急性淋巴细胞白血病免疫分型的特点及其临床意义(英文)

目的为了探讨急性淋巴细胞白血病(ALL)各亚型免疫分型的特点及其临床意义。方法采用 CD45/SSC 双参数散点图设门,应用三色流式细胞术,对81例 ALL 的初诊患者骨髓标本进行免疫分型,并对其中45例进行核型分析。结果 (1)B-ALL 中 CD19表达最常见(阳性率为100%),而 T-ALL 中 CD5和 CD7表达阳性率最高,均为90%;B-ALL 和 T-ALL 都存在抗原交叉表达的现象;两组患者的完全缓解率(CR 率)并无显著差异(P>0.05)。(2)伴髓系抗原表达的急性淋巴细胞白血病(My~+ ALL)比较常见,本组达到39.5%,常累及 B 淋巴系统(占 My~+ ALL 的84.4%);各髓系抗原中以 CD13表达阳性率最高;此类患者的 CR 率较高,儿童 CR 率为72.2%,成人为78.6%。(3)急性杂合性白血病(HAL)的发病率为19.8%,以髓系、B 系共同表达者居多;并且 CD34表达阳性率较高(81.3%),该类患者 CR 率较低(儿童和成人分别为50%和40%)。(4)CD34在 B-ALL,My~+ALL 和 HAL 中表达阳性率较高,而 T-ALL 中少见(P<0.025)。结论免疫分型在诊断特殊类型的 ALL(如 HAL,My~+ ALL)中具有显著优势;CD19和 CD5诊断 B-ALL 和 T-ALL 的灵敏度较好,但特异性不高,存在抗原交叉表达;CD34和髓系抗原的表达与 CR 率无相关性,但在 HAL,CD34的表达与 CR 率成负相关。     

急性淋巴细胞白血病免疫分型的特点及其临床意义

目的为了探讨急性淋巴细胞白血病(ALL)各亚型免疫分型的特点及其临床意义。方法采用CD45/SSC双参数散点图设门,应用三色流式细胞术,对81例ALL的初诊患者骨髓标本进行免疫分型,并对其中45例进行核型分析。结果(1)B-ALL中CD19表达最常见(阳性率为100%),而T-ALL中CD5和CD7表达阳性率最高,均为90%;B-ALL和T-ALL都存在抗原交叉表达的现象;两组患者的完全缓解率(CR率)并无显著差异(P>0.05)。(2)伴髓系抗原表达的急性淋巴细胞白血病(My ALL)比较常见,本组达到39.5%,常累及B淋巴系统(占My ALL的84.4%);各髓系抗原中以CD13表达阳性率最高;此类患者的CR率较高,儿童CR率为72.2%,成人为78.6%。(3)急性杂合性白血病(HAL)的发病率为19.8%,以髓系、B系共同表达者居多;并且CD34表达阳性率较高(81.3%),该类患者CR率较低(儿童和成人分别为50%和40%)。(4)CD34在B-ALL,My ALL和HAL中表达阳性率较高,而T-ALL中少见(P<0.025)。结论免疫分型在诊断特殊类型的ALL(如HAL,My ALL)中具有显著优势;CD19和CD5诊断B-ALL和T-ALL的灵敏度较好,但特异性不高,存在抗原交叉表达;CD34和髓系抗原的表达与CR率无相关性,但在HAL,CD34的表达与CR率成负相关。     

Multiparameter analysis of acute mixed lineage leukemia: correlation of a B/myeloid immunophenotype and immunoglobulin and T-cell receptor gene rearrangements with the presence of the Philadelphia chromosome translocation in acute leukemias with myeloid morphology

