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Query: UMLS:C0023418 (leukemia)
 93,477 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Isolated leukemic B cells from patients with B-chronic lymphocytic leukemia (B-CLL) were tested for proliferative response in vitro to Staphylococcus Aureus strain Cowan 1 (SAC), IL-2, and low molecular weight (MW) BCGF. Patients were classified according to clinical stage and progressiveness. Ten of eighteen cell populations from patients with progressive B-CLL responded in vitro with a stimulation index (SI) > 20. Only 1/16 non-progressive patients had a proliferative but low response. Normal unfractionated tonsillar B cells responded to SAC and BCGF, whereas normal high buoyant density B cells were unresponsive. After 3 days of stimulation, responding B-CLL cells had multiplied and the B cells expressed CD5, CD19, and weakly CD21. No cells in the responding cultures exhibited CD3 or the EBV nuclear antigen EBNA-1. Cell maturation, measured as IgM secretion, was found in some, but not in all responding B-CLL cultures. Thus, B-CLL cells from patients with progressive disease have the capacity to respond to signaling through surface Ig receptors and to certain T-cell factors which was not the case for B-CLL cells from non-progressive patients. The pattern of in vitro response may be related to disease progression, reflecting a dependency of normal immunoregulatory mechanisms and/or a dysregulation of the growth control in the leukemic cells.
Leukemia 1994 Jul
PMID:Leukemic cells from progressive B-CLL respond strongly to growth stimulation in vitro. 803 6

The Epstein-Barr virus (EBV) genome has recently been detected in various non-B cell neoplasms, including various T-cell leukemias and in Reed-Sternberg cells of Hodgkin's disease, but the contribution of EBV genes to the transformed phenotype remains unclear. We have investigated the possible effect which the EBV genes LMP1 and EBNA2, of which the expression has been reported in non-B cell neoplasms, may have on a variety of cell types. The LMP1 and EBNA2 genes were transiently expressed from heterologous promoters in two human T-cell lines (HPB-ALL and Jurkat), two human cell lines of the myeloid lineage (K562 and U937), one type I Burkitt's lymphoma cell line (Rael) and in human primary T cells and B-cell chronic lymphocytic leukemia cells. The cell surface expression of CD23, CD21, ICAM-1 and LFA-1 was monitored on transfected cells. In the cell lines, except U937, the surface antigens CD21 and ICAM-1 were upregulated in a dose-dependent and transient manner by the transient expression of LMP1, and EBNA2 slightly enhanced the effects of LMP1 on CD23 and CD21 upregulation. LMP1 also induced increased CD21, ICAM-1 and LFA-1 surface expression on transfected primary T-cells, and CD21 and ICAM-1 in four of five B-cell chronic lymphocytic leukemias tested. Finally, LMP1 transient expression caused increased cell size of the primary T cells and responding B-cell chronic lymphocytic leukemia cells. Our results strongly suggest that LMP1 can trigger specific responses in a variety of white cell types and thus is probably contributing to the phenotype of EBV-positive tumor cells not only in the B-cell lineage.
Leukemia 1993 Jan
PMID:Transient expression of the Epstein-Barr virus LMP1 gene in B-cell chronic lymphocytic leukemia cells, T cells, and hematopoietic cell lines: cell-type-independent-induction of CD23, CD21, and ICAM-1. 809 69

Surface phenotypes and adhesion activity to human umbilical vein endothelial cells (HUVECs) were studied using leukemic cells from 12 Japanese patients with B-cell chronic lymphoid leukemias including 7 with chronic lymphocytic leukemia (CLL), 1 with prolymphocytic leukemia (PLL), 2 with hairy cell leukemia (HCL) and 2 with HCL variant (HCL-V). CD13 and CD23 were found to be characteristically positive in CLL, whereas they were not expressed in non-CLL cases except for positivity of CD23 in two such cases. Except for CD11b, all other leukocyte integrins examined (CD11a, CD11c and CD18) and their ligand (CD54) were highly expressed in non-CLL cases. Adhesion activity of leukemic cells to HUVECs after co-culture with HUVECs was well correlated with the expression of CD11b, CD18 and CD54, but showed no predilection for any leukemia subtype. Positivity for CD5, CD21, CD23 and CD13 changed after the co-culture with HUVEC. These results suggest that adhesion activity after co-culture. does not correlate with the leukemia subtype and that endothelial cells activate or differentiate leukemic cells.
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PMID:Surface phenotype and adhesion activity of B-cell chronic lymphoid leukemias. 822 Jan 19

