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

Thymocytes from preleukemic mice persistently infected with Moloney murine leukemia virus (MuLV-M-carriers) were vigorously autoaggressive toward normal syngeneic target cells; they exhibited a graded response to allogeneic cells, but they spared xenogeneic cells or syngeneic cells infected with MuLV-M or MuLV-G (Gross). Syngeneic target cells infected with nononcogenic lymphocytic choriomeningitis virus (LCMV), or transformed by the chemical carcinogen 3-methylcholanthrene were not similarly spared. This phenomenon, apparently induced by MuLV-M, is not associated with all persistent virus carrier states. Thymocytes from mice persistently infected with LCMV or with the lactic dehydrogenase virus (LDHV) failed to demonstrate an autoaggressive behavior. That transplantable lymphoma cells (derived from MuLV-M-carriers) were autoreactive in a pattern similar to thymocytes from preleukemic mice suggests a unique role for MuLV in the events leading from altered recognition of "self" to lymphoma.
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PMID:Immunologic mechanisms in the pathogenesis of virus-induced murine leukemia. III. Target cell specificity of autoreactive thymocytes. 18 Jan 78

Most attempts to prolong the survival of allografts have involved treatment of the host to impair its capacity to reject them. Early uncritical attempts to treat the graft rather than the host were received with skepticism because of the prevailing belief that the alloantigens on cell surfaces are immutable. However, over the past decade unequivocal evidence has accumulated that the immunogenicity of allografts is susceptible to alteration. Short-term maintenance in vitro of malignant and normal tissue grafts, such as those of the ovary and thyroid. Weakens their susceptibility to rejection. Various agents have been identified which, when applied to tissues or organs in vitro, have a similar effect. Soaking skin in media containing steroids, urethane, thalidomide, antilymphocyte globulin (ALG), and specific alloantibody is also effective. X-irradiation and perfusion of allogeneic dog kidneys with solutions of concanavalin A or of nucleic acid prepared from the future donor or even from indifferent donors or microoorganisms lead to extended survival. There is also equivocal evidence that soaking mouse skin grafts in RNA prepared from unrelated donors causes them to be treated as allogeneic by syngeneic recipients. Skin from animals suffering from certain diseases displays altered immunogenicity. Skin from mice suffering from virus-induced leukemia or lymphocytic choriomeningitis is frequently rejected by syngeneic recipients. By contrast, skin allografts from some cancer patients and from mice bearing certain tumors give evidence of prolonged survival as do grafts from uremic mice. Some treatments of prospective donors, including cytotoxic drugs, ALG, specific alloantisera, hypoxia, and experimentally produced uremia, also extend the lives of allografts. Trophoblast, a fetal epithelial tissue in immediate contact with maternal tissue, represents a natural example of graft adaptation. Despite its origin from precursor cells with normal transplantation properties, trophoblast fails to elicit transplantation immunity and is unaffected by it. Some of the disparate agents or procedures described here probably act by modifying grafts in such a way that they are more likely to evoke "blocking" or enhancing antibodies rather than the usual destructive cellular immunity, and many of them deplete the grafts of immunogenically effective "passenger" leukocytes. Both of these processes contribute to apparent hypoantigenicity.
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PMID:The feasibility of altering the immunogenicity of grafts. 81 91

A new human leukemia cell line, designated as ME-1, was established from the peripheral blood leukemia cells of a patient with acute myelomonocytic leukemia with eosinophilia (M4E0). This cell line has the characteristic chromosome abnormality of M4E0, inv(16) (p13q22). When cultured in RPMI 1640 medium containing 10% fetal calf serum, ME-1 cells were monoblastoid, but with the addition of cytokines such as interleukin-3 (IL-3), granulocyte-macrophage colony-stimulating factor (GM-CSF), IL-4, or medium conditioned by phytohemagglutinin-stimulated human peripheral leukocytes (PHA-LCM), the cells exhibited differentiation to macrophage-like cells. PHA-LCM also promoted eosinophilic-lineage differentiation of this cell line, although IL-5 did not do so. To elucidate the mechanism of proliferation and differentiation of ME-1 cells, we studied the effect of a potent inhibitor of protein kinase C, 1-(5-isoquinolinyl-sulfonyl)-2-methylpiperazine (H-7), on colony formation of ME-1 cells. H-7 inhibited colony formation of ME-1 cells by IL-3 or GM-CSF dose dependently, but had little inhibitory effect on colony formation by IL-4. These results indicate that the proliferation and differentiation of ME-1 cells by IL-3 or GM-CSF were related to the activation of protein kinase C, while those by IL-4 involved other regulatory systems. ME-1 cells should be useful for studying the pathogenesis of M4E0 and the mechanisms of proliferation and differentiation of leukemic and normal progenitors by cytokines.
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PMID:Establishment and characterization of a new human leukemia cell line derived from M4E0. 207 80