Morphological, immunological, cytogenetic, and molecular features of 28 cases of acute mixed lineage leukemia (AMLL), defined by the co-expression of lymphoid and myeloid cell surface antigens, were correlated in a multiparameter study. These 28 cases were identified in a series of 260 consecutive acute leukemia cases occurring predominantly in adults and were subdivided into 18 cases of AMLL with myeloid morphology and cytochemistry (AMLL-AML) and 10 cases of AMLL with lymphoid morphology and cytochemistry (AMLL-ALL). A lack of correlation was observed between the expression of B- or T-cell associated antigens with the presence of the expected immunoglobulin (Ig) or T-cell receptor (TCR) gene rearrangements in the AMLL cases with myeloid morphology. Only three of the 18 total AMLL-AML cases, each co-expressing B- and myeloid-associated cell surface antigens (B/My), had Ig heavy chain gene rearrangements with or without rearrangements of TCR genes. Ig light chain genes remained in the germline configuration. Strikingly, these three cases were the only AMLL-AML cases in our series to have the Philadelphia (Ph) chromosome translocation t(9;22)(q34;q11), suggesting that a significant percentage of acute leukemias with myeloid morphology and gene rearrangements may be Ph+ AMLL. The fact that three of the 10 B/My AMLL-AML cases in our series were Ph+ suggests that there may be an increased frequency of Ph chromosome, a translocation associated with a poor prognostic outcome, in B/My AMLL-AML occurring in the adult population. Although most AMLL cases with lymphoid morphology had Ig and TCR gene rearrangements associated with a variety of immunophenotypes and karyotypes, two Ph+ AMLL-ALL cases had many similar features (B/My immunophenotype; IgH with or without TCR rearrangements; Ig light chain genes germline) to their Ph+ AMLL-AML counterparts. However, the Ph+ AMLL-ALL cases differed from the Ph+ AMLL-AML cases by the expression of a more mature B-cell lineage immunophenotype and by their additional cytogenetic changes.     

Karyotypic patterns in acute mixed lineage leukemia

We performed cytogenetic and immunologic studies of blast cells from 13 children with acute mixed lineage leukemia (AMLL) to discern patterns of chromosome alteration and antigen expression that would assist in classification of this disease entity. Six patients with 11q23 translocations--including four with the t(11;19), one with the t(9;11), and one with the t(1;11)--were characterized by a young age and hyperleukocytosis. A B cell-associated antigen (CD19) and HLA-DR antigens were expressed by blast cells from all patients; only one case was positive for the common acute lymphocytic leukemia antigen (CALLA, CD10). A myeloid-associated antigen (CD13) was expressed by blast cells from one patient at diagnosis and from another at relapse; it was also expressed by cells from the remaining four patients after brief in vitro culture without addition of differentiating agents. Four patients with t(9;22)(q34;q11) were characterized by an older age and hyperleukocytosis. Each of these cases was positive for CD13, CD19, and HLA-DR, and three were positive for CALLA. The 11q23 translocation was associated with CALLA- ALL marked by a myeloid phenotype, whereas the t(9;22) occurred in cases of acute myeloid leukemia with a CALLA+ lymphoid phenotype. One case had a 7q35-q36 translocation, which involves the region of the T cell receptor beta-chain gene. Our results suggest that karyotypic alterations can be used to refine the classification of AMLL.     

Acute leukemias with the t(4;11)(q21;q23).

The t(4;11)(q21;q23) has been associated with marked lineage heterogeneity. Most of the reported cases were classified as acute lymphoblastic leukemia (ALL). The t(4;11) is one of the commonest specific chromosomal translocations in ALL, occurring in 2% of childhood and 5% of adult cases. In childhood ALL, this translocation is associated with female sex, age less than 1 year, hyperleukocytosis, CD10-/CD19+ B-precursor cell immunophenotype, and myeloid-associated antigen (CD15) expression. There also appears to be an age-related difference in treatment outcome. Adults had the worst prognosis, and children aged 1 to 9 years appeared to have a better outcome than infants or adolescents. Reported cases of acute myeloid leukemia (AML) or secondary leukemia with the t(4;11) have not been well characterized. It is intriguing that virtually all of the reported cases with secondary leukemia had received epipodophyllotoxins or doxorubicin, agents that affect topoisomerase II and are associated with secondary AML characterized by 11q23 abnormalities. Identification of the involved gene(s) in the t(4;11) will provide a molecular approach permitting more accurate classification of these cases.     

Detection of acute leukemia cells with mixed lineage leukemia (MLL) gene rearrangements by flow cytometry using monoclonal antibody 7.1.