The independent significance of CD10 expression in childhood acute lymphoblastic leukemia (ALL) is uncertain because most studies have not adjusted for other risk features, such as age and immunophenotype, or for treatment effects. We reassessed the clinical importance of CD10 expression in patients who received highly effective contemporary treatment. CD10 antigen was detected in blast cells from 384 of 408 patients (94%) with B-lineage ALL and 36 of 90 (40%) with T-cell ALL. In the B-lineage subgroup, CD10 expression was associated with favorable presenting features: age > or = 1 year, lower leukocyte count (< 50 x 10(9)/l), and leukemic cell DNA index > or = 1.16 or hyperdiploidy > 50 chromosomes. One-half of the patients with CD10- B-lineage ALL had 11q23 chromosomal abnormalities. Separate analysis of the marker in T-cell ALL revealed no differences between CD10+ and CD10- cases in clinical features or karyotypic patterns, with the exception of a lower frequency of central nervous system leukemia and a higher frequency of 9p abnormalities in the former subgroup. CD10+ T-cell cases were also significantly more likely than CD10- cases to coexpress CD21, CD1, CD4, or CD8. Lack of CD10 expression was independently associated with an adverse prognosis in T-cell ALL (p = 0.02). However, for the larger subgroup of patients with B-lineage ALL, CD10 expression has no independent prognostic significance.
Leukemia 1993 Jan
PMID:Clinical significance of CD10 expression in childhood acute lymphoblastic leukemia. 841 77

Results of immunophenotypic examinations of peripheral blood and/or bone marrow (BM), involved in low-grade B-cell non-Hodgkin's lymphomas, were compared with the results of cytomorphological and histopathological examinations in 133 adult patients. 69 cases of chronic B-lymphocytic leukaemia (B-CLL), 16 centrocytic (CC) lymphomas, 14 centroblastic-centrocytic (CB/CC) lymphomas, 15 immunocytomas (IC), 10 cases of hairy cell leukaemia (HCL), four prolymphocytic leukaemias (PLL), two B-CLL in transformation, one splenic lymphoma with villous lymphocytes (SLVL), one hairy cell leukaemia variant (HCL-V), and one lymphocytic lymphoma (LC) were classified according to the Kiel and/or FAB classification. Leukaemic disease was found in 105 cases. The following markers were used for immunocytology (APAAP technique) of blood and/or BM smears: CD19, CD5, CD10, CD11c, CD14, CD21, CD22, CD23, CD25, CD38 and TdT. All cases tested showed CD19, but no TdT expression. Every case of HCL had a distinct phenotype with expression of CD11c, CD22 and CD25 and the lack of CD5 and CD23 antigens. In all other NHL cases a very heterogenous expression of CD-antigens with no significant correlations to the cytomorphological subtypes was found. The expression of CD5 is a frequent but inconstant finding in lymphoproliferative diseases other than B-CLL, so 50% of CB/CC, 75% of CC and 80% of IC were CD5 positive. Our results indicate that, with the exception of HCL, the diagnostic relevance of immunophenotyping for the classification of cytomorphologically and histopathologically defined subtypes in blood and/or BM is of very limited value.
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PMID:Immunophenotyping of low-grade B-cell lymphoma in blood and bone marrow: poor correlation between immunophenotype and cytological/histological classification. 825 6

A panel of human hematopoietic cell lines was genetically engineered to express recombinant complement receptor 2 (CR2 or CD21), which is also the Epstein-Barr virus (EBV) receptor. The panel was composed of SupT1, J1.1, and U1.HIV cells. The latter is a promonocytic cell line, whereas the other two are T lymphocytic cell lines. J1.1 and U1.HIV cells are latently infected by human immunodeficiency virus type 1 (HIV-1). These three cell lines were transduced with a murine leukemia virus (MLV)-based retroviral vector system. CR2 was efficiently and consistently expressed on the cell membranes, conferring enhanced susceptibility to EBV infection. The efficient expression of recombinant CR2 in cell lines of hematopoietic origin allowed for study of the interaction between EBV infection and HIV-1 gene regulation in suitable cell-culture models. The effects of EBV and HIV-1 coinfection results were cell-type dependent. In the two T lymphocytic cell lines, HIV-1 expression was rapidly and persistently down-regulated by EBV. Conversely, in the promonocytic cell line U1.HIV-CR2, HIV-1 expression was transiently enhanced by EBV. The EBV and HIV-1 coinfection result in U1.HIV-CR2 cells is potentially important, as the activation of HIV-1 gene expression in monocyte-like cells may play a crucial role in the mechanism of CD4+ T cell depletion by apoptosis. Therefore, the U1.HIV-CR2 cell line may represent a useful cell-culture system to study the synergism between EBV and HIV-1 in inducing apoptosis in primary CD4+ T cells.
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PMID:Differential effects on HIV-1 gene regulation by EBV in T lymphocytic and promonocytic cells transduced to express recombinant human CR2. 934 4

Binding of B cell chronic lymphocytic leukemia (B-CLL) cells to other cells and to extracellular matrices influences the pathophysiology and the clinical presentation of the B-CLL disease. It is still unknown which adhesion pathways regulate the traffic of B-CLL cells within distinct histologic compartments of lymphoid organs. In addition, it is not yet clarified which mechanisms mediate the intercellular adhesion of B-CLL cells. The present study sought to identify the mechanisms that are involved in the binding of B-CLL cells to secondary lymphoid organs in situ and in the homotypic aggregation of these cells. B-CLL cells specifically bound to germinal centers of normal human tonsils via the adhesion pair integrin alpha4beta1/vascular cell adhesion molecule-1 (VCAM-1). Among a large panel of antibodies tested only mAbs against CD19 induced homotypic adhesion of B-CLL cells via the adhesion molecules integrin alphaL (leukocyte function antigen-1 (LFA-1)), intercellular adhesion molecule-1 (ICAM-1) and CD21. Anti-CD19-induced aggregation required protein synthesis. We hypothesize that the observed heterotypic and homotypic adhesion of B-CLL cells reflects the ability of these leukemic cells to migrate in vivo.
Leukemia 1998 Jan
PMID:Differential adhesion pattern of B cell chronic lymphocytic leukemia cells. 943 23