The effect of erythropoietin (Epo) on colony formation by blast progenitors in acute myeloblastic leukaemia other than erythroleukaemia was studied using a blast colony assay. Epo alone did not induce colony formation, but when it was used together with phytohaemagglutinin-stimulated leucocyte-conditioned medium (PHA-LCM) the number of leukaemic colonies significantly increased in nine out of 12 cases studies. Preincubation of Epo with anti-Epo antibody completely abolished this enhancement, indicating that the increase in colony numbers was caused by Epo itself. Cell surface phenotype analysis of colonies produced by Epo plus PHA-LCM showed no increase in percentages of erythroid and megakaryocyte lineages. The addition of Epo also increased the self-renewal capacity of leukaemic blast cells. Fresh leukaemic cells did not express Epo receptors, but they were induced after incubation with PHA-LCM. The present study thus showed that the proliferative response to Epo is not restricted only to the erythroid lineage, but also extends to AML blast cells other than those in erythroleukaemia in the presence of colony stimulating factors.
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PMID:Enhanced growth of clonogenic cells from acute myeloblastic leukaemia by erythropoietin. 237 25

The activity of adenosine deaminase was determined in the cerebrospinal fluid in children with acute lymphoblastic leukaemia in various phases. It was found that an evident rise of this activity occurred during leukaemic meningeal involvement as compared with the initial phase the disease or with the first complete remission. After an episode of recurrent cerebrospinal leukaemia the activity of the enzyme was also higher than during the first complete remission. Such high values as during meningeal leukaemia were not found in inflammatory cerebrospinal fluid which suggests that determinations of this enzyme could be useful for differentiation of leukaemic infiltrations in the central nervous system against lymphocytic meningitis.
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PMID:[Adenosine deaminase activity in the cerebrospinal fluid of children with acute lymphoblastic leukemia]. 263 33

The in vitro effect of recombinant human GM-CSF (rHuGM-CSF) was tested on bone marrow-derived multilineage (CFU-GEMM) as well as megakaryocytic (CFU-Mk), erythroid (BFU-E), and granulocyte-macrophage (CFU-GM) progenitors in a group (n = 16) of patients with myelodysplastic syndromes (MDS). Hematopoietic progenitor cell growth was markedly impaired in MDS patients as compared to normal controls (p less than 0.05, at least). Recombinant HuGM-CSF supported the growth of CFU-GEMM, CFU-Mk, and BFU-E at lower, equivalent, or slightly higher frequencies that those found in cultures plated with medium conditioned by peripheral blood leukocytes (PHA-LCM), but it was invariably ineffective in improving growth values. Recombinant HuGM-CSF supported the growth of granulocyte-macrophage colonies in 15 of 16 cases. The overall incidence (mean +/- SEM) of CFU-GM in cultures containing rHuGM-CSF (5 ng/ml) was significantly higher than the one found in cultures stimulated with PHA-LCM (40 +/- 15 vs. 17 +/- 7, p less than 0.05). Upon culture with rHuGM-CSF (5 ng/ml), in 5 of 15 patients de novo colony formation was observed (8 +/- 4) and in 4 of 15 patients CFU-GM growth (129 +/- 33) fell within normal range. Doses of rHuGM-CSF higher than 5 ng/ml did not result in a further increase of MDS-derived colony formation. It is concluded that rHuGM-CSF (a) does not improve the growth of CFU-GEMM, CFU-Mk, and BFU-E; (b) may completely restore the growth of CFU-GM in a subgroup of MDS patients; (c) while ineffective in improving anemia and thrombocytopenia, its in vivo in MDS may correct leukopenia through an effect at the level of granulocyte-macrophage progenitor cell compartment, at least in a subset of highly responsive patients.
Leukemia 1989 May
PMID:Growth of human hematopoietic colonies from patients with myelodysplastic syndromes in response to recombinant human granulocyte-macrophage colony-stimulating factor. 265 96

