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)

Adoptive immunotherapy of a transplantable AKR leukemia (K36) was carried out as an adjunct to cytoxan chemotherapy using normal allogeneic H-2-incompatible spleen cells as well as sensitized H-2-matched allogeneic spleen cells. A significant therapeutic effect was obtained with cytoxan and allogeneic C57BL/6 splenocytes, demonstrating the potential use of the graft-versus-host reaction. Utilizing specific adoptive immunochemotherapy, a maximum effect was found with splenocytes from allogeneic but H-2-compatible CBA/J mice immunized against an allogeneic Gross-virus-induced lymphoma (E female G2). This therapeutic effect was most likely the result of prior sensitization of donor lymphocytes to common virus-associated tumor antigens.
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PMID:Adoptive immunochemotherapy of a transplantable AKR leukemia (K36). 2 4

Sera from normal C57BL/6 mice contained low titers of antibodies against proteins of MuLV. Sera from C57BL/6 mice that were immunized with allogeneic leukemia cells sometimes contained high-titered antibodies against the p15 protein of MuLV; these antibodies detected group-specific antigenic determinants of the p15 protein, since reactions were observed with the p15 proteins of both AKR and Moloney viruses. In contrast, antisera prepared in C57BL/6 mice against the AKR leukemia K36 reacted strongly with the p30 protein of MuLV, as well as with p15. Antibodies in the C57BL/6 anti-AKR K36 sera detected group-specific antigenic determinants of the p30 protein; reactions were observed with the C57BL/6 anti-AKR K36 serum and the p30 proteins of both AKR and Moloney viruses. It was concluded that mice do have the capacity to respond immunologically to antigenic determinants of the MuLV p30 protein, although in most circumstances this is not observed.
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PMID:Immune response of the mouse to the major core protein (p30) of ecotropic leukemia viruses. 5 85

The Gross cell surface antigen (GCSA), associated with expression of endogenous Gross-type murine leukemia virus (G-MuLV) in tissues of mice, is defined by the cytotoxic reaction of a C57BL/6 antiserum, anti-AKR spontaneous leukemia K36, with cells of the Gross virus-induced C57BL/6 leukemia, Emale symbolG2. Sequential lactoperoxidase-catalyzed radioiodination of Emale symbolG2 cells, Nonidet P-40 lysis, precipitation with anti-K36 serum, and sodium dodecyl sulfate-polyacrylamide gel electrophoresis identified molecules with properties of polyproteins encoded by the gag region of the viral genome. These cell surface species could also be labeled by in vitro culturing of Emale symbolG2 with radioactive glucosamine. The viral specificity of these molecules and their participation in the GCSA typing system were established as follows. (i) Absorption of anti-K36 serum with GCSA(+), but not GCSA(-), leukemias led to a marked decrease in precipitation of these proteins. (ii) The same Emale symbolG2 cell surface proteins were also precipitated by antisera against the MuLV virion proteins p30 and p15. (iii) Anti-K36 was shown to possess antibodies against Gross virus p30 and p15. (iv) "Clearing" the Emale symbolG2 lysate of molecules reactive with anti-p30 or anti-p15 sera removed molecules reactive with anti-K36 serum. (v) Absorption of anti-K36 serum with disrupted G-MuLV virions or with Gross p30 or p15 removed GCSA cytotoxic antibodies; partial absorption was achieved with disrupted Rauscher-MuLV (R-MuLV) or with R-MuLV p30, and no absorption was found with R-MuLV p15. These data show that Emale symbolG2 cells express, on their surfaces, MuLV core polyproteins that apparently can be glycosylated and on which the determinants of GCSA are located.
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PMID:Characterization of molecular species carrying gross cell surface antigen. 6 25

Antisera produced in mice recognize primarily type-specific antigenic determinants on both the major core protein, p30, and the major envelope proteins, gp70 and p15(E), of the endogenous leukemia viruses (MuLV) of BALB/c mice. Three different mouse sera were investigated in detail. (i) Antisera prepared in C57BL/6 mice against the AKR leukemia K36 reacted with the gp70, p15(E), and p30 proteins of MuLV. Certain pools of the C57BL/6 anti-AKR K36 serum contained antibodies which serologically distinguished the p30 proteins of N-ecotropic, B-ecotropic, and xenotropic BALB/c MuLV. (ii) Antisera prepared in BALB/c mice against the BALB/c sarcoma 1315 contained antibodies that reacted with a type-specific antigen of the 1315 MuLV gp70 that is not found on other BALB/c MuLV. (iii) The normal sera of multiparous BALB/c mice contained antibodies that reacted with gp70 and p15(E) proteins of ecotropic MuLV. Sera from some of these mice contained antibodies that serologically distinguished the gp70 of N-ecotropic and B-ecotropic BALB/c viruses. These results emphasize the utility of mouse antisera in the serological typing of MuLV. Furthermore, the antigenic differences observed in the p30 and gp70 proteins should be of particular use in the future analysis of recombinant BALB/c MuLV.
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PMID:Detection of polymorphism in BALB/c leukemia viruses with mouse antisera. 9 60

Several murine tumors were used to determine whether the phenomenon of tumor inhibition in athymic "nude" mice reported previously could be extended to other tumor systems in nude as well as conventional mice. The results with the L5MF-22 tumor line were confirmed, and similar data were obtained with the K36 leukemia of AKR mice and the LAF-17 leukemia of B10.A origin. This phenomenon of tumor inhibition has been called, tentatively, radioresistant inhibition of tumor and may be explained by one of several possibilities. The immunological origin of such tumor inhibition is supported by various observations. The data on tumor cell proliferation in spleens and liver of lethally irradiated mice were similar to previous findings on hemopoietic histocompatibility-incompatible lymphomas. Additionally, the nude mice were stronger responders against lymphoma cells than were conventional hosts. Another explanation is that the tumor inhibition is due to natural cytotoxicity.
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PMID:Radioresistant inhibition of lymphoma growth in congenitally athymic (nude) mice. 83 64

