老年CD+56急性髓系白血病临床生物学特征

目的 研究CD+56老年急性髓系白血病(AML)的临床生物学意义.方法 对102例初治老年AML进行细胞形态学、免疫表型、多药耐药P糖蛋白(PgP)检测,并常规采用HAE方案诱导治疗,判定疗效.结果 老年急性髓系白血病,CD56阳性率39.22%.CD+56AML在FAB分型中以M2b、M5、M7多见,高白细胞计数(57.03×109/L vs 33.65×109/L,P=0.047),多表达PgP(62.50% vs 40.32%,P=0.042).CD+56AML患者髓外浸润现象明显(62.50% vs 37.09%,P=0.015),尤其是脾脏(42.50% vs 19.35%,P=0.014)显著受累,CD56表达与年龄、性别、血红蛋白含量、血小板计数及外周血幼稚细胞数无关,也不影响CR率(P值分别为0.306,0.840,0.564,0.302,0.686,0.547),但无病生存时间(DFS)(5.75个月 vs 30.00个月,P=0.048)和总生存时间(OS)(5.34个月 vs 22.03个月,P=0.032)较短.结论 CD+56AML具有独特的临床生物学特征,多表达耐药蛋白PgP,生物学侵袭性较强,生存期短,预后较差.建议初诊时监测CD56分子表达以判断预后.     

老年CD+7急性髓系白血病生物学特征及其临床意义

目的 研究老年CD7抗原阳性急性髓性白血病（CD^＋7AML）的临床生物学特征。方法 对98便初治老年AML进行细胞形态学、免疫表型、多药耐药P糖蛋白（P120）、细胞遗传学核型分析，并采用常规AML方案诱导治疗，判定疗效。结果 老年AML中CD7阳性表达率28.57%（28/98）,28例CD^＋7老年AML（M/F，20/8）的FAB分型结果为：M03例、M13例、M2a6例、M4a2例、M4b1例、M5a1例、M5b9例。CD^＋7老年AML患者外周血白细胞计数（53.80 vs 25.21 P=0.001）、原始细胞比例（69.00% vs 41.02% P=0.001）及P-糖蛋白表达显著增高（67.85 vs 28.57 P=0.001）,肝脏肿大（46.10% vs 23.50% P=0.044）和髓外白血病易发（28.57% vs 2.78% P=0.001）,且对常规化疗反应差，预后不良，完全缓解率亚型，常提示预后不良，建议监测初诊AML患者CD7表达。     

CD7阳性急性髓细胞白血病免疫表型及临床特点

随着系列单克隆抗体的应用，白血病细胞免疫分型的广泛开展及其研究的深入，伴有ＣＤ７抗原表达的急性髓细胞白血病（ＣＤ＋７ＡＭＬ）不断被发现。有学者认为ＣＤ＋７ＡＭＬ是一类独特的急性髓细胞白血病亚型，具有与不伴有ＣＤ７抗原表达的急性髓细胞白血病（ＣＤ－７Ａ...     

CD56在急性单核细胞白血病细胞表达的意义

目的：探讨CD56分子对急性髓性白血病（AML）之急性单核细胞白血病（M5）细胞生物学及临床特征的影响.方法：应用G显带技术及流式细胞仪对45例M5患者分别进行核型及免疫表型检测，并回顾分析其临床资料.结果：45例患者中CD56表达阳性17例（37.78%），其中正常核型2例（11.76%），异常核型15例（88.24%），以8号三体和11q23异常易见（分别占23.53%，29.41%）;伴CD56抗原表达的患者高表达CD11b，CD14（P＜0.01，P＜0.05），外周血白细胞计数偏高，骨髓及外周血中原始和幼稚细胞百分比明显升高（P＜0.05），较多出现髓外浸润，尤其以淋巴结肿大（P＜0.05）和肝脾肿大（P＜0.05）明显，伴二系以上受累也明显高于对照组（P＜0.05），而中枢神经系统及皮肤浸润与对照组比较差异无统计学意义（P＞0.05），同时伴CD56阳性的患者出现较低的完全缓解率及较短的生存期（P＜0.05）.结论：CD56阳性的M5患者易出现异常核型，高表达CD11b，CD14，预后较差。     