In groups of 26 patients with myeloproliferative disorders (MPD), 8 with chronic myelogenous leukaemia (CML); 8 with polycythaemia vera (PV); 10 with essential thrombocythaemia (ET); and 6 patients with reactive thrombocytosis (RT), we studied the growth characteristics of bone marrow CFU-M in agar culture. The bone marrows from all the patients with MPD formed so called endogenous CFU-M colonies, in the absence of PHA-LCM, that increased in a dose-dependent manner with the addition of increasing concentrations of normal human AB-citrated plasma (NH-ABCP), while the bone marrows from all the patients with RT and from healthy controls formed few or no endogenous CFU-M colonies. In MPD, the endogenous CFU-M growth was enhanced by normal T cells in a dose-dependent fashion, and was decreased with the depletion of T cells from the marrow cells. These results suggest that the formation of endogenous CFU-M colonies is caused by hypersensitivity of CFU-M in MPD to NH-ABCP, which may contain a small amount of Meg-CSF, and/or by in vitro T cell stimulation. Among MPD, the endogenous CFU-M growth in ET was significantly lower than that of other MPD patients; however, the total number of ET CFU-M grown in the presence of PHA-LCM was the highest. These data show that the bone marrow CFU-M in MPD are heterogeneous with respect to in vitro growth pattern or sensitivity to exogenous Meg-CSF.
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PMID:Heterogeneity of in vitro growth pattern of megakaryocyte progenitors (CFU-M) in myeloproliferative disorders. 341 10

The effect of retinoic acid (RA) alone and in combination with cytosine arabinoside (Ara-C) on differentiation of fresh human myeloid leukaemic cells from patients with AML was studied. Cells from six patients: three with acute myelomonocytic leukaemia AMMoL and three with acute monoblastic leukaemia AMoL with a percentage of blasts greater than 70, were treated in an in vitro primary suspension culture with retinoic acid (10(-7) M), cytosine arabinoside (100 ng/ml) or both in combination. Non-adherent mononuclear cells were seeded at a concentration of 5 x 10(5) cells/ml in RPMI 1640 culture medium supplemented with 20 per cent fetal bovine serum and 10 per cent (PHA-LCM) phytohaemagglutinin leucocyte conditioned medium and incubated for 6 days at 37 degrees C in a humidified incubator containing 5 per cent CO2 in air. Morphological and functional differentiation into terminal mature elements was induced in all leukaemia cells of the six patients following exposure to the combination of both agents. These results suggest the potential usefulness of the combination of a differentiating agent (retinoic acid) and an antileukaemic drug (cytosine arabinoside) in the treatment of acute myeloid leukaemias: AMMoL and AMoL. This combination warrants a clinical trial.
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PMID:Retinoic acid alone and in combination with cytosine arabinoside induces differentiation of human myelomonocytic and monoblastic leukaemic cells. 342 32

Persistent infection with lymphocytic choriomeningitis (LCM) virus activates a phenotypic expression of murine leukemia viruis-related antigen. NZB and (NZB x NZW)F(1) mice, which normally carry large amounts of Gross virus, and C57BL/6 and NZW mice, which normally carry little virus, were infected with LCM virus. All had Gross soluble antigen in their plasmas at 3 months of age, while noninfected matched controls of all strains did not. This effect was seen after infection with LCM virus that was tissue passed or plaque purified. Similarly, cultures of mouse-embryo fibroblasts produced Gross soluble antigen when infected with LCM virus, but noninfected cultures failed to do so.
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PMID:Activation of spontaneous murine leukemia virus-related antigen by lymphocytic choriomeningitis virus. 433 Apr 71

Central nervous system (CNS) involvement is a rare complication of chronic lymphoid leukaemia (CLL). The occurrence of lymphocytic meningitis in the course of CLL suggests either CNS involvement by the leukaemic process or infection (especially tuberculosis) related to continuous immunodepression. We report a case of CLL in which leukaemic cells had surface IgM and produced IgM kappa without significant depression of other immunoglobulins. When the patient developed meningitis, measurement of serum and CSF albumin IgG and IgM levels showed that 88% of CSF IgM resulted from local synthesis, while 70% of CSF IgG resulted from serum transsudation. These results suggest that a large number of neuromeningeal lymphoid cells produce the same class of IgM as leukaemic cells and therefore constitute a localization of the disease. Complete remission of the meningitis by intrathecal anti-leukaemic chemotherapy confirmed this hypothesis.
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PMID:[Cerebromeningeal location of chronic lymphoid leukemia. Rapid immunochemical diagnosis and complete remission by intrathecal chemotherapy]. 622 82


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