Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0023418 (leukemia)
 93,477 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Lymphocyte subpopulations in human cord blood have been examined using monoclonal antibodies, visualized with immunogold. The proportions of T11, T4, T8, and B1 cells in cord blood are very similar to values in adult peripheral blood. Some evidence of lymphocyte immaturity in cord blood is suggested by the presence of 12% CALLA-positive cells and the sum of T4 and T8 cells significantly exceeding the number of T11 cells; however, there were no TdT-positive cells. The presence of CALLA-positive lymphocytes in normal cord blood should be borne in mind when investigating blood smears from neonates for congenital leukemia.
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PMID:Characterization of lymphocyte subpopulations in human cord blood using the immunogold staining technique. 244 85

A case of acute leukemia with atypical malignant cells is reported. The clinical picture and coagulation studies were consistent with a disseminated intravascular coagulation syndrome. Morphologically, the leukemic cells from the peripheral blood and bone marrow showed azurophilic granules. More than 80% of cells were hypergranulated, resembling the macrogranular type of promyelocytes. Ultrastructural studies and the pattern of endogenous peroxidase were consistent with the microgranular type of promyelocytes in about 20% of the leukemic cells. Auer bodies were present in both types of atypical promyelocytes. Cytochemically, the whole malignant population exhibited intense peroxidase activity. Studies with monoclonal antibodies showed that about 45% of the proliferating cells expressed T-cell markers T3, T4, T8 and T11, but the cells were not reactive with OKM1 monoclonal antibodies. The chemotherapy for acute promyelocytic leukemia was inefficient, and the prompt disappearance of the blood abnormalities was observed only when chemotherapy for acute lymphoblastic leukemia was started. Therefore, it seems that in some cases of leukemia with hybrid types of malignant cells the morphological features determine the clinical picture, while the patient's response to the therapy is conditioned mainly by the cell surface phenotype.
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PMID:Acute promyelocytic leukemia with T-cell markers and particular response to treatment. Report of a case. 249 88

Pretreatment peripheral and/or bone marrow blasts from 14 patients with acute unclassifiable leukemia (AUL) expressing myeloid related cell-surface antigen (CDII) or megakaryocyte-platelet related cell-surface antigen (OKM6), were isolated for further analysis in this study. Among 11 cases of CD11+AUL, despite a lack of myeloperoxidase (MPO) activity, one patient's blasts possessed Auer rod in a basophilic cytoplasm and another one's blasts expressed MPO maintaining the same surface phenotype after 20 months of his clinical course. The blast from 2 cases possessed both myelomonocytic and monocyte-specific antigens on the cell-surface, whereas the remaining nine cases completely lacked monocyte-specific antigen which is detectable by monoclonal antibodies, Mo2, My4 and Leu M3 (CD14). In addition, we revealed the presence of MPO protein in the cytoplasm of 3 cases of AUL patients by cytoplasmic immunofluorescence test utilizing monoclonal antibody (MA1). Following these results, the former was diagnosed as acute myelomonocytic leukemia (AMMoL) and the latter as acute myelogenous leukemia (AML) by immunophenotypic analysis using flow cytometry (FACS IV) and cytoplasmic immunofluorescence test. We have also described three cases of acute megakaryocytic leukemia which were demonstrated by the presence of megakaryocyte-platelet-related cell-surface antigens detected by utilizing flow cytometry and monoclonal antibodies in addition to both the PPO activity which was shown by ultrastructural cytochemistry, and the emergence of differentiation antigens while culturing these leukemic cells. The blast of 1 case possessed both platelet GPIb and GPIIb/IIIa cell-surface antigens detected by 5F1 (CD36), AN51 (CDw42), and J15, P2 and HPL2 (CDw41), respectively, whereas the remaining two cases almont lacked the GPIb cell-surface antigen. Hence, the former was diagnosed as immature (pro) megakaryocytic leukemia and the latter as acute megakaryoblastic leukemia from the viewpoint of immunophenotypic analysis as will be discussed in this article. These leukemic blasts did not express both T-cell lineage antigens which are detectable by monoclonal antibodies, T6 (CD1), T11 (CD2), T3 (CD3), T4 (CD4), T1 (CD5), Tp40, Leu9 (CD7), T8 (CD8), and B-cell lineage antigens which are detectable by monoclonal antibodies, B4 (CD19), B1 (CD20), B2 (CD21) and J5 (CD10).(ABSTRACT TRUNCATED AT 400 WORDS)
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PMID:[Flow cytometric analysis of myeloperoxidase negative acute unclassifiable leukemias by monoclonal antibodies. Acute myelogenous and acute megakaryocytic leukemia]. 254 Dec 76