急性早幼粒细胞白血病CD56表达的临床意义

全反式维甲酸 ( ATRA)和三氧化二砷 ( As2 O3 )的应用 ,使急性早幼粒细胞白血病 ( APL )的治疗发生了根本性改变。尽管如此 ,仍有一部分患者死于治疗前的出血、治疗无效和早期复发 〔1〕。研究分析表明 ,不良的预后与外周血白细胞过高、血小板过低和存在 S型 PML- RARa融合基因有关〔2〕。近来的研究表明 ,CD56的表达与 APL预后不良亦有直接关系〔3〕。国内目前尚未见 CD56+ APL的报道。我院 1 995～ 1 999年收治 CD56+ APL患者 6例 ,现将其血液及临床特征分析如下。1　材料与方法1 .1 　 研究对象本组 46例 ,经 MIC分型符合 …     

表达CD56抗原的急性非淋巴细胞白血病的临床和MIC分型特征

表达ＣＤ５６抗原的急性非淋巴细胞白血病的临床和ＭＩＣ分型特征陈桂彬贾海蓉卞寿庚沈德诚韩明哲张金香ＣＤ５６被认为是１４００００的神经细胞粘附分子（ＮＣＡＭ），主要表达在正常和肿瘤神经外胚层细胞，也认为是抗全自然杀伤细胞（ＮＫ细胞）的表面标记。现对我院一...     

急性髓细胞白血病CD7、CD34、CD56、P170的表达对完全缓解率的影响

已有文献报道ＣＤ7、ＣＤ3 4、ＣＤ56、Ｐ170 各自的表达与预后有关[1 5] 。但此四种单抗联合表达对预后的影响报道较少。现将我院 1995～ 1999年检测的 2 13例初诊急性髓系白血病(ＡＭＬ)以上 4种分化抗原的单表达和联合表达对完全缓解(ＣＲ)率的影响分析如下。一、材料与方法1 标本来源 :门诊及住院的 2 13例患者 ,经形态、免疫、部分有遗传及细胞组织化学联合诊断为ＡＭＬ。其中男 115例 ,女 98例 ,年龄 1 5～ 82岁 ,中位年龄 31 5岁。2 试验方法及试剂 :(1)白血病细胞分化抗原测定 :取骨髓单个核细胞 ,间接或直接单克隆抗体标记后 ,用…     

CD56^＋巨核细胞白血病

我们检测１例伴ＣＤ５６高表达的巨核细胞白血病患儿，其免疫表型为ＣＤ４１＾＋，ＣＤ＾＋５６；细胞遗传学显示亚二倍体增多；细胞化学染色结果：髓性过氧化物酶，苏丹黑Ｂ染色，特划性脂酶染色，非特异性脂酶且不被ＦＮａ抑制，糖原染色弱阳性；骨髓中的幼稚细胞在体外有较高的ＮＫ细胞介导的细胞毒活性，此细胞经倍体分析发现，８５．８％为二倍体细胞，证明它们属于不分化或分化很差的巨核细胞。     

CD3+ CD41+的急性白血病一例

患者,女,49岁,因浅表淋巴结肿大二月伴发热一月于2002年11月2日入院.患者于2003年9月不明原因的颈部、腋下及腹股沟淋巴结肿大,无痛,10月起伴发热37.6～38.2℃.     

CD34抗原阳性急性非淋巴细胞白血病的临床及免疫表型特征

采用免疫荧光法检测了４３例原发性急性非淋巴细胞白血病（ＡＮＬＬ）细胞ＣＤ３４抗原及其他免疫学标记的表达，其中１３例（３０．２％）表达ＣＤ３４抗原。ＣＤ３４￣（＋）ＡＮＬＬ组在年龄、血红蛋白、白细胞、血小板、外周血和骨髓原始、幼稚细胞比例等方面与ＣＤ３４￣（－）组相比较无显著差别，但表达ＣＤ３４抗原的ＡＮＬＬ多发生在男性患者，常伴有ＨＬＡ－ＤＲ（ＤＰ）、ＣＤ３８、ＣＤ７等不成熟细胞表面标记的表达，而较成熟的髓系细胞表面标记ＣＤ１５则不表达。ＣＤ３４￣（＋）ＡＮＬＬ与ＦＡＢ亚型Ｍ１、Ｍ５ａ有着密切的关系，且对化疗反应较差，证明ＣＤ３４￣（＋）ＡＮＬＬ是一组分化程度较差的类型。     

Phenotypic and clinical heterogeneity of CD56-positive acute nonlymphoblastic leukemia

Summary The precise phenotype and clinical course are described of a subgroup of acute nonlymphoblastic leukemias (ANLL) expressing the NK-cell differentiation antigen CD56. As previously reported, CD56+ leukemias occurred in a frequency of about 20% of ANLL cases showing clinical and immunophenotypical heterogeneity. Carrying various myelomonocytic markers, all cases were diagnosed to be of nonlymphoid origin. Positive or negative expression of CD34 allowed us to distinguish two major subtypes of CD56+ leukemias representing immature and more differentiated cells carrying further differentiation antigens (CD14 and/or CD15) of the myelomonocytic lineages. These phenotypes correlated with the M0, M2, M4, and M5 leukemias of the FAB classification.     

