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)

The phenyl-beta-galactoside (phi-beta-gal)-specific monoclonal antibody (mAb) 49H.8 cross-reacts with the terminal disaccharide structure of the asialo GM1 (AGM1) molecule. It was found to react with phi-beta-gal determinants on murine and rat splenic natural killer (NK) cells, as measured by complement depletion studies. Flow cytometric analysis identified the antigen on two IL 2-dependent cloned murine NK cell lines and the rat large granular lymphocyte leukemia RNK. We have compared the 49H.8 reactivity to that of anti-AGM1 antisera (alpha-AGM1) on NK cells and a panel of NK related killer cells, including bone marrow-derived killer cells, lymphokine-activated killer cells (LAK), and anomalous killer cells (AK). We found that the 49H.8 specificity closely paralleled that of alpha-AGM1. When tested against Con A-reactive T cells, the 49H.8 mAb was less reactive than the alpha-AGM1, indicating that it may be a more specific marker for splenic NK populations than the alpha-AGM1.
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PMID:A phenyl-beta-galactoside-specific monoclonal antibody reactive with murine and rat NK cells. 242 Aug 80

Bone marrow transplantation (BMT) has been used in recent years for the treatment of immunodeficiency diseases, aplastic anemia, and leukemia. However, there are a number of serious problems and limitations associated with autologous or allogeneic BMT. One of these is an increase in opportunistic infections, of which cytomegalovirus (CMV) infection is one of the most important. Cytomegalovirus has been associated with more frequent deaths than any other single agent, with no reproducibly successful or therapy currently available. Recently usage of interleukin-2 or immunomodulation has been suggested as a powerful modality to combat infectious disease. In this study we showed that bone marrow activated in interleukin-2 for 2 days has the ability to lyse spleen cells infected for 3 days with murine CMV (acute infection model) or salivary gland cells infected for 7 days (chronic infection model), while nonactivated bone marrow or natural killer (NK) cells showed no such lysis. The majority of activated cells involved in lysis were antiasialo GM1-, Thy-1+/-, indicating a population of cells other than the natural killer-cell population involved.
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PMID:The potential usefulness of interleukin-2 activated bone marrow cells as an active therapeutic tool against cytomegalovirus infection in a bone marrow transplantation setting. 254 85

It has been found that kinetic parameters of proliferation in a dominating clone of bone marrow blast cells with Ia-positive and Ia-negative phenotype, as well as with expression of myeloid differentiating antigens (ICO-GM1 and ICO-G2), or in the absence of these antigens, do not significantly differ in children with subvariants MO-M4 of acute nonlymphoblastic leukemia, sensitive and resistant to the therapy. A higher rate of the bone marrow blast cell population growth and a lower effectiveness of the combined chemotherapy have been recorded in children with T-cell and pre-B-cell acute lymphoblastic leukemia as compared to acute lymphoblastic leukemia with the phenotype of blast cells that have only Ia-like or "common" antigens.
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PMID:[Comparative evaluation of blast cell proliferation and effectiveness of combined chemotherapy in children with different immunocytological subvariants of acute lymphoblastic and nonlymphoblastic leukemia]. 258 57

Exposure of HL-60 leukemia cells to either 12-O-tetradecanoylphorbol-13-acetate (TPA), dimethylsulfoxide (DMSO), exogenous gangliosides GM3, GM1, or bovine brain ganglioside mixture (BBG) resulted in a marked inhibition of the growth of cells. The order of the inhibitory potency was TPA greater than GM3 greater than DMSO greater than BBG greater than GM1. In contrast, sulfatides were without effect on cellular replication. Treatment of HL-60 cells with TPA or GM3 induced differentiation along the monocyte/macrophage lineage, while treatment with DMSO induced maturation along the granulocytic pathway. These effects were accompanied by more than a twofold increase in protein kinase C (PKC) activity. In contrast, treatment with GM1, BBG, or sulfatides caused only a relatively small increase in PKC activity. The activity of CMP-N-acetylneuraminic acid:lactosylceramide sialyltransferase (ST1), a key enzyme for membrane gangliosides synthesis, in HL-60 cells was also influenced by the exposure to TPA, GM3, DMSO, GM1, or sulfatides. The inducers of differentiation, TPA and DMSO, caused an increase in ST1 activity, whereas GM3, which also induced cellular differentiation, inhibited ST1 activity, perhaps through the action of end-product inhibition. The non-inducers of differentiation, GM1 and sulfatides, also increased the activity of ST1, but to a much lesser extent. The findings suggest that the direct or indirect modulation of PKC activity by some of these agents may be involved, at least in part, in the regulation of cellular growth and differentiation. Furthermore, it is conceivable that differences in PKC activity may be responsible for the changes in ST1 activity associated with cell differentiation and proliferation.
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PMID:Effects of inducers of differentiation on protein kinase C and CMP-N-acetylneuraminic acid:lactosylceramide sialyltransferase activities of HL-60 leukemia cells. 271 23

