Gene/Protein Disease Symptom Drug Enzyme Compound
Pivot Concepts:   Target Concepts:
Query: EC:3.4.24.11 (CD10)
 9,792 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

A panel of B lymphoid-reactive monoclonal antibodies was used to analyze the phenotypic changes that accompany B lymphocyte development in normal human bone marrow. The B lymphoid cells were identified using light scattering and the expression of CD19 on a flow cytometer. Quantitative three-color immunofluorescence was then used to correlate other cell surface antigens on these cells identified as B lymphoid in normal marrow. CD10 and CD20 identified almost exclusive populations and provided a convenient means of discriminating between the less and more mature B lineage cells. The CD10+ cells could be further subdivided using CD34. The population of CD19+, CD10+, CD34+ cells comprised only 0.6% of marrow cells, but these contained the majority of terminal deoxynucleotidyl transferase (TdT+) cells. In the assessment of class II antigens, HLA-DR was expressed on all B lineage cells whereas HLA-DP preceded HLA-DQ in appearance during the developmental process. Among the later antigens expressed on B lineage cells, cell surface IgM, CD20, and HLA-DQ were expressed at essentially the same time. Cell surface CD10 was lost at the time when CD21 and CD22 were acquired on the cell surface. These data illustrate that multiparameter flow cytometry can be used to define a continuous progression of stages of B lymphocyte development based on cell surface antigen expression even though these cells represent a minor fraction of normal marrow cells.
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PMID:Flow cytometric analysis of human bone marrow. II. Normal B lymphocyte development. 311 32

Identification of the antigens expressed on marrow B lineage cells can be used to develop a model for the sequential acquisition of cell surface antigens during B lymphocyte development. The data suggest that the surface antigen expression is highly controlled during the development of B cells with the coordinated acquisition of multiple cell surface antigens during the maturational process. The developmental scheme in figure 6 is inferred from the expression of cell surface antigens on single samples. Confirmation of the progression from one stage to the next requires the isolation of a particular stage with subsequent induction to the next stage in-vitro. These data suggest that the development of B lymphoid cells may be discrete rather than continuous. The most immature cells identifiable in the bone marrow express CD34+ as well as HLA-DR. The earliest recognizable B lineage cells (CD19+, bright CD10+) also express CD34+. These cells are smaller by forward light scattering when compared to the cells which express only CD34+ (precursor of myeloid cells). Cells within stage I also express TdT in the nucleus and are proliferating. As the cells progress from stage I to stage II, the B lineage cells lose cell surface CD34 and nuclear TdT. At this time the density of HLA-DR and CD45 increases while the amount of CD10 decreases. These changes occur with no detectable change in cell size as assessed by forward light scattering. HLA-DP is first detected on the cells at this time. The progression of cells from stage II to stage III is marked by the acquisition of CD20, HLA-DQ, and sIgM. The amount of CD45 increases further in the transition between stage II and stage III. The acquisition CD21 and CD22 as well as the loss of CD10 distinguishes stage IV from stage III. Once the cellular composition of normal marrow has been defined, perturbations from homeostasis can be identified. Since marrow is the tissue most sensitive to injury by most antineoplastic chemotherapy and radiotherapy regimens, a means of quantifying the changes from the normal state can provide an assessment of the cytotoxic injury produced in individual patients. By monitoring the return to normal, it may be possible to more precisely individualize therapy for each patient. With a clear understanding of normal hematopoiesis, it should also be possible to identify maturational blocks which occur in hypoplastic marrow states. This may provide a means of identifying the regulatory points for each lineage and provide strategies for overcoming the inhibition of development.(ABSTRACT TRUNCATED AT 400 WORDS)
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PMID:Flow cytometric analysis of normal B lymphoid development. 326 12

Cell surface phenotypes of 113 B lineage acute lymphocytic leukemia (ALL) cases, defined by the presence of HLA-DR and at least one B-cell-specific antigen (either CD19, CD20, or CD22), were compared with antigen-defined stages of normal B lymphocyte development. The cases were first evaluated for expression of HLA-DR, CD19, CD34, CD10, CD20, and CD22 by indirect one-color immunofluorescence. Pairwise comparisons of cell surface marker expression were performed for each leukemic sample: no correlations were observed for paired antigen expression on the leukemic samples using antigens expressed either early or late during normal B lymphoid development. Complete immunophenotypes of the cases were then compared with normal B-cell developmental stages. Sixteen different complete immunophenotypes were observed on the leukemias that were not found in normal marrow; at least 78% of the cases demonstrated such "asynchronous" combinations of B lymphoid-associated differentiation antigens. Several samples were subsequently studied by two-color immunofluorescence, and the presence of doubly labeled cells with "asynchronous" antigen combinations was confirmed. These results indicate that the majority of B lineage leukemias exhibit "developmental asynchrony," as compared with normal marrow B cells. The data further suggest that ALL cases do not accurately represent cells arrested at the stage where the leukemogenic event occurred. Rather, ALL appears to be a disease in which there may be maturation of leukemic blasts; but this maturation is "asynchronous" when compared with the normal developmental process.
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PMID:Asynchronous antigen expression in B lineage acute lymphoblastic leukemia. 329 83