Translocations involving 11q23 are among the most common genetic abnormalities in hematologic malignancies, occurring in approximately 5-10% of acute lymphoblastic leukemia (ALL) and 5% of acute myeloblastic leukemia (AML). In 11q23 translocations, the mixed lineage leukemia (MLL) gene on chromosome 11, band q23, is usually disrupted. The human homologue of the rat NG2 chondroitin sulfate proteoglycan molecule, as detected by the monoclonal antibody (moab) 7.1, was shown to be expressed on leukemic cells with MLL rearrangements of children with acute leukemia. We further investigated the reactivity of the moab 7.1 on 533 cell samples of adults (n = 215) and children (n = 318) with acute leukemias (271 AML, 217 B-lineage ALL, 37 T-lineage ALL, eight CD7+ CD56+ myeloid/natural killer cell precursor acute leukemias) by flow cytometry. In AML, 38 samples were positive for moab 7.1 ('20%-cut-off-level'). These moab 7.1-positive AML cases revealed a myelomonocytic-differentiated immunophenotype with coexpression of the NK cell marker CD56 in 33 of 38 cases. Two of eight cell samples of the recently described CD7+ CD56+ myeloid/natural killer cell precursor acute leukemia entity reacted with moab 7.1. In ALL, 35 samples mostly of the pro-B-ALL subtype (33 pro-B-ALL, one common-ALL, one pre-B-ALL) were positive for moab 7.1. 58 (81%) of 72 samples with MLL rearrangements were positive for moab 7.1 including 28/31 with a t(4;11), 16/17 with a t(9;11), 3/5 with a t(11;19), and 2/6 with a del(11)(q23). All moab 7.1-positive ALL (n = 34) and childhood AML (n = 17) cases revealed MLL rearrangements as detected by Southern blot analysis and RT-PCR. However, 11 adults with AML, and one adult with moab 7.1-positive CD7+ CD56+ myeloid/natural killer cell precursor acute leukemia were negative for MLL rearrangements as proved by Southern blot analysis. We conclude that moab 7.1 is a sensitive but not entirely specific marker for the identification of 11q23-associated AML and ALL by flow cytometry in children and adults.     

Characterization of myeloid leukemias with monoclonal antibodies 3C5 and MY9

The expression of two membrane antigens identified by the monoclonal antibodies (McAb) My9 and 3C5 has been investigated in cells from 80 acute leukemias. My9 was positive in the blasts of 33 out of the 38 (87 per cent) cases of acute myeloid leukemia (AML) tested, regardless of FAB subtype, and in 13 of 18 (72 per cent) cases of chronic granulocytic leukemia (CGL) in myeloid blast crisis. The reactivity of 3C5 was confined to myeloblastic (M1) AML, 85 per cent of cases, and to lymphoblastic leukemia (ALL) of B-lineage, 70 per cent of cases, including CGL in lymphoid transformation. My9 was negative in ALL except for an unusual case. The phenotype My9+, 3C5+ was seen exclusively in M1 (69 per cent) and M2 (14 per cent) AML. Ultrastructural analysis with the immunogold method in combination with the myeloperoxidase (MPO) reaction showed that expression of My9 increased in parallel with MPO activity whereas 3C5 was expressed mainly in myeloblasts with little MPO content. We conclude that the use of these two McAb will contribute to the diagnosis and classification of AML and may throw some light to the pathogenesis of biphenotypic acute leukemias, including TdT + AML.     

Determination of Myloid Antigen Expression on Childhood Acute Lymphoblastic Leukaemia Cells: Discrepancies Using Different Monoclonal Antibody Clones

Prospective clinical studies including large numbers of patients have led to the conclusion that co-expression of myeloid antigens in childhood acute lymphoblastic leukaemia (My+ ALL) does not have prognostic significance. However, reports of the frequency of My+ ALL in children vary widely across laboratories using different mAb clones and staining and analysing procedures. Taking two commonly accepted thresholds of positivity for myeloid antigens (20 and 30%), we analysed the immunoreactivity of the most widely employed mAb clones against CD13 (SJ1D1, L138 and My7) and CD33 (My9, P67.6 and D3HL60) and compared the proportions of My+ ALL detected by these clones in childhood ALL. The correlation between myeloid antigen expression and the presence of the t(12;21) translocation was analysed concomitantly in the same samples.

The percentage of ALL cases positive for myeloid markers varied significantly depending on the mAb clone and the positive threshold. Among patients with B-ALL, the proportion of CD13+ ALL was significantly lower using SJ1D1 than using L138 or My7, while the proportion of CD33+ ALL was significantly higher for My9 than for P67.6 or D3HL60. Analysis of the co-expression of CD13 and CD33 on B-ALL cells using combinations of mAb clones showed that this frequency was either underestimated by the SJ1D1/D3HL60 or overestimated by the L138/P67.6 and My7/My9 combinations. A correlation between CD13/CD33 positivity and the t(12;21) translocation was uniformly observed in B-ALL patients for a positive threshold of 30%, whereas SJ1D1/D3HL60 detected no correlation between t(12;21) and CD13/CD33 ppositivity when the threshold was lowered to 20%. These data show that the mAb clones commonly used to detect the CD13 and CD33 surface antigens have variable immunoreactivity against childhood ALL cells, which may partly explain the conflicting reports concerning the prognostic significance of myeloid antigen expression in paediatric ALL and its association with different translocations. The present findings may also be of clinical importance for therapeutic choices.     

