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 availability of membrane receptors for the 71,000-dalton envelope glycoprotein (gp71) of Rauscher murine leukemia virus on splenic and thymic cells from BALB/c mice during Rauscher murine leukemia virus-induced leukemogenesis was determined utilizing a radiolabeled gp71 binding assay. Shortly after infection, the relative cellular [125I]gp71 binding level decreased, first with splenic cells (at day 7 to 10 after infection) and later with thymic cells (at day 10 to 20 after infection). The dependency of the reduction of binding on the replication of the inoculated virus was demonstrated by regression analyses using cellular gp71 binding level as the dependent variable and infectious virus titer, as well as viral gp71 and p30 levels, of spleens and thymuses from infected mice as independent variables. With each independent variable, the reduction of gp71 binding for both cell types was highly dependent (P less than 0.01) on the level of virus detected in their respective organ. In the early stages of leukemogenesis, the [125I]gp71 binding level declined to approximately 20 to 30% of control values. During this period the rate of reduction of binding was very rapid and, in general was similar for both splenic and thymic cells. Further progression of the disease resulted in little or no further reduction in binding. The application of this technique to monitor host ecotropic virus synthesis and to study cell surface virus receptor control mechanisms in vivo is discussed.
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PMID:Depression of Rauscher leukemia virus envelope glycoprotein gp71 binding by lymphoid cells during leukemogenesis in mice. 46 72

The comparison of the biological effects of FVP and FVA showed that leukemogenesis appears to be delayed in FVA infected mice as compared to FVP infected animals after injection of comparable quantities of virus as measured in spleen focus forming units. In addition, no CFU-EI, characteristic for FVP induced leukemia, were found in leukemic spleen or bone marrow of FVA infected mice. Since it was possible to distinguish both viruses by their different host ranges, which are helper virus determined, it is suggested that the observed differences, especially the lack of CFU-EI in FVA infected mice, might be due to differences in the helper virus component of the FV complex.
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PMID:Comparison of the biological effects of anemia inducing and polycythemia inducing Friend virus complex. 48 68

Specific cDNA probes of Moloney and AKR murine leukemia viruses have been prepared to characterize the proviral integration sites of these viruses in the genomes of Balb/Mo and Balb/c mice. The genetically transmitted Moloney provirus of Balb/Mo mice was detected in a characteristic Eco RI DNA fragment of 16 x 10(6) daltons. No fragment of this size was detected in tissue DNAs from Balb/c mice infected as newborns with Moloney virus. We conclude that a viral integration site, occupied in preimplantation mouse embryos, is not necessarily occupied when virus infects cells in post-natal animals. Balb/Mo and Balb/c mice do carry the AkR structural gene in an Eco RI DNA fragment of 12 x 10(6) daltons. Further restriction analysis of this fragment indicated that both mouse lines carry one AKR-type provirus. Leukemogenesis in Balb/Mo and newborn infected Balb/c mice is accompanied by reintegration of Moloney viral sequences in new chromosomal sites of tumor tissues. Part of the reintegrated Moloney viral sequences are of subgenomic size. The AKR viral sequences, however, are not found in new sites. Further restriction analysis revealed that the development of Moloney virus-induced leukemia in Balb/Mo mice does not lead to detectable structural alteration of the genetically transmitted Moloney and AKR structural genes. Possible mechanisms of the reintegration process are also discussed.
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PMID:The integration sites of endogenous and exogenous Moloney murine leukemia virus. 50 16

A group of mouse leukemia cell lines induced by the Friend murine leukemia virus (F-MuLV) was examined for a cell membrane antigens (regulated by the I-region of the H-2 complex), as well as for erythroid characteristics. Erythroid traits tested were hemoglobin synthesis, incorporation of 59Fe into heme, and presence of globin mRNA. Of 19 lines, 13 were positive for erythroid characteristics. All of these 13 lines were a-negative. Of 19 lines, 6 were negative for erythroid characteristics, and 5 of the 6 were a-positive. The data suggested that F-MuLV-induced leukemogenesis may operate in more than 1 cell type. In addition to the primitive erythroid type of cell usually involved in leukemia induced by F-MuLV, nonerythroid Ia-positive cells may also be transformed. The exact origin of the Ia-positive leukemia cells is unknown.
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PMID:Lack of erythroid characteristics in Ia-positive leukemia cell lines induced by Friend murine leukemia virus: brief communication. 56 10

Dietary administration of N-[4-(5-nitro-2-furyl)-2-thiazolyl]acetamide to mice for 14 weeks followed by 16 weeks of control diet resulted in a high incidence of lymphocytic leukemia and a low incidence of forestomach squamous cell papillomas. The coadministration of p-hydroxyacetanilide at a dose of 1.0% with either 250 or 500 ppm of N-[4-(5-nitro-2-furyl)-2-thiazolyl]acetamide resulted in inhibition of leukemogenesis, whereas when p-hydroxyacetanilide was coadministered with 1000 ppm of N-[4-(5-nitro-2-furyl)-2-thiazolyl]acetamide the leukemia incidence was not significantly reduced, but the latent period was prolonged. When sodium sulfate was administered with p-hydroxyacetanilide and N-[4-(5-nitro-2-furyl)-2-thiazolyl]acetamide, leukemogenesis was partially restored. L-Methionine, fed in place of sodium sulfate, unblocked leukemogenicity inhibition by p-hydroxyacetanilide. None of these chemicals, p-hydroxyacetanilide, sodium sulfate, or L-methionine, significantly affected the incidence of forestomach papillomas induced by N-[4-(5-nitro-2-furyl)-2-thiazolyl]acetamide, although tumor incidences in all groups were low. p-Hydroxyacetanilide and sodium sulfate had no significant effect on the high incidence of stomach tumors induced by formic acid 2-[4-(5-nitro-2-furyl)-2-thiazolyl]hydrazide or bladder tumors induced by N-[4-(5-nitro-2-furyl)-2-thiazolyl]formamide.
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PMID:Effect of p-hydroxyacetanilide, sodium sulfate, and L-methionine on the leukemogenicity of N-[4-(5-nitro-2-furyl)-2-thiazolyl]acetamide. 63 67