T cell activation via the CD2 molecule involves phospholipase C and phosphoinositide hydrolysis. Here we demonstrate that the triggering of subclones of the human T leukemia Jurkat cell line by anti-CD2 as well as anti-CD3 monoclonal antibodies is able to induce activation (i.e. translocation from cytosol to cell membrane) of protein kinase C (PKC), which is dependent on the formation of 1,2-diacylglycerol from inositol 4-5-bisphosphate. The kinetics of PKC translocation parallels the rise in intracellular calcium following both CD2 and CD3 stimulations. These results further demonstrate that CD2 and CD3 activation pathways use similar signal transduction mechanisms.
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PMID:T cell activation via the CD2 molecule is associated with protein kinase C translocation from the cytosol to the plasma membrane. 256 74

Human T-cell leukemia virus type I (HTLV-I) is etiologically associated with adult T-cell leukemia, an aggressive lymphoproliferative disorder, and with chronic neurological diseases. In vitro it can infect several types of cells but transforms only human T lymphocytes. We have previously shown that HTLV-I viral particles, even when noninfectious, were able to activate human resting T lymphocytes, suggesting that this activation step may be important in the initiation of the lymphoproliferative process. In the present study, we first demonstrate that in contrast to other mitogenic stimuli, HTLV-I has the unique property to activate human resting T cells in the absence of accessory cells. We then investigate the relationship between HTLV-I-induced T-cell activation and the classical well-known pathways of activation, namely, the CD3/TCR and CD2 pathways. Competitive blocking experiments were performed in which the effects of monoclonal antibodies (MAb) to the CD3/TCR complex or to the CD2 molecule were evaluated on the HTLV-I activation of T cells and compared with that obtained on phytohemagglutinin (PHA)-stimulated cells. It was found that anti-CD3 or -TCR MAb strongly suppress the proliferative response of T cells to PHA, but are significantly less efficient in inhibiting the activation initiated by HTLV-I. By contrast, MAb recognizing specific epitopes of the CD2 molecule inhibit the proliferative response of T cells to PHA or to HTLV-I to the same extent. The results provide evidence that HTLV-I virions interfere mainly with activation via CD2 but not via the CD3/TCR complex. Considering the earlier expression of the CD2 molecule on human T-cell precursors, these observations might be relevant to the characterization of the differentiation stage at which viral infection could interfere with the development and the maturation of T lymphocytes.
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PMID:Peripheral T-lymphocyte activation by human T-cell leukemia virus type I interferes with the CD2 but not with the CD3/TCR pathway. 257 39

The cell surface marker profile and functional analysis of peripheral blood lymphocytes from 11 Japanese adult T cell leukemia patients were studied. The phenotypic analysis of Japanese adult T cell leukemia (ATL) cells by a series of 13 monoclonal antibodies showed that all ATL cells are anti-T4 reactive but some differ in their expression of T3, T11, and T12 antigens. Thus, considerable phenotypic heterogeneity exists in these populations of leukemia cells. When analyzed in functional assays, ATL cells were suppressive when added to a pokeweed mitogen- (PWM) driven Ig synthesis system. However, the suppression mechanism seemed to be more complex than originally conceived. ATL cells examined in this study seem to function mainly as an inducer of suppressor cells, and as such, activate normal T8 precursors of suppressor cells rather than function as suppressor effector cells. In addition, no evidence was obtained to suggest that suppression of PWM-stimulated IgG synthesis was mediated by natural killer (NK) activity of ATL cells. Rather, ATL cells seem to be markedly deficient in NK activity. These studies suggest that the majority of ATL cells tested are representative of and seem to be the leukemic counterparts of the T4+ suppressor inducer subset.
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PMID:Functional and phenotypic studies of Japanese adult T cell leukemia cells. 285 96