Cholera holotoxin produces both stimulation and inhibition of the growth of different cell populations. These opposite effects were both attributed to the enzymatic activity of the subunit A that activates adenylate cyclase, increasing the intracellular level of cAMP. We observed that the B subunit of cholera toxin produced by itself an inhibition of the 'in vitro' growth of two murine leukemia cell lines (L1210 limphoid leukemia and WEHI-3B myelomonocytic leukemia). The sensitivity of WEHI-3B cells towards cholera toxin was about 5000-times higher than that of the L1210 cells, whereas the two leukemias showed an identical sensitivity to the B subunit (IC50 = 5.10(-10) M for L1210 and 10(-10) M for WEHI-3B). The inhibition produced by the B subunit was neutralized by GM1 and in a minor degree by type II gangliosides. The two leukemias showed a remarkable difference in their gangliosides contents (L1210 cells contained GM1 (80.6%) and GM2 (19.4%), while WEHI-3B cells contained GM1 (28.2%), Fuc-GM1 (44.9%) and a band (26.9%) with a chromatographic mobility between GD1a and GD1b). The inhibition could be explained by a competitive mechanism between the B subunit and some autocrine factor binding GM1-containing receptors. Our data strengthen the suggestion to consider gangliosides as very important pleiotropic biomodulators.
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PMID:Inhibition of murine leukemia (WEHI-3B and L1210) proliferation by cholera toxin B subunit. 280 81

A method that could be facilitated for the quantitation and qualitation of gangliosides in human plasma was developed and applied in the present study for characterization of ganglioside patterns in plasmas of patients with neoplastic diseases including gastric cancer, adult T-cell leukemia (ATL), and acute lymphocytic leukemia (ALL). As a retrovirus-infected disease with different clinical entity, human T-cell lymphotropic virus type I-associated myelopathy (HAM) was also subjected to this study. The results were compared with the patterns obtained from normal control plasmas. The analytical data revealed that GM3 increased in gastric cancer, GT1b decreased in HAM and ATL, and GD3, GM1 and GM3 decreased in ALL. There were close correlations between various human diseases and the presence of gangliosides with their specific patterns. Furthermore, gangliosides purified from plasma of patients with HAM significantly inhibited the expression of CD4 antigen on human T lymphocyte membrane. Therefore, analytical studies of plasma gangliosides could provide diagnostic and therapeutic values in retroviral infections.
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PMID:Diagnostic value of ganglioside patterns in plasma of human diseases. 280 80

Spleen cells from acutely diabetic (AD) and non-diabetic but diabetes prone (DP) BB/Wor rats lysed insulinoma target cells to a significantly greater degree than did diabetes resistant (DR) cells as determined using a 51Cr release cytotoxicity assay. There were no differences between the AD and DP groups. Lysis was not target cell specific, since somatostatin secreting RIN 14B cells, Wistar Furth leukemia cells designated LW12, PC12 cells and NK sensitive YAC-1 cells were also lysed. Lysis of all target cells was significantly reduced by pretreatment of the effector lymphocytes with antiserum to NK cells (anti-asialo GM1) and complement suggesting that NK cells mediated destruction of these cells. These data demonstrate a generalized increase in non-specific NK cell activity in BB/Wor rats. Since NK cells have been shown to mediate antibody dependent cell mediated cytotoxicity (ADCC), splenic lymphoid cells from AD rats were tested for their ability to lyse insulinoma target cells in the presence of diabetic rat sera which were demonstrated to contain islet cell surface antibodies. Three different ADCC protocols were tested but in each case the addition of serum dilutions from AD rats reduced the lysis of insulinoma cells by AD spleen cells in a dose dependent manner. This inhibition was also demonstrated when sera and effector cells from control rats were used. As a positive control, DR spleen cells were incubated with 51Cr labelled target cells that were untreated or pre-treated with anti-rat class 1 antibody (OX18). Pre-treatment of the target cells resulted in a marked increase in their subsequent lysis.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:In vitro natural killer cell activity in the spontaneously diabetic BB/Wor rat: effects of serum on lysis of insulinoma cells. 285 69