Tumor induction by fractionated whole-body X-irradiation (400 rad) was studied in spayed Sprague-Dawley rats. Ovariectomy was chosen as an intensifying factor for radiation leukemogenesis. Ovariectomized rats gained more body weight and responded more quickly (but transiently) in the recovery of WBC levels after the last (3rd or 4th) X-irradiation. A total of 26 tumors developed in 21 out of 47 ovariectomized rats, 11 tumors in 6 out of 13 ovariectomized and ovary-grafted rats, and 44 tumors in 25 out of 29 sham-ovariectomized rats during the observation period up to 64 weeks after starting X-irradiation. Eighty per cent of tumors were of mammary gland origin in the latter two groups with intact or grafted ovaries. By contrast, 61.1% of tumors in the spayed rats were derived from the subcutaneous mesenchymal tissue and the hematopoietic tissue. This may imply that some forms of mesenchymal tumors including leukemia are under the suppressive influence of female sex hormones.
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PMID:Effect of ovariectomy on x-ray carcinogenesis in rats. 66 36

Administration of ovine growth hormone to young C3Hf mice inhibited Gross passage A virus-induced leukemogenesis as manifested by a delayed onset and a lower incidence of thymus leukemia. These results can be interpreted that growth hormone inhibited thymus-dependent leukemogenesis perhaps through thymotrophic influences which prevented or delayed the thymus involution believed to be essential for leukemia change. In female but not in male Gross passage A virus-infected mice, development of a thymus-independent leukemia appeared to be promoted by growth hormone.
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PMID:Inhibitory effect of growth hormone on Gross passage A virus-induced thymus leukemia in C3Hf mice. 76 Dec 14

The radiation- and radiation leukemia virus-induced leukemias in C57BL/6 strain mice were found to be of the thymus-derived (T) lymphocyte origin. Experimental evidence indicated that the interaction of the radiation leukemia virus with thymus-derived lymphoid cells and specifically with the thymus subpopulation bearing high levels of H-2 alloantigens were prerequisites for the development of high leukemia incidence in these test systems. In radiation leukemogenesis in C57BL/6 mice it was shown that within several days following the radiation treatment a "released" leukemogenic agent was found in the irradiated bone marrow; whereas, several days following chemical carcinogen leukemogenesis in SJL/J mice, established preleukemic or leukemic cells could be detected in the bone marrow. The analysis concerned with the lymphoid origin of chemical carcinogen-induced lymphatic leukemias in SJL/J mice indicated clearly that the carcinogen could affect different lymphoid populations. The majority of the chemical-induced leukemias were of the bone marrow-derived (B) lymphocyte origin, although some leukemias were of T lymphocyte origin, and some tumors could not be classified as either T or B leukemias, perhaps representing stem cells which do not carry the characteristic surface antigens for mature T and B cells.
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PMID:Pathways in thymus- and bone marrow-derived lymphatic leukemia in mice. 80 36

The study of Friend and Rauscher murine leukemia viruses has produced a variety of evidence regarding the nature of the target cell(s). These viruses produce in mice leukemias with a strong erythroid component. However, they are also pancytotic in their action, with demonstrable effects on differentiating myeloid and thromboid cells, the immuno-responsive cells, and the peripheral lymphoid cells as well. In addition, it has been noted that a variety of factors can influence disease expression, including the variety of mouse strain, the hematopoietic cell line being observed, and the tissue microenvironment in which leukemogenesis is taking place, as well as the viral substrain itself. The data available indicates that the target cells are definitely to be found among the most primitive of the hematopoietic progenitor cells of both the marrow and the spleen. However, from an analysis of this data it would appear that the virus target is not exclusively limited to a single type of hematopoietic precursor cell. Rather it is suggested that there is a closely related family of targets, consisting of the uncommitted pluripotent stem cell and the committed progenitor stem cells of the erythroid, myeloid, thromboid and immune cell lines. The evidence for each of these types of hematopoietic cells is reviewed.
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PMID:The role of committed and uncommitted hematopoietic stem cells as targets for Rauscher and Friend leukemia virus. 89 10

The correlation of murine leukemia virus (MuLV) infection and leukemogenesis was examined by XC plaque assay in W/F rats neonatally infected with the rat-adapted Gross virus (RAGV). Thymic lymphomas developed in 100% of infected rats, with a mean latent period of 64 days. The virus infectivity was first detected in the thymus as early as 15 days after the virus infection; the titer steadily increased thereafter until the development of thymic lymphoma. No other tissues of virus-infected rats showed virus infectivity until the development of localized thymic lymphoma, though sera of a few rats showed low infectivity titers. In rats with generalized leukemia, however, high titers were detected in the sera and leukemic tissues. In untreated controls, all tissues tested invariably showed negative titers for MuLV infectivity at any age up to 7 months after birth. The results indicated that those tissue sites were common to both RAGV infectivity and the leukemogenic process, with the primary involvement of the thymus, and that the appearance of RAGV infectivity in various tissues represented the expression of the oncogenic genome of RAGV.
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PMID:Type C RNA viruses and leukemogenesis: association of Gross strain of murine leukemia virus infection and leukemogenesis in rats. 99 3


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