Determination of Myeloid Antigen Expression on Childhood Acute Lymphoblastic Leukaemia Cells: Discrepancies Using Different Monoclonal Antibody Clones

Prospective clinical studies including large numbers of patients have led to the conclusion that co-expression of myeloid antigens in childhood acute lymphoblastic leukaemia (My+ALL) does not have prognostic significance. However, reports of the frequency of My+ ALL in children vary widely across laboratories using different mAb clones and staining and analysing procedures. Taking two commonly accepted thresholds of positivity for myeloid antigens (20 and 30%), we analysed the immunoreactivity of the most widely employed mAb clones against CD13 (SJ1D1, L138 and My7) and CD33 (My9, P67.6 and D3HL60) and compared the proportions of My+ ALL detected by these clones in childhood ALL. The correlation between myeloid antigen expression and the presence of the t(12;21) translocation was analysed concomitantly in the same samples.

The percentage of ALL cases positive for myeloid markers varied significantly depending on the mAb clone and the positive threshold. Among patients with B-ALL, the proportion of CD13+ ALL was significantly lower using SJ1D1 than using L138 or My7, while the proportion of CD33+ ALL was significantly higher for My9 than for P67.6 or D3HL60. Analysis of the co-expression of CD13 and CD33 on B-ALL cells using combinations of mAb clones showed that this frequency was either underestimated by the SJ1D1/D3HL60 or overestimated by the L138/P67.6 and My7/My9 combinations. A correlation between CD13/CD33 positivity and the t(12;21) translocation was uniformly observed in B-ALL patients for a positive threshold of 30%, whereas SJ1D1/D3HL60 detected no correlation between t(12;21) and CD13/CD33 positivity when the threshold was lowered to 20%. These data show that the mAb clones commonly used to detect the CD13 and CD33 surface antigens have variable immunoreactivity against childhood ALL cells, which may partly explain the conflicting reports concerning the prognostic significance of myeloid antigen expression in paediatric ALL and its association with different translocations. The present findings may also be of clinical importance for therapeutic choices.     

Determination of myeloid antigen expression on childhood acute lymphoblastic leukaemia cells: discrepancies using different monoclonal antibody clones.

Prospective clinical studies including large numbers of patients have led to the conclusion that co-expression of myeloid antigens in childhood acute lymphoblastic leukaemia (My+ ALL) does not have prognostic significance. However, reports of the frequency of My+ ALL in children vary widely across laboratories using different mAb clones and staining and analysing procedures. Taking two commonly accepted thresholds of positivity for myeloid antigens (20 and 30%), we analysed the immunoreactivity of the most widely employed mAb clones against CD13 (SJ1D1, L138 and My7) and CD33 (My9, P67.6 and D3HL60) and compared the proportions of My+ ALL detected by these clones in childhood ALL. The correlation between myeloid antigen expression and the presence of the t(12;21) translocation was analysed concomitantly in the same samples. The percentage of ALL cases positive for myeloid markers varied significantly depending on the mAb clone and the positive threshold. Among patients with B-ALL, the proportion of CD13+ ALL was significantly lower using SJ1D1 than using L138 or My7, while the proportion of CD33+ ALL was significantly higher for My9 than for P67.6 or D3HL60. Analysis of the co-expression of CD13 and CD33 on B-ALL cells using combinations of mAb clones showed that this frequency was either underestimated by the SJ1D1/D3HL60 or overestimated by the L138/P67.6 and My7/My9 combinations. A correlation between CD13/CD33 positivity and the t(12;21) translocation was uniformly observed in B-ALL patients for a positive threshold of 30%, whereas SJ1D1/D3HL60 detected no correlation between t(12;21) and CD13/CD33 positivity when the threshold was lowered to 20%. These data show that the mAb clones commonly used to detect the CD13 and CD33 surface antigens have variable immunoreactivity against childhood ALL cells, which may partly explain the conflicting reports concerning the prognostic significance of myeloid antigen expression in paediatric ALL and its association with different translocations. The present findings may also be of clinical importance for therapeutic choices.     

