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

Spleen cells taken from mice infected as adults with two different variants of the spleen focus-forming virus (SFFV), SFFVP and SFFVA, as well as spleen cells taken from mice infected as newborns with Friend murine leukemia virus (F-MuLV) were assayed in a proliferation assay in the presence or absence of the erythroid hormone erythropoietin (Epo). Infection of NIH Swiss mice with SFFV resulted in excessive proliferation of erythroid cells that could still differentiate, and spleen cells taken from these mice were able to incorporate high levels of tritiated thymidine ([3H]dThd) in the absence of Epo, even in the presence of antibodies to Epo. In contrast, the level of proliferation of spleen cells from SFFVA-infected mice, but not those from SFFVP-infected mice, could be greatly enhanced by the addition of Epo to the cultures. Infection of newborn mice with F-MuLV resulted in the generation of Friend mink cell focus-inducing virus, which caused excessive proliferation of erythroid cells that appeared to be blocked in differentiation, resulting in severe anemia. Spleen cells from these mice were unable to proliferate in the absence of Epo. However, when increasing doses of Epo were added to the cultures, the cells proliferated at levels equivalent to the levels seen with SFFV. These results indicate that a proliferation assay based on the incorporation of [3H]dThd into spleen cells in response to Epo can be used as a quantitative means of assessing and comparing the effects of erythroleukemia-inducing retroviruses on the proliferation of their target cells.
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PMID:Employment of a [3H]thymidine-incorporation assay to distinguish the effects of different Friend erythroleukemia-inducing retroviruses on erythroid cell proliferation. 345 16

To determine whether hemopoietic cells infected with Friend polycythemia-inducing spleen focus-forming virus (SFFVp) are conserved or suppressed via natural surveillance in leukemia-resistant adult mice, we engrafted C57BL/6 recipients with isologous transgenic (donor origin marker) or natural killer (NK) cell-deficient B6 beige marrow cells exposed to SFFVp in vitro. Both groups of primary recipients were viremic and nonleukemic. Spleen cells from primary SFFVp-infected chimeras were engrafted into irradiated leukemia-susceptible secondary recipients to reveal dormant leukemia and grew as tumors of donor origin in 8 of 38 (21%) and 33 of 47 (70%) instances, respectively. Treatment of marrow donors and recipients with anti-asialo GM1 serum resulted in the depression of NK cell activity and the rapid development of dormant leukemia. We conclude that NK cells are an effective surveillance mechanism able to suppress SFFVp-induced preleukemic stem cells.
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PMID:Natural killer cell suppression of Friend virus-induced preleukemic hemopoietic stem cells. 347 19

Spleen and light density peripheral blood leukocytes of 10 hairy cell leukemia (HCL) patients and total leukocytes of one patient and blood donor cells were stained quantitatively for cellular DNA. The DNA content of single cells was measured by flow cytometry (FC) and compared to the DNA content of sheep cells admixed as an internal control. Eight of eleven patients (72 per cent) showed deviations from blood donor DNA content. Two female patients showed increased cellular DNA content, the six male patients had hypodiploid cells. Chromosomal aberrations are therefore likely to exist in the majority of HCL patients. Separation of HCL cells into sheep erythrocyte rosette and non rosette forming cells revealed similar DNA abnormalities in both cell populations, suggesting that the leukemia encompasses cells with B and with T markers.
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PMID:DNA-abnormality in hairy cell leukemia. 357 Jan 74

Thymus, spleen, and bone marrow of 1-month-old neonatally Moloney murine leukemia virus-inoculated mice have been transferred to 400-R-irradiated syngeneic recipients of the opposite sex. The donor or recipient origin of T-cell lymphomas arising in the host animal was identified by the sex chromosome marker. Spleen and bone marrow of athymic BALB-nu/nu mice contain cells with the potential to develop into T-cell lymphomas upon transfer to thymus-bearing BALB/c recipients. Such lymphomas arise from at least two subsets of T-cells, one terminal deoxynucleotidyl transferase (TdT) positive and the other 20 alpha-hydroxysteroid dehydrogenase positive. The enzyme-negative precursor T-cells from the BALB-nu/nu spleen and bone marrow can thus mature to enzyme-positive cells and give rise to lymphoma in the thymus-bearing recipient. Preleukemic spleen and bone marrow, but not thymus, from CBA and BALB/c mice regularly contained cells with the potential to develop lymphoma. The subset of T-cell involved was influenced by the genotype since lymphomas arising after the transfer of CBA and BALB/c spleens were TdT positive and 20 alpha-hydroxysteroid dehydrogenase positive, respectively. In thymus-bearing mice, but not in nude mice, the transfer of preleukemic spleen cells gave lymphomas earlier than did transfer of bone marrow cells. This suggests that the more mature lymphoid cell population in the spleen of thymus-bearing mice may allow leukemic transformation to occur more rapidly than do the less mature cells in the bone marrow. In one-third of the cases, the virus produced by the preleukemic cells transferred induced new lymphomas involving recipient host cells. These de novo-induced lymphomas were all TdT positive. We suggest that leukemic transformation of TdT-positive cells may occur through a different mechanism than does transformation of cells bearing the 20 alpha-hydroxysteroid dehydrogenase marker.
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PMID:Influence of genotype and the organ of origin on the subtype of T-cell in Moloney lymphomas induced by transfer of preleukemic cells from athymic and thymus-bearing mice. 387 60

