬ） 患者完全缓解（ＣＲ） 后强化治疗的效果。方法：对６７ 例ＣＲ后的成人ＡＬ患者进行强化治疗,急性髓细胞性白血病（ＡＭＬ）以中剂量阿糖胞苷（ＩＤ－ Ａｒａ－ Ｃ）方案为主,急性淋巴细胞性白血病（ＡＬＬ）以中剂量氨甲蝶呤（ＩＤ－ ＭＴＸ）方案为主。结果：４８ 例ＡＭＬ患者中位ＣＲ 期１６ 个月,预期３ 年和４ 年无病生存（ＤＦＳ）为３６９％ 和２１１ ％ ;２３ 例（４７９ ％） 患者复发。１９ 例ＡＬＬ 患者中位ＣＲ 期１４ 个月,预期４ 年ＤＦＳ 为３１５％ ;１０ 例（５２６％ ） 患者复发。结论：以ＩＤ－ Ａｒａ－ Ｃ 为主的强化方案及以ＩＤ－ ＭＴＸ 为主的强化方案分别能延长ＡＭＬ及ＡＬＬ患者的ＤＦＳ,降低复发率     

10例巨核细胞白血病免疫表型特点

急性巨核细胞白血病（Ｍ＿７）由于缺乏足够特异的形态学和细胞化学特征，不易诊断。８０年代血小板过氧化酶反应（ＰＰＯ）在电镜中的发展以及抗血小板单克隆抗体（ＭｃＡｂ）的应用，使急性巨核细胞白血病较易被识别出来。最近资料表明：Ｍ＿７占成人ＡＮＬＬ的２～８％，儿童的１４％，婴幼儿可高达２０％。约占全部急性白血病的８～１０％，成人Ｍ＿７多见于二次性白血病，即实体瘤化疗后发生白血病，或慢粒急变后，或ＭＤＳ、ＭＦ变为白血病者。本文检测１０２例急性白血病患者免疫表型，发现与证实１０例Ｍ＿７，发生率９．８％。其中３例为慢粒急变；７例为原发。１０例患者均至少有一种抗血小板膜糖蛋白ＭｃＡｂ阳性＞３０％。ＨＬＡ－ＤＲ阳性率低者ＣＤ＿（４１）、ＣＤ＿（１２）阳性率高。免疫表型为ＨＬＡ－ＤＲ３／１０（＋）、ＣＤ＿５（—）、ＣＤ＿９（＋）、ＣＤ＿（１０）（—）、ＣＤ＿（１９）（—）、ＣＤ＿（２０）（—）、ＣＤ＿（１３）５／９（＋）、ＣＤ＿（３３）２／２（＋）、ＣＤ＿（４１ａ）８／８（＋）、ＣＤ＿（４１ｂ）９／９（＋）、ＣＤ＿（４２ｂ）５／５（＋）。表明原始巨核细胞可同时表达早期髓系抗原ＣＤｓ＿（３３），部分表达ＣＤ＿（１３）。ＣＤ＿（４     

分化抗原与小儿急性淋巴细胞白血病的临床关系

目的：为了探讨免疫分型与临床表现的关系，为该病型的诊断和分型的治疗奠定基础。方法：将取自患者骨髓标本处理后依次与１０种识别人白细胞分化抗原的单克隆抗体经ＡＰＡＡＰ方法反应，根据实验结果将３３例急淋分为Ｔ－ＡＬＬ和非Ｔ－ＡＬＬ以及各自的亚型。在所有病例中，将ＣＤ７＋与ＣＤ７－的急淋作为一组对比，在非Ｔ－ＡＬＬ中，将ＣＤ１０＋与ＣＤ１０－的急淋作为一组对比，用χ２检验、ｔ检验统计方法分别比较和分析这些不同的免疫表型之间的临床各指标的差异。结果：ＣＤ７＋的急淋其外周血白细胞均数明显高于ＣＤ７－的急淋（Ｐ＜００１），出血情况和严重脏器侵润都较多（Ｐ＜００５，Ｐ＜００５），且达到缓解的时间较长（Ｐ＜００１）。ＣＤ１０＋的非Ｔ－ＡＬＬ达到缓解的时间明显短于ＣＤ１０－的非Ｔ－ＡＬＬ（Ｐ＜００１）。结论：提示细胞表面分化抗原标记分析具有临床鉴别意义     

THE EFFECT OF ACTIVE COMPONENTS OF LYCIUM BARBARUM AND GARLIC（LB－GO）ON THE SYNTHESIS OF DNA AND ULTRASTRUCTURE OF U_（14） CERV

ＴＨＥＥＦＦＥＣＴＯＦＡＣＴＩＶＥＣＯＭＰＯＮＥＮＴＳＯＦＬＹＣＩＵＭＢＡＲＢＡＲＵＭＡＮＤＧＡＲＬＩＣ（ＬＢ－ＧＯ）ＯＮＴＨＥＳＹＮＴＨＥＳＩＳＯＦＤＮＡＡＮＤＵＬＴＲＡＳＴＲＵＣＴＵＲＥＯＦＵ_（１４）ＣＥＲＶＩＸＣＡＮＣＥＲＣＥＬＬＳＩＮＭＩＣ?..     