Bone marrow-derived leukocytes of murine epidermis can express two phenotypes: typical Langerhans cells, which are Ia+ and Thy-1-, and a recently discovered second population that is Thy-1+ and Ia-. To verify that these phenotypes are expressed by two different cell types, and to help understand their lineage and function, we have studied morphology and reactivity with a large panel of antibodies. Dual antibody immunofluorescence combined with electron microscopy showed that Thy-1+ and Ia+ cells were each distributed in a regular fashion and formed adjacent dendritic systems in or close to the basal layer. Double-labeling studies with anti-Ia and a second monoclonal antibody revealed that all Langerhans cells expressed F4/80 (macrophage), Mac-1 (C3bi receptor), and 2.4G2 (Fc receptor), as well as the thymus leukemia (TL) and heat-stable (M1.69/16) antigens. A large fraction expressed S100 and all exhibited membrane ATPase and nonspecific esterase. In contrast, Thy-1+ cells lacked all these features of Langerhans cells, except that a minority were strongly reactive with 2.4G2. Thy-1+ cells also lacked differentiation antigens of most other types of leukocytes, except they were rich in asialo GM1. By electron microscopy, Thy-1+ cells had cytoplasmic granules that were similar in structure and in their aryl sulfatase content to those previously described in natural killer cells. The granules were enlarged in beige mice, suggesting a lysosomal origin, and were present in mast cell-deficient W/Wv mice, indicating no relation to mast cells. We conclude that Thy-1+ epidermal cells are thoroughly distinct from Langerhans cells. On the basis of morphology and phenotype, they may represent a type of tissue natural killer cell. Thy-1+ natural killer cells are now being identified in several nonlymphoid sites, such as gut epithelium and the livers of mice given adjuvants. If Thy-1+ epidermal cells prove to be natural killer cells, it is noteworthy that they represent a resident population regularly distributed in the basal layer of all mouse strains. The notion that Thy-1+ epidermal cells are immature natural killer cells is intriguing in light of recent evidence that Ia+ Langerhans cells are also immature with respect to accessory cell function. The epidermis may not have the functional capacities of a lymphoid organ, but it could contribute immature cells important for both natural and acquired resistance.
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PMID:The Thy-1-bearing cell of murine epidermis. A distinctive leukocyte perhaps related to natural killer cells. 286 Dec 45

Gangliosides (GM3, GD3, GM2, gangliotetraose-series gangliosides) and their asialo derivatives of several adult T-cell leukemia (ATL) cell lines (ATL-1K, ATL-3I, ATL-5S, and MT-2 cells) and the lymphocytes from a patient with ATL were quantified by highly sensitive enzyme-immunostaining on silica gel thin layer chromatograms using specific antiglycolipid antibodies. GM2 and GD3 gangliosides and asialo GM1 (GA1) newly appeared in all cultured ATL cells and the lymphocytes from patients with ATL but not in normal human T-lymphocyte-rich fraction. Gangliotetraose-series gangliosides, GM1a, GD1a and GD1b, were also found in cultured ATL cells, but were not detected in normal human lymphocytes or the lymphocytes of a patient with ATL. Quantitative immunostaining analysis of GM2, GD3 gangliosides and GA1 in T-cell lines from non ATL leukemia (Molt-3, CEM and Jurkat) revealed GM2 gangliosides in all the T-cells from non ATL tested and GA1 in Jurkat cells, but no GD3 ganglioside was found in the non ATL leukemia cells tested. The above results indicate that ganglioside GD3 may be a T-cell glycosphingolipid antigen associated with ATL, and ganglioside GM2 and GA1 may be useful as surface markers related with ATL, as well as T-cell lymphoma. The contents of GA1, GM3, GD3, GM2 and gangliotetraose-series gangliosides in ATL cells were all different, even though all the cells used have a common antigen reactive with monoclonal OKT-4 antibody, indicating that there are several subsets of human inducer/helper T-cells, which possess different metabolism and expression of gangliosides.
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PMID:Aberrant expression of ganglioside and asialoglycosphingolipid antigens in adult T-cell leukemia cells. 289 Jun 14

We previously described the interleukin 3 (IL-3)-dependent cell line, M1-A5, which has both natural cytotoxic (NC) and suppressor cell activities, the latter of which is mediated, in part, by the release of two cytokines which activate suppressor cells from unprimed lymphoid precursor cells. In this study we have compared the M1-A5 cell line with four other IL-3-dependent cell lines to determine whether these dual activities are universally associated with IL-3 dependence and to test the hypothesis that there is a direct relationship between the cytotoxic and the suppressive activities. The cell lines tested were a bone marrow derived Dexter culture derived line (FDC-P1), two Moloney leukemia virus induced leukemias (DA-1 and DA-3), and a mast cell line (PT18(A17]. All lines were dependent on IL-3 for survival but FDC-P1, DA-1, and DA-3 showed varying degrees of short-term proliferation in granulocyte-macrophage colony stimulating factor (GM-CSF). The cell lines all expressed asialo GM1 and Ly-5 surface markers but differed with respect to other markers. DA-1 expressed MAC-1, FDC-P1 and DA-3 expressed Thy-1, and PT18(A17) expressed receptors for the Fc portion of IgE. The cell lines varied greatly in their cytotoxic activity against WEHI-164. FDC-P1, DA-1, and PT18(A17) had low NC activity. DA-3 had consistently high activity, greater than that seen with M1-A5 cells. However, none of the cell lines secreted constitutively a suppressor cell inducing factor (SIF). In addition, it was demonstrated that recombinant murine TNF did not activate suppressor cells capable of inhibiting antibody synthesis and that anti-TNF did not block SIF activity, thus suggesting that TNF contamination of the M1-A5 derived SIF preparation is not responsible for the induction of suppressor cells. We conclude that suppressor cell inducing factors are not universally secreted by IL-3-dependent cell lines, that there is no correlation between NC and SIF activity, and that the dual activities of M1-A5 cells are not mediated by TNF.
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PMID:Secretion of a suppressor cell inducing factor by an interleukin 3-dependent cell line with natural cytotoxic activity. III. Comparison with other interleukin 3-dependent cell lines. 297 53


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