Childhood acute leukemia with t(11;19) (q23;p13).

From 583 cases of acute lymphoblastic leukemia (ALL) and 181 cases of acute myeloid leukemia (AML) in childhood, seven patients were identified to have t(11;19) (q23;p13) by sequential cytogenetic analyses. The t(11;19) was associated with B-precursor ALL at diagnosis in three patients and at relapse in one patient. All four tested patients with B-precursor failed to express the CD10 antigen when the t(11;19) was detected, and one of three patients tested expressed myeloid-associated markers. In three other patients the translocation was detected either at lineage conversion from ALL to M5 AML (n = 2) or from AML to CD10- B-precursor ALL (n = 1). Leukemic blasts of four patients had an entirely different karyotype at the time of lineage conversion or loss of CD10 expression, suggesting an induction of a second neoplasm. Thus the t(11;19) can be found in de novo or secondary acute leukemia with lymphoid (CD10-) or myeloid (monoblastic) phenotype. Further investigation of the gene(s) involved in the 11q23 chromosomal region and the breakpoints in the 19p13 region is needed to understand the leukemogenesis of this apparently heterogeneous group of disorders.     

Significance of aberrant immunophenotypes in childhood acute lymphoid leukemia

Leukemic cells from 51 pediatric patients (younger than 18 years) diagnosed with acute lymphoid leukemia by standard morphologic and cytochemical methods were subjected to flow cytometric studies using a panel of monoclonal antibodies against T-cell (CD1, 2, 3, 4, 5, 7, 8), B-cell (CD10, 19, 20, 21), myeloid (CD13, 14, 15, 33), and HLA-DR antigens. Cases of "conventional" acute lymphoid leukemia (leukemic cells with a normal configuration of B-cell or T-cell differentiation antigens) were observed in 26 of 51 (51%) cases, whereas cases of "aberrant" acute lymphoid leukemia (cells with abnormal patterns of B-cell or T-cell antigens or with concomitant myeloid antigens) were noticed in 25 (49%) cases. Myeloid antigen-positive acute lymphoid leukemia was observed in the leukemic cells of eight (16%) individuals. No significant differences were observed between conventional and aberrant ALL in the distribution of sex, age, leukocyte count, hemoglobin concentration, platelet count, blast count, French-American-British (FAB) type, lymphadenopathy, organomegaly, rate or duration of remission, or survival. When only myeloid antigen-positive cases were compared with myeloid antigen negative-cases, no significant correlations were observed except for duration of first remission (myeloid antigen positive, 26+ +/- 22 months; myeloid antigen negative, 40+ +/- 18 months; P less than 0.001), and duration of survival (myeloid antigen positive, 27+ +/- 24 months; myeloid antigen negative, 62+ +/- 17 months; P = 0.001). These data suggest that pediatric patients with ALL blasts possessing myeloid antigens may represent a high-risk group for length of remission and survival.     

Characterization of Philadelphia-chromosome-positive acute leukemia by clinical, immunocytochemical, and gene analysis.

Philadelphia chromosome (Ph') was detected at presentation in 10 out of 110 patients with acute lymphoblastic leukemia (ALL) and five of 168 patients with acute myelogenous leukemia (AML). Two other ALL patients who had studies at relapse were also included in the analyses. One of the 12 Ph'-positive (Ph+) ALL patients had simultaneous expression of myeloid-associated antigen on the leukemic blasts, while all the five AML patients coexpressed markers of lymphoid cells. Double labeling of the cells with myeloperoxidase and CD10 on three Ph+ AML cases showed that most leukemic blasts expressed either myeloperoxidase activity or CD10 but not both. Cross-lineage gene rearrangements of T-cell receptor (TCR) beta-chain gene were detected in three of the eight Ph+ ALL patients tested. All the four Ph+ AML cases studied showed immunoglobulin heavy chain gene rearrangements, and three of them also had simultaneous rearrangements of TCR beta-chain gene. The results revealed that Ph+ acute leukemia in this study belonged either to ALL or mixed lineage leukemia, and none was pure AML. This finding is contrary to that of acute blast crisis of chronic myelogenous leukemia in which the majority of patients had myeloid transformation. Rearrangements of bcr were detected in four of the 10 Ph+ ALL and three of the four Ph+ AML patients tested. No significant difference was noted in the clinical or hematologic manifestations among Ph+ leukemia with or without bcr rearrangements.     