PCR扩增TCR_γ基因重排检测急性淋巴细胞白血病微量残留病的研究

应用多聚酶链反应（ＰＣＲ）技术检测急性淋巴细胞白血病（ＡＬＬ）骨髓白血病细胞ＴＣＲγ基因重排，敏感性达１０￣（－５）水平以上。２７例急性期ＡＬＬ有２１例检测到约４００ｂｐ的扩增产物，阳性检出率为７７．８％（２１／２７）；７例完全缓解（ＣＲ）的ＡＬＬ有２例检测阳性，其中１例于检测后１．５月复发，另１例随访６个月仍ＣＲ；而其余５例检测阴性者于检测后平均随访７．１月均持续ＣＲ。提示本法对ＡＬＬＴＣＲ＿γ基因重排的检测较具普遍性，可用于其微量残留病（ＭＲＤ）的检测，对ＡＬＬ预后的判断、复发的监测可能有重要意义。     

恶性淋巴瘤骨髓累及的细胞化学特点

目的：用细胞化学染色的方法诊断恶性淋巴瘤骨髓累汲并与白血病相鉴别。方法：细胞化学染色方法：结果：前躯淋巴母细胞性淋巴瘤（ＰＬＢ）、中心小裂细胞性淋巴瘤（Ｓ－ＦＣＣ）和伴毛细胞的脾淋巴瘤（ＳＬＶＣ）ＰＯＸ、ＳＢＢ和ＣＥ均为阴性，ＰＡＳ：Ｓ－ＦＣＣ和ＳＬＶＬ反应弱，ＰＬＢ反应较强，淋巴瘤珠状占２２．２２％，ＡＬＬ珠状占７０．５９％。ＮＡＥ：Ｓ－ＦＣＣ反应强度以＋＋为主，ＳＬＶＬ和ＰＬＢ较弱。ＡＣＰ：Ｓ－ＦＣＣ较ＳＬＶＣ和ＰＬＢ略强，Ｓ－ＦＣＣ和ＳＬＶＣ均可见＋＋＋＋。ＴＲＡＰ：Ｓ－ＦＣＣ阳性率２％－５４％，ＰＬＢ阳性率１０％－１６％，SLVC性率均为１８％，真性组织细胞性淋巴瘤（ＴＨＬ）ＡＣＰ４例均为阳性，阳性率为１００％，１例ＴＲＡＰ阳性。淋巴瘤与ＣＬＬ、ＨＣＬ和ＡＬＬ相比较发现，淋巴瘤较ＣＬＬ和ＡＬＬ ＴＲＡＰ明显增高，Ｓ－ＦＣＣＴ ＳＬＶＣ的ＡＣＰ和ＴＲＡＰ与ＨＣＬ相同，结论：细胞化学染色在诊断淋巴瘤骨髓转移，并与ＡＬＬ和ＣＬＬ相鉴别上有一定的意义，淋巴瘤骨髓累及PAS阳性率和阳性指数较ALL弱。ACP阳性较ALL和CLL强，具有较强的抗酒石酸的功能，但与HCL难鉴别。     

Residual bone marrow leukemic progenitor cell burden after induction chemotherapy in pediatric patients with acute lymphoblastic leukemia.

