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)

Bone marrow lymphoblasts from 109 children admitted with untreated acute lymphoblastic leukemia (ALL) were tested for spontaneous rosette formation with sheep erythrocytes. Twenty-six children (24%) had lymphoblasts that formed rosettes (E+). Of 13 initial clinical characteristics, 8 were significantly associated with E+ lymphoblasts: mediastinal enlargement (86% of patients E+), leukocyte counts over 100 X 10(9)/liter (65% E+), nodes greater than 2 cm in any diameter (65% E+), age over 5 yr (46% E+), hemoglobin over 8 g/dl (44% E+), hepatomegaly greater than 5 cm (38% E+), boys (35% E+), and lymph node enlargement outside of the cervical area (28% E+). Spleen size, initial platelet counts, and periodic acid-Schiff scores did not distinguish E+ from E- patients. Since few patients were black and few presented with central nervous system leukemia, the association of these two characteristics with E+ blasts could not be determined. A hierarchical classification scheme and a linear logistic regression model were used to define the patterns of characteristics associated with E+ lymphoblasts. The initial clinical characteristics and the poorer course of E+ patients suggest that ALL comprises at least two biologically and clinically distinct types. The E+ ALL may result from a leukemic transformation of a non-Hodgkin lymphoma.
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PMID:Initial prognostic factors and lymphoblast-erythrocyte rosette formation in 109 children with acute lymphoblastic leukemia. 26 81

Spleen cells from normal, nonimmune, CBA or (CBA X AKR)F1 mice markedly and rapidly inhibited the incorporation of [3H]thymidine by two different T-cell lymphomas in an in vitro cytostasis assay. These were the I-529 lymphoma of spontaneous AKR origin and the Moloney murine leukemia virus-induced YAC lymphoma of A mouse origin. Spleen cells were the most efficient inhibitors for both types of target cells, whereas lymph node cells were much less active and thymus cells showed little or no activity. Granulocytes, as well as conventional T- and B-lymphocytes, were excluded as important contributors to the cytostatic cell population. Spleen cells were separated on nylon wool, Sephadex G-10 columns, or plastic petri dishes and tested for activity in the cytostasis assay or for cytotoxicity against 51Cr-labeled lymphoma target cells. Adherent cells carried almost all cytostatic activity against the AKR lymphoma but also showed significant cytotoxic activity against these target cells. In addition, the cytostatic activity against the YAC lymphoma was mainly due to adherent spleen cells, but nonadherent cells were relatively more active against this target than against I-529 cells. Such nonadherent spleen cells further showed increased cytotoxic activity, compared to the whole spleen cell population.
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PMID:Natural cell-mediated immunity to lymphoma cells. I. Characteristics of effector cells in a cytostasis assay in vitro. 30 67

A spontaneous BALB/c B lymphocyte leukemia could be stimulated in vitro by the polyclonal B cell activator lipopolysaccharide (LPS) and the conditions for activation were studied. Spleen cells or peripheral blood lymphocytes from tumor-bearing animals responded by increased DNA synthesis and the peak of activation occurred earlier than with normal mouse spleen cells. Tumor cells harvested from the spleen, but not from the peripheral blood, could be induced by LPS to secrete IgM. Direct demonstration that the response was due to tumor cell activation and not that of contaminating normal B lymphocytes was provided by karyotype analysis and by immunoprecipitation, which showed the restriction of light chains on secreted IgM molecules to the lambda isotype.
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PMID:Characterization of a spontaneous murine B cell leukemia (BCL1). II. Tumor cell proliferation and IgM secretion after stimulation by LPS. 38 13