Biologic and clinical significance of CD7 expression in acute myeloid leukemia

CD7 antigen, a T-cell lineage associated antigen, is expressed in a minority of patients with acute myeloid leukemia (AML). The biologic and clinical significance of this finding is not clearly established. In this retrospective study of patients with de novo acute myeloid leukemia, we have identified CD7 expression and analyzed its association with markers expressed early in hemopoietic ontogeny and clinical parameters. Among 60 consecutive AML patients, we found six (10%) expressing CD7 on leukemic cells. There were five males and one female and the mean age was 59.6 years (age range: 32–76 years) with no demographic peculiarities. The FAB subtypes were: M0 (2), M1 (1), M2 (1), and M4 (2). CD7 expression was associated with immature antigens CD34, HLA-DR, and terminal deoxynucleotidyl transferase (TdT) and antigen receptor gene rearrangements (rearrangements of T-cell receptor gamma chain in 6/6 and immunoglobulin heavy chain in 2/6). Hepatomegaly was present in three and this was associated with splenomegaly with lymphadenopathy in one patient. Mediastinal or central nervous system involvement was absent. Complete remission was achieved in two patients with standard chemotherapy; one of these is in remission and alive (5 years later), while one died following relapse 9 months later. Three patients had significantly lower response to standard therapeutic regimen (two died during induction and one died 7 months later without ever achieving complete remission). One patient has been excluded in determining the prognostic significance of CD7 due to early death. Our results suggest origin of CD7+ AML from early hemopoietic precursors and indicate biologic aggressiveness in a significant proportion of patients. We suggest evaluation of CD7 in all patients with AML at the time of diagnosis in view of poor clinical outcome. Am. J. Hematol. 58:278–284, 1998. © 1998 Wiley-Liss, Inc.     

Prognostic significance of CD7+CD56+ phenotype and chromosome 5 abnormalities for acute myeloid leukemia M0

Myeloid/natural killer (NK) cell precursor acute leukemia is an entity of acute leukemia characterized by poor prognosis and a CD7+CD56+ myeloid antigen+ phenotype without light-microscopic myeloperoxidase reactivity. This disease shares several clinical characteristics with acute myeloid leukemia (AML) M0. To clarify the relationship between these 2 leukemias, we analyzed 105 cases of AML M0. Among them, 17 were CD7+ and CD56+, 77 were negative for either antigen, and 11 could not be determined. CD7+CD56+ AML M0 showed onset at significantly lower patient age (median 46 versus 63 years, P = .004). The disease localization and the hematological manifestations were significantly different: CD7+CD56+ AML showed more frequent extramedullary involvement, fewer circulating leukemic blasts, less anemia, and less thrombocytopenia than did AML M0. The cytogenetic aberrations were also unique, because no 5q abnormalities were found in CD7+CD56+ M0. The prognosis of CD7+CD56+ M0 was poor in patients younger than 46 years (P = .03). Multivariate analysis showed that the CD7+CD56+ phenotype was a significant prognostic factor for AML M0, as well as age, circulating blast percentage, and chromosome 5 abnormalities These findings suggest that AML M0 consists of heterogeneous subgroups to be managed separately, and CD7+CD56+ M0 constitutes a distinct subtype of AML M0.     

CD56 expression in myeloperoxidase-negative FAB M5 acute myeloid leukemia

CD56 is a natural killer (NK) cell marker that has been identified in approximately 15-20% of acute myeloid leukemia (AML) cases, where it has been associated with monocytic morphology and chromosomal abnormalities such as trisomy 8, t(8;21), t(15;17), and 11q23 rearrangements. The clinical presentation, chromosomal abnormalities as detected by fluorescent in-situ hybridization (FISH), and clinical outcomes of 7 patients with AML are presented. These cases were characterized by French-American-British (FAB) M5 morphology, myeloperoxidase (MPO) negativity, and co-expression of myelomonocytic and NK cell-associated antigens (CD11c(+), CD13(+), CD15(+), CD33(+), HLA-DR(+), and CD56(+)). All patients presented lymph node, hepatic, or splenic involvement at diagnosis. Despite the homogeneous morphologic and immunophenotypic characteristics the outcomes varied considerably. Two patients died during induction therapy, but the other five patients attained complete remission (CR). Of these five patients, 4 have received a bone marrow transplantation (autologous or allogeneic) and 3 of them are in CR (median follow-up: 45 months). The three patients with 11q23 rearrangements had a poor outcome and died of their disease within 1 year of diagnosis. Further studies with a larger group of patients would help establish the actual prognostic value of these morphologic, immunophenotypic and cytogenetic features.     