We used highly sensitive multiparameter flow cytometry and blast colony assays to quantify the leukemic progenitor cell (LPC) burden of postinduction chemotherapy bone marrows from newly diagnosed and relapsed pediatric patients with acute lymphoblastic leukemia (ALL). Of 890 newly diagnosed patients, 243 (27%) had detectable LPC in the postinduction bone marrow samples with an average (mean +/- SE) LPC content of 22+/-9 LPC/10(6) mononuclear cell (MNC; range, 0-7199/10(6) MNC; median, 0/10(6) MNC). By comparison, 24 of 50 (48%) patients with relapsed ALL had detectable LPC in their postinduction bone marrow specimens (P = 0.003), and their average LPC content was 202+/-139 LPC/10(6) MNC. Fewer patients with B-lineage ALL (170 of 786; 22%) than patients with T-lineage ALL (73 of 104; 70%) harbored residual LPC in their postinduction bone marrow specimens (P < 0.0001). This correlation with immunophenotype was independent of the National Cancer Institute risk classification. Similarly, 19 of 44 (43%) patients with relapsed B-lineage ALL versus 5 of 6 (83%) patients with relapsed T-lineage ALL harbored residual LPC in their postinduction bone marrow specimens (P = 0.09). Among newly diagnosed patients, those with high-risk ALL seemed to have larger numbers of residual LPC in their bone marrow after induction chemotherapy than those with standard risk ALL (53+/-26, n = 286 versus 7+/-1, n = 604, P = 0.04). LPC of patients with standard risk ALL who had a slow early marrow response at day 7 seemed to be more resistant to the three-drug induction chemotherapy than patients who had a rapid early marrow response. Overall, the order of chemosensitivity of LPC was: newly diagnosed standard risk B-lineage > newly diagnosed higher risk B-lineage > newly diagnosed standard risk T-lineage > newly diagnosed higher risk T-lineage > relapsed B-lineage > relapsed T-lineage. Notably, LPC- patients whose end-of-induction remission bone marrow specimens had zero LPC had an excellent early event-free survival outcome. Within the standard and high-risk subsets, LPC- patients had a 2.6-fold lower and 2.4-fold lower incidence of events, respectively, than LPC+ patients. At 6 months, 12 months, as well as 24 months, the ranking order for better event-free survival was: standard risk, LPC- > high risk, LPC- > standard risk, LPC+ > high risk, and LPC+.     

Flow cytometric detection of rare normal human marrow cells with immunophenotypes characteristic of acute lymphoblastic leukemia cells.

Rare subpopulations of normal marrow B lymphoid cells expressing immunophenotypes typically found in B-lineage acute lymphoblastic leukaemias (ALL) were sought by multiparameter flow cytometry. First, CD34+ marrow leukocytes were isolated by immune adherence using immunomagnetic microspheres, and analyzed for coexpression of the following pairs of membrane antigens: CD34 CD22; CD34 CD20; and CD10 CD22. Terminal deoxynucleotidyl transferase expression was not assessed. All three antigen combinations were found on small percentages of the CD34-enriched cell population. Second, unseparated normal low density marrow leukocytes were examined by 'gating' on cells with the right-angle light scatter of lymphoid cells, plus either CD34+ or CD10+ immunofluorescence. This independent approach confirmed that rare subsets of normal cells coexpress 'immature' and 'mature' differentiation antigens. In addition, remission marrow cells were examined from two children who had completed therapy for ALL two and four months earlier. Both specimens had a more than threefold increase in CD34+ cells over normal marrow, and cells coexpressing immature and mature cell surface antigens were easily detected. These findings demonstrate that immunophenotypes characteristic of B-lineage ALL, previously labeled 'asynchronous' with respect to the developmental sequence of the majority of normal B lymphoid cells, exist at low frequency in normal human bone marrow.     

Inhibition of normal human in vitro colony forming cells by cells from leukaemic patients.

Co-culture in agar of normal bone marrow cells from different individuals gave granulocyte macrophage colony counts that were expected from counts made when the marrows were cultured separately. Co-culture of normal marrow with normal peripheral blood leucocytes (which did not themselves give rise to colonies) caused inhibition of colony growth only when the ratio of peripheral blood to bone marrow cells was of the order of 4 : 1. Peripheral blood or bone marrow cells from 7 of 9 patients with acute myelomonocytic leukaemia, which did not give rise to colonies, caused a marked reduction in the number of colonies obtained from normal marrow cells when cultured with them. This inhibitory effect of leukaemic cells was found when ratios of leukaemic to normal cells were as low as 1 : 4. Additional evidence that the inhibition of normal colony formation was related to the leukaemic process was obtained from follow-up studies on one of the patients whose cells lost the capacity to inhibit normal colony formation during remission and became inhibitory again on relapse.     

Prognostic significance of CD34 expression in childhood B-precursor acute lymphocytic leukemia: a Pediatric Oncology Group study.