Cell-mediated immunity to Moloney murine leukemia virus (M-MuLV) and to tumor-associated surface antigens of leukemia cells induced by the virus was studied with an in vitro migration inhibition factor assay. Spleen cells of C57BL/6N mice at Day 14 following inoculation with Moloney murine sarcoma virus, produced migration inhibition factor in response to M-MuLV. The Moloney murine sarcoma virus-immune spleen cells, however, did not respond to other murine type C viruses, to AKR and Rauscher viruses, or to murine mammary tumor virus. The immune spleen cells also responded specifically to purified glycoprotein with molecular weights of 69,000 and 71,000 and proteins with molecular weights of 30,000 and 12,000, but not to protein with a molecular weight of 10,000, of the homologous M-MuLV. Migration inhibition factor production was also observed in response to soluble 3 M KCl extracts of leukemia cells, MBL-2, induced by M-MuLV. Similarly, the immune spleen cells responded to membrane fractions purified from the MBL-2 cells. Comparable membrane fractions prepared from a Gross virus-induced leukemia, E male G2, and a radiation-induced leukemia, RL male 1, were not active. The tumor-associated surface antigens of MBL-2 membranes could be solubilized by the detergent, Nonident P-40. Thus, C57BL/6N mice inoculated with Moloney murine sarcoma virus developed cell-mediated immunity to envelope and some internal antigens of M-MuLV and also to tumor-associated surface antigens of a tumor induced by this leukemia virus.
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PMID:In vitro studies of cell-mediated immunity to Moloney murine leukemia virus and Moloney leukemia-associated surface antigens. 38 18

The ultrastructure of T and B lymphocytes has been examined in long-term syngeneic chimaeras and age-control mice. Spleen cell suspensions from these mice were passed through glass wool columns to obtain pure lymphocyte populations. These cells were then separated into T and B lymphocytes by nylon wool columns, and their purity was tested by cytotoxicity assays with anti-phi serum. Electron microscopic observations on such separated T and B lymphocytes did not reveal morphological differences except when the cells were fully differentiated, either as mature (T2) cells or plasmacells. In particular, T2 cells showed a very high cytoplasmic density, attributable to the presence of a larger number of microfilaments with respect to immature (T1) cells. In long-term chimaeras a significantly larger number of T2 cells was found as compared to age-control mice, and this morphological observation is correlated with the differences in immune reactivity and leukemia incidence previously described in these mice.
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PMID:Electron microscopic observations on T and B lymphocytes from spleens of syngeneic radiation chimaeras. 79 64

Spleen cells from normal (C57BL/6 X DBA/2)F1 mice were sensitized in vitro for 5 days with irradiated C57BL/6 or DBA/2 parental stimulating cells. Effector cells were generated which specifically lysed 51Cr-labeled targets (leukemia or mitogen-stimulated lymphoid cells) H-2-matched with the parental genotype used for sensitization. The response of F1 spleen cells to the C57BL/6 parent was stronger and more reproducible than that to the DBA/2 parent. The kinetics of generation of effector cells were similar for the F1 anti-parent and an F1 anti-allogeneic response. However, the magnitude of the F1 anti-C57BL/6 cytotoxic response was considerably lower than the F1 response to allogeneic cells. The ratio of responder to stimulator cells in the cultures was more critical for the former than for the latter response. Several lots of fetal bovine serum were found to be adequate for supplementing the medium in the induction of J1 hybrid anti-parent and anti-allogeneic cytotoxic effector cells. Based on these and other studies, it would appear that the F1 hybrid anti-parent cytotoxic response provides an in vitro model of murine hemopoietic graft rejection in vivo. This response may be elicited by a mechanism distinct from T cell-mediated cytotoxicity and involve different subpopulations of spleen cells.
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PMID:In vitro induction of F1 hybrid anti-parent cell-mediated cytotoxicity. 95 51