Immunoglobulin and T-cell receptor gene rearrangements in acute lymphoblastic leukemia--a higher incidence of double rearrangements in patients with myeloid antigen expression.

Among 160 patients who were diagnosed as having acute lymphoblastic leukemia (ALL) by French American British (FAB) criteria, 32 patients (20%) expressed myeloid-associated antigens on leukemic blasts (My+ALL). Correlation of immunophenotype with rearrangement of immunoglobulin (Ig) heavy chain and T-cell receptor (TCR) beta chain genes was performed on 73 of these patients (21 were My+ALL). Rearrangements of both Ig and TCR genes (double rearrangements) were detected in 24 patients, including three (19%) of 16 T-lineage ALL. 17 (33%) of 52 B-lineage ALL, and four of five ALL expressing both B and T-cell surface markers. Also a higher incidence of double rearrangements in My+ALL was found as compared with My-ALL (43% vs 29%). This difference was more evident when only B-lineage ALL was considered (50% in My+ patients vs 24% in My- patients). However the difference is not statistically significant yet possibly due to the small number of patients in the study. Further studies on more patients are needed to confirm this. In My-B-lineage ALL, rearrangements of TCR beta chain gene were restricted to certain subgroups (Groups III & IV) of patients who expressed CD10 surface antigens but lacked cytoplasmic Ig. In My+ B-lineage ALL, rearrangements of TCR beta chain gene could be found in various subgroups studied (Groups II through V). Cross-lineage gene rearrangement in My+ALL may involve mechanisms different from those in My-ALL.     

急性白血病细胞中CD19的表达

目的观察CD19在急性白血病(AL)中的表达与分布,为白血病的诊断、鉴别以及导向治疗提供依据.方法采用27个荧光直标单克隆抗体(单抗)及CD45/SSC双参数设门多色流式细胞术对321例AL细胞进行免疫诊断和分型,并对CD19在各类型AL细胞中的表达情况进行分析.结果在116例B细胞系急性淋巴细胞性白血病(ALL)患者中,CD19的阳性率(99.1%)明显高于B细胞系其它相关性抗原的阳性率;CD19在17例含B细胞系成分的杂合型白血病(HAL)中全部表达,而在29例T细胞系ALL和7例T/My HAL则均无表达;在152例急性髓系白血病(AML)中,仅11例(7.2%)CD19阳性,明显低于其在B细胞系ALL中的阳性率(P=0.001);CD22在B/My HAL的阳性率(12/15,80.0%)明显高于CD19 -AML(0/11,0%,P＜0.001).结论 CD19对B系ALL细胞的特异性较好,敏感性较高,是诊断B细胞系ALL较为可靠的表面标记,也可作为导向治疗B细胞系ALL的理想靶点.     

In vivo and in vitro expression of myeloid antigens on B-lineage acute lymphoblastic leukemia cells.

The expression of myeloid antigens has been extensively examined using two-color analysis in 43 children with B-lineage acute lymphoblastic leukemia (ALL). On pre-culture cells, CD33 expression was frequently observed in CD19+, CD10- B-precursor ALL, and CD14 was expressed only on the cells from B-precursor ALL expressing CD19, CD10 and CD20, and B-ALL. After 2 or 3 days of culture without TPA, CD13 emerged on the cells from 21 of 29 patients irrespective of the presence or the absence of fetal calf serum in the culture. Of four patients with CD10+ B-precursor ALL, which showed no expression of CD13 after culture, two had T-cell associated antigens. Whereas the addition of TPA to the culture enhanced the expression of CD13 on the cells from acute non-lymphocytic leukemia (ANLL), TPA reduced the expression of this antigen on B-precursor cells. These findings suggest that the regulatory mechanism of CD13 expression may be different between B-precursor ALL and ANLL. Co-culture with cycloheximide mostly abrogated the induction of CD13, suggesting that CD13 expression was mainly dependent on de novo protein synthesis.     