We studied the change in cytoplasmic free calcium ion concentration ([Ca2+]i) in the peripheral blood leukemic cells from adult T-cell leukemia (ATL) patients stimulated by anti-T3 (CD3) or anti-T11 (CD2) antibodies in order to see whether there is an abnormal response in the early activation processes following T3 or T11 antigen stimulation. Peripheral blood mononuclear cells (PBMC) from four T-cell chronic lymphocytic leukemia (T-CLL) patients showed a rapid and clear increase in [Ca2+]i (from 165 +/- 26 nM to more than 299 nM) when stimulated by OKT3 antibody and anti-mouse IgG antibody. This response was comparable to that of PBMC from 10 normal individuals (from 151 +/- 20 nM to 252 +/- 34 nM). In contrast, PBMC from 10 ATL patients showed only a slight increase in [Ca2+]i (from 137 +/- 21 nM to 176 +/- 32 nM) following T3 stimulation. The experiments with higher concentrations of OKT3 antibody suggested that this attenuated increase in [Ca2+]i in ATL cells was not exclusively due to impaired expression of T3 antigen. The [Ca2+]i increase in ATL cells induced by the stimulation with two anti-T11 antibodies recognizing different epitopes of the T11 antigen, however, was comparable to that of normal PBMC. The abnormal response of [Ca2+]i to the T-cell receptor/T3 antigen stimulation in ATL may be related to dysfunction or leukemogenesis of HTLV-I-infected cells.
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PMID:Increase in cytoplasmic free calcium concentration initiated by T3 antigen stimulation is imparied in adult T-cell leukemia cells. 289 98

A 27-year-old male patient with ataxia telangiectasia (AT) developed atypical chronic lymphocytic leukemia with increasing bone marrow infiltration in the absence of organomegaly. One-third of the leukemia cells expressed a mature suppressor/cytotoxic T cell phenotype (T3+ T4- T6- T8+ T10-), two-thirds demonstrated additional helper/inducer T cell-associated antigens (T3+ T4+ T6- T8+ T10-), and a small fraction reacted with a natural killer (NK) cell-specific monoclonal antibody (Leu 11+). The proliferative response to stimulation in vitro with lectins and various monoclonal antibodies resembled the proliferation pattern of mature thymocytes: The cells responded to phytohemagglutinin (PHA), concanavalin A (ConA), stimulation of the T3-Ti receptor complex with Sepharose-bound anti-T3, and stimulation of the sheep erythrocyte receptor protein with anti-T11(2) and anti-T11(3) in conjunction with exogenous interleukin-2 (IL 2); they failed, however, to proliferate after stimulation with anti-T11(2) and anti-T11(3) alone. There was no response in the mixed lymphocyte reaction (MLR) and no suppression of the MLR between two healthy donors. Antibody-dependent cell-mediated cytotoxicity and NK activity could not be demonstrated. Cytogenetic analysis revealed complex clonal aberrations, including an interstitial deletion of the long arm of chromosome 14 concerning bands q21-31, loss of chromosome 20, and loss of the Y chromosome. Cytostatic chemotherapy was of little use and caused serious side effects, whereas leukapheresis proved effective in reducing the tumor load. The clinical data and laboratory findings in this case correspond to three previously described patients with AT who developed chronic T cell leukemia. Thus, in adult patients with AT, malignant proliferation of cytogenetically marked and phenotypically heterogeneous mature T cells seems to be a frequent complication.
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PMID:Chronic T cell leukemia with unusual cellular characteristics in ataxia telangiectasia. 294