The effect of Corynebacterium parvum on the immune response of C57BL/6 mice (H-2b) to the allogeneic leukemia L1210 (H-2d) was investigated. Mice were either left untreated or given C. parvum i.v. or i.p. in various dosages. Seven days later they were challenged with 2.5 to 10 X 10(6) live L1210 cells i.p. Control animals almost always rejected the challenge. In contrast, most mice pretreated with either 1.0, 0.5, or 0.25 mg of C. parvum i.v. and 1.0 or 0.5 mg i.p. exhibited enhanced growth of leukemia L1210 as indicated by gross ascites and significantly greater weight gain. This sometimes progressed to the death of the animal, but more often regressed after several days. Spleen cell-mediated cytotoxicity to alloantigens, evaluated in vitro by release of 51Cr from P815Y (H-2d) target cells, was significantly decreased in the mice pretreated with either 1.0 or 0.5 mg of C. parvum i.v. or 0.5 mg of C. parvum i.p. This suppression could not be reversed by reduction of the concentration of macrophages in the spleen cell suspensions. Complement-dependent cytotoxic antibody, measured by release of 51Cr from L1210 cells, was profoundly suppressed in mice pretreated with C. parvum i.v. in dosages ranging from 1.0 to 0.1 mg. These data suggest an immunological basis for the enhanced growth of leukemia L1210 caused by C. parvum at these schedules.
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PMID:Immunological enhancement of leukemia L1210 by Corynebacterium parvum in allogeneic mice. 97 53

It has previously been demonstrated that an in vitro antineoplastic treatment may induce new antigenic specificities in murine lymphomas. L1210 leukemia has been altered by DIC (L1210/DIC); drug-treated L1210 subline has been rejected by syngeneic animals. Here spleen cells from mice, normal or immune to L1210/DIC, have been stimulated in vitro by the L1210/DIC cells as measured by 3-h-thymidine uptake. Spleen cell stimulation did not occur with other syngeneic tumor cells and, as expected, spleen cells have been triggered by allogeneic cells. DIC-induced antigens stimulating syngeneic lymphocytes, as allogeneic cells did, have been demonstrated on L1210/DIC cells.
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PMID:[Pharmacological alteration of the antigenic properties of experimental leukemias detected by lymphocyte transformation]. 102 82

Lipid constituents were examined in the spleen of mice 10, 14 and 18 days after infection with Rauscher leukaemia virus. (i) The total lipid content, as related to the amount of protein, decreased with the development of the tumour. (ii) Spleen cells of control and infected mice synthesized the same lipids. (iii) In the infected spleen, free fatty acids increased by 80% and triglycerides decreased by 44% as compared to the control. The percentage distribution of phospholipid components showed a change in tumour cells: lecithin and phosphatidylethanolamine increased, lysolecithin and sphingomyelin decreased. (iv) After intraperitoneal injection of [32P] orthophosphate, in infected mice the incorporation of 32P into phosphatidylcholine and phosphatidylethanolamine increased, while 32P incorporation into lysophosphatidylcholine + sphingomyelin and phosphatidylinositol + phosphatidylserine fractions decreased.
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PMID:Lipid composition of the mouse spleen in Rauscher leukaemia. 105 75

Spleen cells from 2- to 3-month-old normal mice of some strains having a low incidence of spontaneous leukemia were found to lyse cells of the spontaneous AKR leukemia K36 in the 51Cr release assay. Incubation of 51Cr-labeled ADR K36 cells with spleen cells from normal C57BL/6, C57L, C57BL/10, and RF mice resulted in the release of significantly more 51Cr than that released in the presence of medium alone. In contrast, 51Cr released from AKR K36 cells after incubation with spleen cells from mice of the high leukemic strains AKR and C58 was less than that released spontaneously. The results of competitive inhibition tests when C57BL/6 spleen cells were incubated simultaneously with 51Cr-labeled AKR K36 target cells and varying numbers of nonlabeled cells demonstrated that the cytotoxic activity of normal C57BL/6 spleen cells was directed against an antigen(s) associated with several leukemias, but that was undetectable on normal thymocytes. Pretreatment of C57BL/6 spleen cells with carbonyl iron and a magnet, which removed phagocytic macrophages, did not decrease the cytotoxic acitivity for AKR K36 cells.
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PMID:Lysis of leukemia cells by spleen cells of normal mice. 105 93


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