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)

Mouse thymocytes and spleen cells from unprimed C57BL/6 donors generate broadly reactive cytotoxic cells during 5 days of culture in vitro with polyinosinic acid (5') (poly(I] and/or supernatant from PMA-treated EL4 leukemia cells which contains interleukin 2 (IL-2) activity. We refer here to such cytotoxic cells as "supplement-induced cytotoxic cells" or SICC. Thymocytes are dependent on the supernatant factor(s), whereas spleen cells are usually stimulated by poly(I) alone. Polyinosinic acid acts synergistically with supernatant factor(s) to stimulate generation of SICC by both thymocytes (SICC-T) and spleen cells (SICC-S) when the IL-2 activity of the supernatant is inadequate alone. SICC can be generated by both splenocytes and thymocytes in medium supplemented with fetal calf serum or syngeneic plasma. SICC are active in 4 hr 51Cr-release tests against syngeneic, allogeneic, and xenogeneic tumors but not against lipopolysaccharide-induced lymphoblasts. Embryonic fibroblasts, too, are sensitive to SICC generated by thymocytes. In complement-dependent depletion tests, cytotoxic activity is partially sensitive (SICC-T) or fully sensitive (SICC-S) to anti-Thy-1 and -H-2 but not to anti-Lyt-1, -Lyt-2, or -asialo GM1.
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PMID:Supplement-induced cytotoxic cells (SICC) generated from mouse thymus or spleen cells cultured in the presence of interleukin 2 and/or polyinosinic acid. 660 5

Leukemias were induced by 7,12-dimethylbenzanthracene feeding of intact, thymectomized, or Freund's adjuvant-pretreated SJL mice. Four of six Thy-1-positive thymomas that arose in intact mice had a pseudodiploid stemline with one morphologically similar or identical marker. Banding analysis showed that the marker had arisen by the translocation of the distal part of one chromosome 15 to one X chromosome [t(X;ter 15)]. Two normal No. 15 chromosomes were also present in the same metaphase plates. These four Thy-1-positive lymphomas were thus trisomic for the distal part of chromosome 15. All 8 Thy-1-negative lymphomas, originating in the spleen or lymph nodes of thymectomized or adjuvant-pretreatment mice, had a trisomy of chromosome 12 and also a trisomy of either chromosome 3 or chromosome 18. These results further stress the importance of gene dosage effects, related to the distal part of chromosome 15, in Thy-1-positive T-cell leukemogenesis. The cytogenetic difference between the Thy-1-positive and -negative leukemias supports our hypothesis that nonrandom chromosomal changes in murine leukemias are dependent on the target cell type, rather than the inducing agent.
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PMID:Nonrandom chromosomal changes in thy-1-positive and thy-1-negative lymphomas induced by 7,12-dimethylbenzanthracene in SJL mice. 677 Oct 2

Neoplastic thymocytes from rat thymic lymphoma-leukemias induced by the rat-adapted Gross-leukemia virus (RAGV) were analyzed for a variety of differentiation markers to define their differentiation state and possible cellular origin. A majority of thymocytes from leukemic rats had the phenotypic characteristics of subcapsular cortical thymocytes that are the most ancestral of the thymocytes. These cells exhibited readily detectable levels of Thy-1 and histocompatibility antigens on their surfaces, they contained terminal deoxynucleotidyl transferase (TdT) and they contained low adenosine deaminase (ADA) and high purine nucleoside phosphorylase (PNP) specific activity. The leukemic thymocytes also contained a sub-band of the LDH-5 isozyme (LDH-5') that was not detected in normal thymocytes but that was present in lymphocyte-rich fractions of postnatal bone marrow, fetal and prepubertal spleen, and fetal and neonatal liver. The tissue distribution and ontogeny of LDH-5'-containing cells is similar to prethymic TdT+ cells in the rat and both TdT and LDH-5' are enriched in a subset of bone marrow "null" cells. These results suggest that TdT+ thymocyte progenitors or their precursors are the targets of leukemic transformation of RAGV.
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PMID:Evidence for the cellular origin of Gross virus-induced leukemia in the rat: description of a unique LDH isozyme sub-band in leukemic lymphoid cells and lymphohemopoietic precursor cells. 677 89