We studied the blasts from 795 children greater than 1 year of age with newly diagnosed, untreated B-precursor acute lymphoblastic leukemia (ALL) for expression of the hematopoietic stem cell-associated antigen CD34. All cases were confirmed as B-lineage lymphoblastic leukemia by virtue of expression of CD19 and/or CD22, lack of T-cell antigens, and lack of surface-membrane immunoglobulin (Ig). The CD34 antigen was present in at least 10% of blast cells in 587 (73.8%) of the patients. There was no significant difference in presenting clinical characteristics between CD34+ and CD34- patients save for an increased incidence of CNS involvement at diagnosis in the latter. Patients with CD34+ leukemia were more likely to have blasts expressing CD22, CD9, and CD13 antigens but were less likely to coexpress CD20. Patients with pre-B (cytoplasmic mu) ALL were significantly more likely to lack CD34 on their blasts, while children with hyperdiploid ALL were more likely to be CD34+. Although remission induction rates were not significantly different between patients with CD34+ and CD34-ALL (P = .23), event-free survival was shorter for patients with CD34- leukemia (P = .0014). Even though CD34 expression was associated with certain other known prognostically favorable variables including hyperdiploidy and lack of cytoplasmic Ig, it had an independent favorable effect on treatment outcome, even after adjusting for competing prognostic factors.     

Growth requirements for human acute lymphoblastic leukemia cells: refinement of a clonogenic assay

Since freshly obtained acute lymphoblastic leukemia (ALL) cells rarely replicate spontaneously in vitro in a sustained way, development of a useful clonogenic assay for ALL blast progenitors is dependent on identifying the cellular growth requirements. Thus, marrows from 25 ALL cases were cultured in methylcellulose to determine the optimal conditions for cell growth. Blast colonies were confirmed as leukemic by morphology, cytochemistry, surface markers, and cytogenetics. Irradiated (7000 rads) normal peripheral blood feeder cells were an absolute requirement and produced number-dependent increases in ALL colonies; added growth factors enhanced the feeder cell effect. ALL cell-feeder cell contact was essential since their physical separation in a two-layer culture system drastically interfered with colony growth. Feeder cells from various donors, including new and relapsed cases of ALL, yielded colony numbers that differed widely when tested on the same marrow with and without added growth factor; thus, identification of a "good" feeder cell donor was key to an optimal assay. Neither recombinant interleukin-2 nor recombinant GM-CSF had ALL growth-promoting properties when tested alone or in combination but in the presence of feeder cells they moderately enhanced the feeder cell effect. The most effective growth factors were derived from cells exposed to phytohemagglutinin (PHA) for 72 h. In order of magnitude for colony growth-promoting activity, PHA-T cell conditioned medium (CM) was more stimulatory than PHA-blast cell CM followed by PHA-leukocyte CM; removal of PHA from CM by affinity chromotography did not alter the results. The most potent PHA-TCM was prepared from T-cells from a phlebotomized hemochromatosis patient; PHA-TCM from transfused thalassemia patients and normal donors were less active. Concanavalin-A blast cell CM had modest colony promoting properties whereas CM prepared with other B-cell mitogens and supernatants from ALL blasts in liquid culture had none. Our studies illustrate the complex and fastidious growth needs of ALL cells. The data have allowed us to refine a clonogenic blast progenitor assay that should facilitate study of proliferative properties of B and T lineage leukemias. The assay could be adapted further for detection of residual leukemia cells in marrow samples used for autologous transplantation, and in patients during complete hematological "remission."     

Identification of gene expression profiles that segregate patients with childhood leukemia.

To identify genes whose expression correlated with biological features of childhood leukemia, we prospectively analyzed the expression profiles of 4608 genes using cDNA microarrays in 51 freshly processed bone marrow samples from children with acute leukemia, over a 24-month period, at a single institution. Two supervised methods of analysis were used to identify the 20 best discriminating genes between the following cohorts: acute myelogenous leukemia (AML) versus acute lymphoblastic leukemia (ALL); B-lineage versus T-lineage ALL; newly diagnosed B-lineage standard-risk versus high-risk ALL; and B-lineage leukemia harboring the TEL-AML 1 fusion versus patients without a molecularly characterized translocation. These methods identified overlapping sets of genes that segregated patients within described subgroups. Cross-validation demonstrated that the majority of patients could be correctly classified based on these genes alone, and hierarchical clustering grouped patients with similar clinical and biological disease features. The potential for select genes to discriminate patients was validated using real-time PCR in samples that were analyzed by microarray profiling and in other uniformly processed leukemic marrow samples. As expected, microarray technology can successfully segregate patients defined by traditional measures such as immunophenotype and cytogenetic alterations. However, among specific subgroups, this preliminary analysis also suggests that microarrays can identify unanticipated similarities and diversity in individual patients and thus may be useful in augmenting risk-group stratification in the future.     