Single- and multicolor flow cytometry were used to define progenitor subsets in normal human bone marrow and peripheral blood, cord blood, and blood following mobilization of CD34+ progenitor cells by cyclophosphamide or cyclophosphamide/etoposide/G-CSF treatment. CD34 cells were quantitated and subsets of CD34+ cells were defined by coexpression of CD33, CD13, CD10, CD19, CD45RA, and CD71. Myeloid and erythroid progenitors were quantitated by sorting single CD34+ cells into individual wells of 96-well plates containing methylcellulose, IL-3, GM-CSF, G-CSF, IL-6, and erythropoietin. Comparative studies of CD34 cells showed that the percentage of CD34+ mononuclear cells was greatest in blood samples from patients following mobilization treatment with cyclophosphamide/etoposide/G-CSF averaging 2%. By comparison, the remaining sample groups ranged from 1.68 to 0.15% CD34 cells in this order, bone marrow > cord blood > cyclophosphamide mobilized blood > peripheral blood. Comparison of CD34 cells per milliliter of bone marrow or blood showed a range of 22.4 x 10(4) to 0.65 x 10(4)/ml in the following order, bone marrow > chemotherapy/etoposide/G-CSF > cord blood > cyclophosphamide-mobilized blood. Comparative analysis of CD34 subsets from different sources showed significant differences, particularly bone marrow and blood samples. A distinct population of CD34+ CD19+ (Leu 12) CD10+ (CALLA) pre-B lymphocyte cells was defined in bone marrow with lower side and forward light scatter characteristics and was variable between donors (29.8 +/- 16.9%, mean +/- 1 SD; range, 3-54%; n = 8). This population was not found to a significant degree in blood and also expressed CD45RA (Leu 18). Coexpression studies of CD45RA and CD71 (transferrin receptor) expression on CD34+ cells defined a CD45RA- CD71+ population containing 89 +/- 6.3% (n = 4) BFU-E and a CD45RA+ CD71+ population that contained all CFU-GM (n = 4). LeuM7 (CD13) stained a larger percentage to a greater intensity than MY7 (CD13). Coexpression of CD45RA (Leu 18) and CD13 (LeuM7) defined a subset of CD13+ CD45RA+ cells enriched for CFU-GM and CFU-M with a cloning efficiency of 31%. Coexpression of CD33 (MY9) and CD13 (MY7) defined a population that was predominantly CFU-GM with a cloning efficiency of 38%. These studies define CD34+ phenotypes containing pure populations of B lymphocyte, granulocyte-macrophage, or erythroid progenitors and demonstrate the utility of multiparameter flow cytometry to define lineage-committed CD34+ cells.
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PMID:Phenotypic analysis and characterization of CD34+ cells from normal human bone marrow, cord blood, peripheral blood, and mobilized peripheral blood from patients undergoing autologous stem cell transplantation. 750 11

The blast cells of peripheral blood and bone marrow of eleven acute leukemia patients with CD34 surface membrane antigen expression were investigated by immunophenotyping, cytochemistry and biochemical analysis. CD34 expression is a characteristic marker of very immature leukemic cells. Nine of eleven CD34+ acute leukemia cases had the immunophenotype of poorly differentiated myeloid cells. CD34+ blasts of two patients expressed the phenotype of very early lymphoid differentiation. Significant correlation was found between the expression of HLA-DR and CD34. The absence of CD10 antigen expression was observed in all cases of CD34+ myeloid blasts. The strong activity of SBB along with simultaneous absence of light microscopy MPO staining, 5'NT and moderate BG reactivity were characteristic enzyme features of CD34+ myeloid cells. The enzyme features of more mature stages of myeloid differentiation lacked. In lymphocytes, the CD34 expression correlated with CD10 antigen positivity and 5'NT activity. The activity of ADA was higher than that of PNP in all cases of CD34+ acute leukemia blast cells. The SBB, 5'NT and BG reactivity in correlation to CD34 antigen expression in acute leukemia may be an additional marker of very early stages of differentiation, either lymphoid or myeloid. The contribution to clinically important differential diagnosis of immature acute leukemia is discussed.
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PMID:Relation of some cytochemical activities to the expression of CD34 marker in acute leukemia. 750 88