Leukemia cells enriched from peripheral blood of a patient with myelogenous leukemia were induced to differentiate with a purified T cell lymphokine neuroleukin. With sufficient neuroleukin concentrations, cells with macrophage-like morphology were identified among the developing adherent cells. After 2-5 days, approximately 38-50% of the suspension cells became macrophage-like and acquired CD21, alpha-naphthyl acetate reactivity and immune adherence capability. The amount of these nonproliferating cells increased along with cells containing fragmented DNA. Induction with insufficient neuroleukin quantity or with patient plasma alone developed few or no mature cells, indicating differentiation to mature cells is dose-dependent. The possibility of insufficient quantity of neuroleukin in regulation of patient plasma for differentiation was discussed.
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PMID:Neuroleukin mediated differentiation induction of myelogenous leukemia cells. 993 30

Epstein-Barr virus (EBV) was first reported as the causative virus of Burkitt's lymphoma in 1964. Since then, EBV has also been associated with infectious mononucleosis, AIDS and transplant-related B cell lymphomas, and nasopharyngeal cancer. The virus has further been linked with T cell lymphomas, Hodgkin disease, and NK leukemia or LGL leukemia, establishing a concept of a wide spectrum of EBV associated malignant disorders. EBV DNA encodes several proteins such as EBNA1-6, LMP 1, 2 and others. Recent studies have demonstrated that EBNA2, EBNA5, EBNA3A, EBNA 3C are essential for transformation, and that any gene product is not sufficient to transform cells by itself. Further there are different mechanisms of virus-associated transformation or carcinogenesis among EBV-associated malignant disorders. On the other hand, human T lymphotropic virus type I (HTLV-I) is known as a causative virus of adult T cell leukemia (ATL). However, precise molecular mechanisms of leukemogenesis in ATL still remains unclear. Some additional factors to HTLV-I infection are supposed to be involved in complete leukemogenesis. We demonstrated that HTLV-I infected T cells and primary ATL cells express EBV receptor/CD21 on the cell surface. Therefore, it is possible that EBV infection is one of the factors. We further investigated this possibility in 6 HTLV-I infected T cell lines and primary ATL cells from 18 patients with ATL. However, no EBV genome was detected in both T cell lines and primary ATL cells. EBV involved T-cell lymphoma has unique clinical manifestations as compared to non-EBV involved T-cell lymphoma. Therefore, it is still possible that a small group of ATL patients with unique clinical manifestations is associated with EBV.
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PMID:Epstein-Barr virus involvement in T-cell malignancy: significance in adult T-cell leukemia. 1034 73

Antigen CD5 is the glycoprotein which belong to the scavenger receptor cysteine-rich family. Mainly there is on the T cells subpopulation. During fetal life B CD5+ cells are major subpopulation of B cells in the spleen, lymph nodes and there are also in the cord blood. In adult CD5+ cells are minor subpopulation (27%) of B cells from the peripheral blood. CD5 there are on chronic lymphocyte leukaemia B cells (B-CLL) also. Usually expression CD5 on B-CLL cells associated with weak or lack expression of the surface immunoglobulins and CD79 beta, CD20, CD22, CD21 (CR-2), CD35 (CR-1) antigens. It appeared interesting to compare the expression of CD5 antigen (the mean fluorescence intensity--MFI of CD5) on B cells from the cord blood, adults peripheral blood and B-CLL patients. MFI of CD5 on B and T cells were also compared in each groups. MFI of CD 19 was studied too. Lymphocytes from the cord blood (11 assays), adult peripheral blood of healthy volunteers (18 assays) and the peripheral blood of no treated patients with B-CLL (56 assays) were studied. The immunological phenotype of lymphocytes was evaluated with the monoclonal antibodies anti-CD5 and anti-CD19 by the flow cytometry method. We have demonstrated that MFI of CD5 on B cells from patients with B-CLL was strongest and weakest from normal individuals. MFI of CD5 on T cells from patients with B-CLL is stronger in comparison to healthy volunteers. MFI of CD19 is weakest on cells from patients with B-CLL and strongest in normal individuals. On the basis of the our results and other medical papers we suggest on the one hand that biology of B-CLL depend on deficit antigens specific for B cells lines on the other hand depend on overexpression of CD5 antigens on leukaemic B and T cells also.
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PMID:[Expression of CD5 antigen in B and T cells from umbilical cord blood, from blood of healthy adults and patients with chronic lymphocytic B-cell leukemia (PBL-B)]. 1074 Apr 8


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