CD13、CD33在BCR-ABL+急性淋巴细胞白血病患者骨髓中的表达及其与临床特征和预后的相关性

目的:探讨髓系抗原CD13、CD33在BCR-ABL+急性淋巴细胞白血病（acute lymphoblastic leukemia,ALL）患者骨髓中的表达及其与临床特征和预后的相关性。方法:应用实时荧光定量聚合酶链反应（real time quantitative-polymerase chain reaction,RQ-PCR）检测119例初诊ALL患者骨髓BCR-ABL表达水平。用流式细胞学检查检测ALL的抗原表达水平。对照分析单纯BCR-ABL+患者中CD13+和CD13-以及CD33+和CD33-患者在初次诱导缓解率（initial-induction remission rate,CR1）和总生存率（overall survival rate,OS）的区别。结果:在BCR-ABL+ 的ALL患者中,初诊时CD13+患者较CD13-患者具有较低的首次诱导缓解率,差异具统计学意义（P＜0.05）,但CD33+患者较CD33-患者首次诱导缓解率无统计学差异。CD13+组及CD33+的OS显著低于CD13-组及CD33-组（P＜0.05）。结论:BCR-ABL+ALL患者中CD13+及CD33+提示预后不良。     

Molecular evidence for central nervous system involvement in children with newly diagnosed acute lymphoblastic leukemia

Central nervous system (CNS) involvement in children with newly diagnosed acute lymphoblastic leukemia (ALL) would have profound implication for the prognosis and accurate stratification of CNS prophylactic therapy. Using PCR technique with specific primers for V, D and J segments of TCRD gene, the pattern of TCRD gene rearrangements in bone marrow lymphoblasts and in cells from cerebrospinal fluid (CSF) have been investigated. The study involved 21 children at the time of diagnosis with B-lineage ALL. In nine of 21 patients incomplete TCRDVD gene rearrangement has been found in CSF cells, which was identical to that observed in bone marrow of the same children. It can be concluded that at least in 43 per cent of all analysed cases, there were signs of CNS involvement in newly diagnosed ALL patients.     

Bone marrow leukemic progenitor cell content in pediatric T-lineage acute lymphoblastic leukemia patients with an isolated extramedullary first relapse.

Isolated extramedullary relapse in childhood acute lymphoblastic leukemia (ALL) is associated frequently with the T-lineage immunophenotype and may be accompanied by occult bone marrow disease. We employed highly sensitive multiparameter flow cytometry and blast colony assays to quantify the leukemic progenitor cell (LPC) burden in the pretreatment bone marrows of 15 pediatric T-lineage ALL patients with an isolated extramedullary first relapse. Sites of extramedullary relapse were CNS (11 patients), testes (3 patients), and both CNS and testes (1 patient). Bone marrow LPC were detectable in 8 patients (53%) and undetectable in 7 patients (47%) at day 0 of post-relapse induction therapy, with LPC counts ranging from 0/10(6) mononuclear cells (MNC) to 518/10(6) MNC (mean +/- SEM, 50+/-34/10(6) MNC). Five of 9 patients with an early relapse (< 18 months after achieving a first complete remission [CR1]) and 3 of 6 patients with a late relapse (> or = 18 months from CR1) had detectable bone marrow LPC at day 0. Five of 8 patients with NCI-defined poor risk ALL and 3 of 7 patients with NCI-defined standard risk ALL had detectable LPC at day 0. Following post-relapse induction chemotherapy. LPC counts were detectable in bone marrows of 4 of 6 evaluated patients. Thus, approximately half of the extramedullary relapse T-lineage ALL patients studied had substantial occult involvement of the bone marrow. These findings may partly explain the previously observed poor prognosis of T-lineage patients following a CNS relapse.     

Clinical significance of human bone marrow stromal cell colonies in acute leukemias

Human bone marrow-derived fibroblastoid colony-forming cells (CFU-F) and adipocyte colonies in 36 patients with acute leukemia were studied, and were serially analysed at different clinical stages. At untreated stage, CFU-F number in acute lymphoblastic leukemia (ALL) was lower than that in acute non-lymphoblastic leukemia (ANL). In ANLs, CFU-F number in M1 was lower than that in M2. Adipocyte colonies were frequently developed at regenerating and relapsing stages, but rarely at untreated and remission stages. The adipocyte colony formation did not correlate with any of CFU-F number, marrow cellularity nor number of leukemic cells, but might be associated with hemopoietic regeneration. The favorable prognosis was associated with normal CFU-F number and with adipocyte colony formation at regenerating or bottom stage. As adipocytes in marrow samples were completely removed before cultures, adipocyte colony was probably originated from preadipocytes. Thus, our results suggest that adipocyte precursor cells increase in regenerating marrow and that they are essential in active hemopoiesis.