A method for automatic lineage assignment of acute leukemias was developed. Input are eight list mode data files acquired with a FACScan flow cytometer. For each cell, four parameters are measured: forward light scatter, orthogonal light scatter, fluorescein fluorescence, and phycoerythrin fluorescence. Eight data files are acquired in the following sequence: unstained, isotype controls, CD10/CD19, CD20/CD5, CD3/CD22, CD7/CD33, HLADR/CD13, and CD34/CD38. First, each of the data files 3 to 8 are clustered independently employing an algorithm based on nearest neighbors. Next, the clusters are associated across the data files to form cell populations, using the assumption of light scatter invariance across tubes for each population. The mean positions of each cell population are fed into a decision tree. The decision tree first identifies normal cell populations, i.e., monocytes, neutrophils, eosinophils, basophils, NK cells, T-lymphocytes, and B-lymphocytes. After elimination of the normal cell populations from the data space, the residual cell populations are classified as B-lineage ALL, T-lineage ALL, AML, AUL, B-CLL, or unknown. The effectiveness of this novel approach is shown with case studies of B-lymphoid, T-lymphoid, and Myeloid acute leukemias.
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PMID:Automatic lineage assignment of acute leukemias by flow cytometry. 750 22

A strategy to phenotype rare populations of hematopoietic cells expressing the cell-surface marker CD34 was studied. The antigenic phenotype of umbilical core blood (CB) CD34+ cells was investigated using flow cytometry and compared with the mRNA-phenotype determined by cDNA-polymerase chain reaction (cDNA-PCR) analysis. The cDNA-PCR method allowed an mRNA evaluation of small numbers of cells. Monoclonal antibodies and oligonucleotide primers that recognize myeloid, lymphoid, erythroid and platelet/megakaryocytic cell membrane antigens or corresponding mRNA transcripts were used. Evaluation by flow cytometry showed that the vast majority of CD34+ CB cells coexpressed CD38, CD18, HLA-DR, and CD33. Rare subpopulations of CD34+CD38-, CD34+CD18-, CD34+HLA-DR-, and CD34+CD33- were also identified. A large proportion of CD34+ CB cells expressed CD13, CD45R, and to a lesser extent CD71. The CD36, CD51, and CD61 antigens were identified on a small number of CD34+ cells. The three-color flow cytometry analysis showed that CD34+ cells stained with antibodies to CD61 and CD36 or CD51 can be divided into subsets that may represent progenitor cells committed to the erythroid and/or megakaryocytic lineage. A variety of other lineage-specific cell-surface antigens including pre-T-cell marker CD7 and markers of early B cells, ie, CD10 and CD19, were not coexpressed with CD34+. Using the cDNA-PCR it was seen that the mRNA phenotype of a small number of sorted CD34+ cells (purity > 98%) was negative for the markers CD2, CD14, CD16, CD20, CD21, CD22, CD41b, and glycophorin A that are expressed on differentiated cells but positive for CD34, CD7, CD19, CD36, and CD61. The results suggest that circulating CD34+CD7+ and CD34+CD19+ CB cells cannot be distinguished by flow cytometry but can be detected by cDNA-PCR. This indicates that CB either contains very low numbers of these progenitors or that the antigen density of CD7 and CD19 on CD34+ cells is below the detection limit of the flow cytometer. In contrast to flow cytometry, cDNA-PCR allows the phenotypic analysis of cells even if their number is small. Thus, the cDNA-PCR method can be useful in linking phenotype analyses, ie, markers of differentiation, to studies on gene expression within rare populations of hematopoietic stem cells.
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PMID:Phenotype analysis of hematopoietic CD34+ cell populations derived from human umbilical cord blood using flow cytometry and cDNA-polymerase chain reaction. 751 40