A clone of the interleukin 2-producing Jurkat leukemia cell line termed JA3 (surface phenotype, T3+, Ti+, T44+, T11+, T40+) has been used to induce and select cell variants lacking surface molecules involved in T-cell activation. Following 200 rad of gamma-radiation (1 rad = 0.01 Gy), cells were treated with monoclonal antibodies (mAbs) directed to T3, Ti, T44, or T11 antigen and complement. After growth of the residual cells in culture, "negative" cells were cloned under limiting conditions. Depending on the specificity of the mAb used for the immunoselection, three groups of variants were obtained. (i) The use of mAbs directed to T3 or Ti resulted in cell variants that expressed the T3 Ti- T44+ Leu1+ T11+ T40+ 4F2+ HLA class I+ surface phenotype. (ii) Immunoselection with anti-T44 mAb resulted in 2 variants that shared the T3- Ti- T44- Leu1- T11+ T40+ 4F2+ HLA class I+ phenotype. (iii) Cell treatment with anti-T11 mAb resulted in 15 variants characterized by the lack of T11 antigen expression and of all the other T-cell-specific surface antigens. Therefore, it appears that the different sets of JA3 cell variants, like T cells at discrete stages of intrathymic differentiation, may follow a coordinated expression of surface differentiation antigens. Analysis of the functional responsiveness of the three distinct groups of JA3 cell variants to different stimuli showed that all produced interleukin 2 in response to A23187 calcium ionophore plus phorbol 12-myristate 13-acetate. The first group of variants (T3- Ti-) did not respond to stimulation with anti-T3, anti-Ti, or anti-T44 mAbs. Eight of 9 did not respond to phytohemagglutinin either; however, all responded to appropriate stimulatory combinations of anti-T11 mAbs (and to calcium ionophore). The second group of variants (T3-, Ti-, T44-, T11+), similar to the first group, did not respond to anti-T3, anti-Ti, anti-T44 mAbs, and phytohemagglutinin, but they were fully responsive to anti-T11 mAb. The last group of variants (lacking all the T-cell-specific surface antigens) only responded to calcium ionophore A23187.
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PMID:Selection and characterization of T-cell variants lacking molecules involved in T-cell activation (T3 T-cell receptor, T44, and T11): analysis of the functional relationship among different pathways of activation. 295 35

A human leukemia cell line (TALL-101) was established from the bone marrow of a patient with an undifferentiated acute T cell leukemia using the conditioned medium (CM) of the human T cell leukemia virus (HTLV) II-transformed human cell line J-LB1. Immunofluorescence analysis on the original leukemic cells indicated the presence of T cell markers (Leu-1, Tdt, and T11); however, the established TALL-101 cell line expressed only antigens commonly present on progenitor cells, thymocytes, and myelomonocytic cells, but not on mature T cells. A high percentage of TALL-101 cells displayed the Tac antigen which was down-regulated upon incubation in the presence of recombinant human (rH) interleukin 2 (IL 2). Interferon (IFN)-gamma induced the appearance of class II histocompatibility leukocyte antigens (HLA) and of a T cell marker (3A1), and enhanced the expression of transferrin receptors on these cells. Further evidence for a T cell lineage of the TALL-101 cell line was provided by both chromosomic and genotypic analysis showing a translocation in chromosome 14 typical of T cell leukemias, and a rearrangement of the T-beta receptor locus. The growth-promoting activity in the J-LB1-CM was identified as granulocyte-macrophage colony stimulatory factor (GM-CSF), a growth factor which stimulates proliferation of normal myelomonocytic cells and other progenitor cells, but not known to have an effect on T cells. Dose response curves of [3H]thymidine incorporation and growth indicated that TALL-101 cells were sensitive to very low concentrations of rHGM-CSF, 5 ng/ml inducing maximal proliferation in chemically defined medium. The TALL-101 cell line is strictly GM-CSF-dependent for growth: upon depletion of GM-CSF from the culture medium, the cells stop proliferating immediately and die within 1 to 2 wk. The overall data, showing that GM-CSF is able to support the growth of a highly undifferentiated T cell leukemia, strongly suggests that this factor might have similar growth promoting effects on other immature T cell leukemias, and possibly, on normal T cell progenitors.
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PMID:Establishment and characterization of an undifferentiated human T leukemia cell line which requires granulocyte-macrophage colony stimulatory factor for growth. 295 97


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