新疆地区450例急性白血病的免疫分型研究

 目的　研究新疆地区急性白血病（AL）患者免疫表型分布特点。方法　采用间接免疫荧光法对450例AL患者进行免疫表型分析。结果　106例急性淋巴细胞白血病（ALL）,334例急性髓系白血病（AML）,10例为FAB不能分类的急性白血病（UAL）;ALL中髓系抗原的表达15 %,AML中淋系抗原的表达25 %,表达最频繁的是CD7;研究了295例AL患者MPO mRNA基因表达,81例ALL中有1例表达MPO基因;所有髓系均不同程度地表达MPO基因,9例UAL有6例表达MPO基因;ALL免疫分型特点在汉族和维吾尔族（简称维族）中差异无统计学意义（P＞0.05）,在AML中,汉族髓系抗原的表达率依次为CD33＞CD13＞CD15,维族髓系抗原的表达率依次为CD15＞CD33＞CD14。结论　免疫表型的检测对AL更精确地诊断和分型有重要意义。联合分析AL形态学、细胞化学、免疫学及MPO mRNA表达等特点,对于AL的诊断和指导治疗均有重要意义。     

Kinetic and Immunophenotypic Heterogeneity in Acute Myeloid Leukemia Subpopulations

Bone marrow samples of 27 cases of acute myeloid leukemia were studied by double staining with 3H-Thymidine and monoclonal antibodies (APAAP method). 3H autoradiography labels the nucleus of S-phase cells and immunocytochemistry (APAAP) detects cytoplasmic antigens. Different myeloid subsets were characterized with the monoclonal antibodies My7 (CD13), My9 (CD33), My4 (CD14), IOM11c (CD11c), Ber Mac3 and anti-HLA-DR. We have shown that there are different myeloid subsets with different proliferative patterns. The most notable finding was that in M4 acute leukemia only myeloid subsets were in the S-phase, while in M5 acute leukemia the highest percentage of proliferating cells was in the monocytic subsets.     

Acute leukemia expressing the normal human hematopoietic stem cell membrane glycoprotein CD34 (MY10)

Thirty-one cases of acute leukemia with blast cells greater than or equal to 70% positive for the hematopoietic stem cell Ag, CD34 (MY10, HPCA-1), were identified from the University of Nebraska Medical Center and The Johns Hopkins Oncology Center over an 18-month period. Fourteen of the cases were classified as early B-lineage ALL, 3 cases were other ALL subtypes, and 14 of the cases were ANLL. Five of the 17 cases of ALL expressed one or more myeloid-associated surface Ags, 3 ANLL cases expressed CD10 (CALLA, J5), and T-lymphoid Ags were present in 12 of 31 cases (1 T-cell ALL, 3 of 16 B-lineage ALL cases, and 8 of 14 ANLL cases). Eleven of 12 CD34+ ALL cases studied had abnormal karyotypes; only 7 of 12 CD34+ ANLL cases studied had abnormal karyotypes, and 3 of these were CD10+ ANLL. Six cases were Ph1 positive, including the one mature B cell ALL, 4 early B-lineage ALL, and 1 CD10+ ANLL case. Good and poor prognosis subgroups of high frequency of expression of CD34 leukemias could be identified, generally, as would have been predicted by previously defined criteria. Thus, of the 10 Ph1-negative early B-lineage ALL patients, 9 achieved CR (90%). At the other extreme, the CR rate of CD10- ANLL was 4 of 11 (36%). The leukemias characterized by greater than or equal to 70% of cells positive for CD34 form a relatively undifferentiated subset of the leukemias which may show features associated with more than one lineage, and if CD10- and myeloid morphology, may respond poorly to therapy.     

成人急性B淋巴细胞白血病核型t(9;22)易位与免疫表型关系探讨

目的 探讨成人急性B淋巴细胞白血病(B-ALL)染色体t(9;22)易住与免疫表型之间的关系。方法 对154例初治成人B-ALL进行形态学(M)免疫学(I)和细胞遗传学(C)分型。结果 发现有t(9;22)易位(Ph^ )的B-ALL占46例(29．9％),其中伴髓系抗原(CD13或CD33表达(My^ )有28例(60．9％),伴T细胞抗原(CD2或CD3或CD33)表达(T细胞抗原阳性)3例(6．5％),cd34^ 39例(84．8％),CD10^ 45例(97．8％)。经分析发现,Ph^ 与My^ 高度相关,而与T细胞抗原和CD34^ 无相关。结论 伴髓系抗原表达的成人B-ALL与核型t(9;22)易位密切相关。这可能是影响成人My^ B-ALL缓解率低,持续缓解时间短,预后差的原因之一。