CD4+ and CD56+ acute monoblastic leukemia.

We report here a patient with acute monoblastic leukemia whose leukemia cells had CD4 (T4) and CD56 (NKH-1) antigens, in addition to CD36 (OKM5) antigen. The leukemia cells did not have NK or ADCC activities. They showed no rearrangements of immunoglobulin heavy (IgH) chain and T cell receptor (TCR)-beta chain genes, indicating that the leukemia cells were nonlymphoid. The presence of this case suggests that leukemia cells could be originated from monocytes with NK-associated antigen without IgH or TCR rearrangements.     

淋系分化抗原在急性髓细胞白血病中的表达及其意义

目的 探讨淋系分化抗原在急性髓细胞白血病（ＡＭＬ）的表达及其临床意义。方法 采用ＡＰＡＡＰ法和流式细胞术检测６４例ＡＭＬ的免疫表型。结果 ９例除表达髓系抗原外尚有淋系抗原表达（Ｌｙ＾＋ＡＭＬ）。Ｌｙ＾＋ＡＭＬ组于初诊时肝脾肿大明显,白细胞总数较Ｌｙ＾－ＡＭＬ组高。用标准方案诱导化疗,其中仅１例部分缓解。结论 Ｌｙ＾＋ＡＭＬ细胞对于常规诱导缓解方案不敏感,选择兼顾ＡＬＬ＋ＡＭＬ的方案可提高治疗效果。     

Aberrant co-expression of CD19 and CD56 as surrogate markers of acute myeloid leukemias with t(8;21) in Taiwan

Aberrant antigen expression in acute myeloid leukemia (AML) has been extensively studied in the West with limited reports from Taiwan. We carried out this retrospective study to characterize the frequency and significance of aberrant antigen expression of AML in Taiwan. Among 111 cases, 58 (52%) showed aberrant antigen expression, most frequently CD7 (27%) and CD56 (23%). Aberrant CD7 expression was observed in all non-AML-M3 subtypes, most frequently in AML-M7 (4/6, 67%); while CD19 expression was only observed in AML-M2 (5/36, 14%). CD56 expression was most common in AML-M5 (4/8, 50%). The relative frequency of CD19 and CD56 expression in AML with t(8;21) was higher than those with other chromosomal abnormalities or normal karyotype (P = 0.011 and 0.005, respectively). In non-M3 AML, aberrant antigen expression was identified in 56/96 (58%) cases, in contrast to 2/15 (13%) AML-M3 cases (P = 0.001). CD7, CD19 and CD56 expression was not correlated with remission rate. We concluded that aberrant immunophenotype was more frequent in non-M3 leukemias in Taiwan. The relative frequency of CD19 and/or CD56 expression in AML with t(8;21) was significantly higher than those without this translocation and co-expression of these two antigens may serve as the surrogate markers for AML with t(8;21).     

CD33 directed bispecific antibodies in acute myeloid leukemia

Despite the approval of a number of new targeted therapies for acute myeloid leukemia (AML), median overall survival still remains poor, ranging from 12 to 18 months in most patients. Based on the success of blinatumomab, the CD19-targeted bispecific antibody for the treatment of acute lymphoblastic leukemia, the development of several CD33-targeted bispecific antibodies for AML are being investigated in clinical trials. In this review article of CD33-targeted bispecific antibodies, we describe the rationale for targeting CD3 x CD33, summarize the data from four ongoing phase 1 studies, review the major toxicity associated with CD33-targeted bispecific antibody therapy of cytokine release syndrome (CRS) and steps to mitigate CRS, and describe possible mechanisms of resistance to CD33-targeted bispecific antibody therapy. Future development to try to improve outcomes include combination therapies to reduce the tumor burden prior to starting treatment, combining with immune checkpoint inhibition therapy such as anti-PD-1/PDL1 antibodies, and the use of second generation bispecific antibodies that target two different antigens and recruit other effector cells such as nature killer cells and macrophages.