Using two-color flow cytometry, we analyzed the subpopulations of CD34+ stem and progenitor cells in the blood and bone marrow from 10 patients with hematological malignancies. Peripheral blood mononuclear cells (PBMNC) harvested after chemotherapy (high-dose Ara C and VP-16) and rhG-CSF, and BM mononuclear cells, which were obtained before chemotherapy (BMMNCbefore) and after the stem cell collection (BMMNCafter) were isolated by Ficoll-Hypaque centrifugation. The purified cells were stained with FITC-conjugated anti-CD34 antibody and one of the following PE-conjugated antibodies: anti-CD7, CD10, CD11b, CD11c, CD13, CD19, CD33, CD38, CD45RO, CD56, and HLA-DR. CD34+ PBMNC harvested and the CD34+ BMMNCafter expressed CD13 and CD33 more frequently than CD34+ BMMNCbefore but expressed CD10 and CD19 less frequently than CD34+ BMMNCbefore. These data suggested that harvested PBMNC contain more myeloid lineage committed progenitors than BMMNCbefore, which might contribute to the rapid recovery of neutrophils after peripheral blood stem cell transplantation. No significant phenotypic differences of CD34+ cells between harvested PBMNC and BMMNCafter were observed except for the expression of CD11c. CD34+ PBMNC harvested coexpressed CD11c more frequently than both CD34+ BMMNCbefore and CD34+ BMMNCafter, which expression might be associated with commitment to the monocyte lineage.
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PMID:Phenotypic differences of CD34-positive stem cells harvested from peripheral blood and bone marrow obtained before and after peripheral blood stem cell collection. 751 35

Seventy-five adult patients with newly diagnosed acute lymphoblastic leukemia (ALL) were analyzed for CD34 expression on leukemic cells. CD34 was significantly associated with B-cell lineage ALL (p = 0.0002). In B-lineage ALL, CD34 positivity was significantly associated with expressions of CD9 (p = 0.001), CD19 (p = 0.00001) and CD22 (p = 0.002). CD34 was more expressed in B-ALLs with higher WBC cell count (p = 0.04), and higher percentage of peripheral blood leukemic cells (p = 0.005), total or partial monosomy of chromosome 7 (p = 0.0001) or Ph+ chromosome (p = 0.01); and less expressed in cases with hyperdiploidy (> or = 50 chromosomes) (p = 0.03). CD34 was more expressed in poor risk B-ALLs patients, defined according to Hoelzer criteria (p = 0.01). In T-lineage ALL, CD34 positivity was inversely correlated with the expression of CD10 (p = 0.05). After intensive induction therapy, 58 of 73 evaluable patients (79%) achieved a complete remission (CR). CD34 positivity was correlated with the persistence of blast cells in day 15 bone marrow aspirates (p = 0.001) and after one course of induction chemotherapy (p = 0.01). With a median follow-up of 11 months, no statistical differences were seen in leukemia-free survival and overall survival between CD34 positive and negative cases, even when stratifying by immunophenotype. We conclude that CD34 expression is associated with features of poor prognosis in adult ALL. Its study might therefore become useful in the design of future prognostic models.
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PMID:CD34 expression is associated with major adverse prognostic factors in adult acute lymphoblastic leukemia. 753 67

We have previously demonstrated that the immunoglobulin (Ig) heavy chain variable region (VH) sequences expressed by the malignant clone in multiple myeloma (MM) contain a high degree of somatic mutation without clonal diversity. This sequence can be used to identify all members of the malignant clone in this B cell malignancy. We sequenced the variable regions expressed by patients with MM and generated primers from the complementarity determining region (CDR) sequences specific for each patient's tumor. Using these primers, we performed PCR amplification on highly purified subpopulations of cells separated by expression of CD10, CD34 and CD38. The results of these experiments demonstrate: 1) there is a small fraction of CD10-expressing tumor cells in MM patients, 2) CD34-bearing malignant cells do not exist in MM, and 3) although the vast amount of tumor is in the CD38-expressing cells, a small amount of tumor is in the CD38-negative population. We also used these primers to determine whether pre-class switch (i.e., Cmu-expressing lymphocytes) clonal cells exist in these patients. After PCR amplification with CDR1 and Cmu primers, colony hybridization was performed using both framework 3 (FR3) and CDR3 probes. Out of > 200 FR3-hybridizing colonies, < or = 5 colonies also hybridized with the CDR3 probe. Colonies which hybridized with both these probes were sequenced, and none of these sequences matched even closely the CDR3 expressed by the malignant clone. These results make the existence of a pre-class switch malignant cell unlikely in MM. Overall, these results suggest that the malignant clone in MM derives from a cell late in B lymphocyte development.
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PMID:Multiple myeloma clones are derived from a cell late in B lymphoid development. 753 71


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