One of the characteristic cellular immune responses associated with the regression of Moloney leukemia/sarcoma virus-induced tumors is a T cell proliferative response against the major viral envelope glycoprotein, gp70. The results described here demonstrated that associated with this proliferative response is the production of a lymphokine, Interleukin 3 (IL-3). The production of IL-3 was immunologically specific and showed the same specificity as that observed in blastogenic responses. IL-3 production was dependent upon an antigen-specific Thy-1.2+, Lyt-1+, 2- lymphocyte subpopulation but did not require the presence of an Ia+ or an adherent accessory cell. The results also suggested that IL-3 may constitute one of the blastogenic factors previously shown to be involved in the proliferative response to gp70. In particular, purified IL-3 was found to induce proliferation of both normal and immune nylon wool purified splenic lymphocytes. The phenotype of the responding lymphocyte subpopulation was Thy-1.2-, Lyt-1-, 2-, Ig-, and Ia-. Maximal IL-3 production occurred approximately 48 hr after the addition of antigen and its production was significantly blocked by mitomycin C. These characteristics were unlike those for the general production of blastogenic factor activity suggesting that IL-3 is responsible for only a minor component of the proliferative response.
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PMID:T cell recognition of Moloney leukemia virus proteins. III. T cell proliferative responses against gp70 are associated with the production of a lymphokine inducing 20 alpha-hydroxysteroid dehydrogenase in splenic lymphocytes. 679 77

We have identified previously a quantitatively minor membrane protein (p28) with an apparent reduced m.w. of 28,000, which is biosynthetically labeled in activated human lymphocytes. Rabbit antisera with activity directed against p28 (alpha-ATC) were prepared and p28 was identified by immunoprecipitation in NP-40 extracts of activated, extrinsically labeled lymphocytes. p28 was not expressed in appreciable amounts by unstimulated T cells, stimulated or unstimulated B cells, null cells, or adherent cells. Protein p28 was only minimally represented on resting thymocytes but was easily detected on 4-hr activated thymocytes and the T lymphoblastoid cell lines HSB2 and MOLT-4. Absorption and immunoprecipitation studies with alpha-ATC indicated that p28 was not present on erythrocytes, platelets, neutrophils, six B cell lines, six null cell lines, and seven other T lymphoblastoid cell lines. Protein p28 from HSB2 cells was absorbed by lentil lectin, concanavalin A, and wheat germ agglutinin affinity columns and was eluted with the appropriate sugars. Gel filtration column chromatography of unreduced p28 in the presence of 0.5% NP-40 or 0.1% deoxycholate gave elution characteristics consistent with a m.w. of approximately 60,000 to 100,000. In preparative isoelectric focusing (IEF) studies the isoelectric point (pI (p28) = 5.2 to 6.1) was similar or identical to that described for the reduced and denatured protein in two-dimensional polyacrylamide gels (pI = 5.5 to 6.2). Protein p28 was eluted from DEAE-cellulose (Whatman DE-52) ion exchange columns at 0.05 to 0.15 M NaCl. Experiments with monoclonal antibodies or heteroantisera specific for other T cell and B cell antigens and various lymphoblastoid cell lines and normal peripheral blood cells indicated that p28 is distinct from the human Ia-like antigens, from T3, T4, T5, T8, and from several other reported human T cell antigens that appear to correspond to Thy-1, the sheep erythrocyte receptor, and a human thymus-leukemia antigen.
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PMID:Properties of a surface antigen expressed on activated human thymus-derived lymphocytes. 680 Nov 23

Five rat leukemia cell lines induced with chemical agents and/or leukemia viruses were investigated in terms of their surface antigens. One of them, KNL-14, which was induced with 1-butyl-1-nitrosourea in WKA rats had RT1-B region-associated antigens on the cell surface. In addition, Thy-1.1 antigens and surface and cytoplasmic mu chains were detected by serological and immunochemical means. From the results it was concluded that this leukemia originated from immature B cells. In the present work, RT1 antigens on the KNL-14 cells were further investigated. The class I and class II antigens were examined and KNL-14 cells were found to have phenotypical antigens and immunogenicity similar to those of B cells from the WKA lymph nodes. As for class II antigens, which are responsible for various immunologic functions, two specificities were detected, Ba-1.2 and Ba-2.7. These KNL-14 cells should be useful for studying the process of rat B cell differentiation and for immunochemical studies of the rat MHC gene products.
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PMID:Chemically induced rat B cell leukemia KNL-14, and its major histocompatibility complex products. 681 90