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

Oxygenated derivatives of cholesterol are known to exhibit potent cytotoxic effects against many different cell types. The cellular basis of this cytotoxicity is not understood. Using two murine cancer cell lines (the EL4 lymphoma and the K36 leukemia cell line) and two oxygenated sterols (7-ketocholestanol and 25-hydroxycholesterol), our laboratory attempted to determine whether the cytotoxic action of oxysterols was mediated by a mechanism requiring protein or RNA synthesis. The addition of 5 microM 7-ketocholestanol or 25-hydroxycholesterol to the culture medium regularly caused the viable cell count to fall below 10-20% of control within 48-72 h. In the presence of inhibitors of protein or RNA synthesis, however, cell viability was consistently and significantly increased in a dose-dependent manner. For cultures of EL4 cells grown in the presence of 5 microM 7-ketocholestanol, for example, the addition of appropriate concentrations of cycloheximide, puromycin, emetine, and actinomycin increased the percentage of viable cells from a control value of less than 6% to 66%, 28%, 76% and 42%, respectively. Qualitatively similar results were obtained with the K36 cell line. Additional studies revealed that macromolecular synthesis inhibitors, while effective in inhibiting protein or RNA synthesis to varying degrees, did not affect the cellular uptake of 7-keto[3H]cholestanol, suggesting that their ability to protect cells against oxysterol-induced cytotoxicity was not due to an inhibition of the cellular oxysterol uptake. These observations suggest that the cytotoxicity of oxygenated sterols may be mediated by mechanisms requiring de novo protein or RNA synthesis and that oxysterol-induced cytotoxicity may provide a useful system for the identification of proteins involved in cell death.
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PMID:Inhibitors of protein and RNA synthesis block the cytotoxic effects of oxygenated sterols. 137 72

Cancers are the result of somatic heritable changes in certain genes. The AKR leukaemia K36.16 has been extensively studied in our laboratory. When compared to normal AKR thymocytes, the K36.16 tumour cells do not express the H-2Kk antigens and have an unexpected antigenic determinant that could be detected by anti-H-2Dd monoclonal antibodies. To understand the molecular mechanisms that could be responsible for these changes, we have compared the genomic composition of the class I MHC genes in the K36.16 tumour cells to that of normal AKR lymphocytes. A unique polymorphic 2.6-kb Hind III fragment was detected in DNA obtained from the K36.16 tumour cells after hybridization with a 3'-gene-coding H-2 probe. This fragment is not present in DNA of normal AKR lymphocytes. In an effort to further understand the mechanism underlying the nature of this MHC gene polymorphism, we have cloned and sequenced this Hind III fragment. When compared with the reported sequences of a number of mouse class I MHC genes, the nucleotide sequence of this polymorphic Hind III fragment is similar to that of a reported Tla gene.
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PMID:Cloning and characterization of a polymorphic class I MHC gene in the AKR lymphoma K36.16. 263 6

Two new serological specificities were identified on the surface of murine leukemia virus (MuLV)-infected cells by direct and absorption immunofluorescence tests. Both antigens were detected with antisera prepared in rats that were growing transplants of syngenic MuLV-induced leukemias. Antigen G(L) was defined with the AKR leukemia K36 as the test cell; antigen G(T) was defined with the W/Fu leukemia C58(NT)D as the test cell. G(L) and G(T) antigens were serologically and genetically independent of the MuLV-induced Gross and G(IX) cell-surface antigens. G(L) and G(T) antigens were found in normal lymphoid cells of mice from high-leukemic strains, but not in lymphoid tissues of mice from most low-leukemic strains. Tumors and leukemias of mice of low-leukemic strains often were G(L) and G(T) positive. Similarly, infection of normal cells with MuLV resulted in expression of G(L) and G(T). With ferritin-labeled antibody the G(L) and G(T) antigens were observed on virus-free segments of the cell surface. Genetically, G(L) and G(T) antigens were each controlled by two dominant unlinked genes in AKR mice; these same antigens were each controlled by three or more dominant unlinked genes in C58 mice. Penetrance of G(L) and G(T) regulatory genes was dependent upon the Fv-1 genotype of the host. Expression of G(L) antigen was closely associated with virus production, whereas expression of G(T) antigen was less closely associated.
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PMID:Cell surface antigens associated with murine leukemia virus: definition of the GL and GT antigenic systems. 435 63

By inhibiting techniques using indirect immunofluorescence tests and indirect immunoelectron microscopy, the G(Gross) soluble antigens (GSA) in the body fluids of AKR and C58 mice, which have a high incidence of spontaneous leukemia, were classified according to the known specificity of G antigens in the murine Gross leukemia system. GSA existing in the plasma of nonleukemic and leukemic AKR mice and in the ascitic fluid of transplanted AKR spontaneous leukemia K36 showed the several specificities corresponding to G cell surface antigens, GCSAa, b, and c, and type-specific and group-specific viral envelope antigens, tsVEA and gsVEA, respectively. However, the plasma of nonleukemic C58 mice lacks GSAc, which can be recognized by the G-typing mouse serum. GSA corresponding to G(IX) antigen was not detected in the body fluids.
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PMID:Wild-type gross leukemia virus: classification of soluble antigens (GSA). 456 40


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