Monoclonal antibodies against a thymus cell differentiation antigen (Thy-1.1) were effective in the therapy of a transplanted mouse leukemia. Passive immunization resulted in high titers of cytotoxic antibody in the serum of treated mice and the suppression of metastatic tumor cells. The tumor-suppressive effects of the monoclonal antibodies were amplified by the administration of exogenous complement. This combined antibody and complement therapy resulted in the cure of leukemia in a significant proportion of the treated animals.
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PMID:Mouse leukemia: therapy with monoclonal antibodies against a thymus differentiation antigen. 696 28

Potentially leukemic cells have been identified among bone marrow cells of AKR/J mice from the age of 14 days onward. Transfer of AKR/J bone marrow into irradiated hybrid mice (AKR/J X DBA/2)F1 caused a high leukemia incidence (50-100%) of AKR origin, very often within a short latent period. Similar transfer of AKR/J marrow into irradiated AKR/J recipients did not enhance spontaneous tumor development. In contrast to the leukemic AKR cells that express the T-cell surface component Thy-1.1, the potential leukemic cells among bone marrow cells of young AKR mice were shown to lack the expression of this antigen. The development of preleukemic AKR marrow into overt leukemia in hybrid mice was dependent on the presence of an intact thymus and exposure of the recipients to x-rays shortly before marrow transfer. Evidently, preleukemic AKR bone marrow undergoes sequential changes, affected by host factors, leading ultimately to development of overt leukemia.
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PMID:Potential leukemic cells among bone marrow cells of young AKR/J mice. 696 16

Antisera to the 1-butyl-1-nitrosourea-induced "non-T, non-B" rat leukemia line DBLA-6 were raised in rabbits. Following absorption with syngeneic hepatoma cells, the antisera were very similar in specificity to antisera raised to rat Thy-1 antigen. Anti-DBLA-6 serum was cytotoxic in the presence of complement against 70 to 90% of thymocytes and 40 to 50% of neonatal spleen cells. In contrast, no significant cytotoxicity was observed against cells from bone marrow, lymph node, spleen, and peritoneum. An absorption test revealed that an antigen recognized by anti-DBLA-6 serum was present in brain tissue but absent in liver and kidney tissues. Nineteen rat leukemias and lymphomas were divided into six groups based on antigenic and morphological characteristics and the presence of receptor for guinea pig red blood cells. These tumors were investigated for the presence of the antigen recognized by anti-DBLA-6 serum. Of the leukemias and lymphomas studied, anti-DBLA-6 serum reacted with all thymic (Group 1) and extrathymic (Group 2) lymphomas and unclassified leukemias (Groups 3 and 4), while all myelogenous leukemias (Group 5) and erythroleukemias (Group 6) were negative. The position of leukemias and lymphomas reactive with anti-DBLA-6 serum in the lymphocyte maturational pathway is discussed.
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PMID:Heterologous antiserum to chemically induced rat non-T, non-B leukemia and its application to characterization of rat leukemias. 696 31

A method for infection of lymphocytes with Moloney(Abelson) murine leukemia virus [M(A)-MuLV] is described. Only lymphoblasts obtained after stimulation of normal spleen cells by the B cell mitogen lipopolysaccharide (LPS) were satisfactory targets for virus-specific, secondary cytotoxic T lymphocytes (CTL), whereas spleen cells stimulated by the T cell mitogen concanavalin A were not. The secondary CTL response against M(A)-MuLV could be efficiently measured using M(A)-MulV-infected LPS blasts as stimulating cells for secondary in vitro restimulation and as target cells for virus-specific destruction. Cold target inhibition demonstrated virus specificity of CTL. The T cell character of the cytotoxic cells was demonstrated by their sensitivity to anti-Thy-1.2 treatment. Using syngeneic virus-infected LPS blasts as target and stimulator, CTL responses were measured with effector cells from C57BL mice of the H-2b haplotype and of recombinant haplotypes sharing either K or D alleles with H-2b. In analogy with previous studies on Moloney virus-specific CTL, it was observed that C57BL/6 (H-2b) effector cells predominantly lysed Db-compatible, virus-infected target cells; B10.A(5R), (KbDd) effector cells showed a poor CTL response against syngeneic, virus-infected target cells. The combined findings indicate the existence of an Ir gene in the H-2D region regulating the CTL response against Moloney leukemia virus.
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PMID:Cytotoxic T cell response against lymphoblasts infected with Moloney (Abelson) murine leukemia virus. Methodological aspects and H-2 requirements. 697 10


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