Brown, Eric R. (Northwestern University Medical School, Chicago, Ill.), Peter Buinauskas, and Steven O. Schwartz. Immunofluorescent antibody studies of a murine leukemia virus. J. Bacteriol. 92:978-982. 1966.-Correlation was close between in vitro complement fixation, immunodiffusion, and passive cutaneous anaphylaxis tests with the S-63 and GC murine leukemia viruses and immunofluorescence reactions with these viruses. When fluorescein-isothiocyanate-conjugated convalescent sera obtained from mice initially infected with S-63 leukemia virus were used, the reactive site was within the cytoplasm of the infected cell. By electron microscopic examination, virus particles were demonstrated in the same areas within the cells that exhibited specific fluorescence with the conjugates. Spleen and mesenteric nodes contained the most virus, whereas kidney tissues contained the least amount. Fluorescence was not observed within the nuclei of infected cells.
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PMID:Immunofluorescent antibody studies of a murine leukemia virus. 416 60

Spleen cells from BALB/c or CAF(1) mice released little or no detectable leukemia virus when cultured 2-7 days in vitro. In contrast, spleen cells of CAF(1) mice previously inoculated with parental BALB/c spleen cells released leukemia viruses in 10 of 11 cases studied. Cultures of a mixture of spleen cells from normal BALB/c and CAF(1) mice also contained leukemia viruses. Phytohemagglutinin induced the transformation of lymphocytes in cultures of CAF(1) or BALB/c spleen cells, but this transformation did not activate leukemia viruses. It is concluded that mixed lymphocyte cultures in vitro, just as graft-versus-host reactions in vivo, can activate leukemia viruses that are normally present in a repressed form. This activation is not solely a function of lymphocyte transformation. The activated mouse leukemia virus may subsequently account for the observed high incidence of neoplasia in graft-versus-host disease.
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PMID:Activation of leukemia viruses by graft-versus-host and mixed lymphocyte reactions in vitro. 440 35

Spleen cells from W/Fu rats 40 days or more after immunization with a syngeneic Gross virus-induced leukemia were unreactive in direct cytotoxic assays. Incubation of these immune cells at 37 degrees C for 12 hr or longer, in the absence of antigen, resulted in the appearance of specific cytotoxic reactivity. Other lymphoid cells from the immune rats also were activated upon in vitro incubation, but to a lesser extent. Experiments were performed to define the necessary conditions and the mechanism for the in vitro incubation. Activation was temperature dependent, occurring at 37 degrees C but not at 4 degrees C. Immune serum suppressed the activation, but normal rat serum also had some inhibitory activity. Passage of immune cells through a nylon column, before preincubation, prevented activation. In contrast, exposure to nylon after preincubation did not remove cytotoxic reactivity. These findings demonstrate the reversal of a central inhibition of immune cell activity. The explanations offered for this phenomenon included change in surface characteristics of the immune cells during in vitro incubation, and the possible need for an adherent helper cell.
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PMID:In vitro activation of cellular immune response to Gross virus-induced lymphoma. 508 73

Thymus and spleen grafts from neonatal C57BL mice were implanted beneath the kidney capsule of (A x C57BL) F(1) hybrids. At various intervals after implantation, the grafts were analyzed serologically. Cells of each graft were tested for the presence of cells of host origin, TL (thymus-leukemia) antigenicity, and sensitivity to the cytotoxic effect of guinea pig serum (GPS). Thymus grafts showed partial repopulation by host cells 11 days after grafting, and some grafts were completely repopulated by host cells 13 days after grafting. All thymus grafts were fully repopulated 18 days after grafting. With one exception, thymus grafts contained no significant number of TL-positive cells within 14 days after grafting. TL-positive cells appeared in thymus grafts examined 15 days after implantation, and their number increased up to the 18th day after implantation. Cells residing in thymus grafts remained sensitive to GPS throughout the period of observation. The acquisition of thymus-distinctive serological properties by host cells repopulating thymus grafts was similar in intact and in thymectomized recipients. Spleen grafts were completely repopulated by host cells as early as 8 days after grafting. The cells residing in spleen grafts remained TL-negative throughout the period of observation, and were refractory to the cytotoxic effect of GPS. It is thus apparent that, while both spleen and thymus grafts are invaded by TL-negative cells, only those entering the thymus acquire the antigen. The nature of the process by which the thymus endows thymus-distinctive properties on cells entering it is discussed.
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PMID:Serological analysis of thymus and spleen grafts. 565 21

Spleen cells from DBA/2 mice did not proliferate, but released interferon (IFN) when cultured in the presence of mitomycin C-treated syngeneic L1210 leukemia cells apparently free from mycoplasma and common non-oncogenic viral infections. IFN titers reached a plateau after 18 h of culture. The biological activity of this IFN was stable at pH 2 and could be inactivated by antibody raised against alpha and beta-IFN. Removal of phagocytes from the spleen cell suspensions caused a decrease in IFN production. By contrast, suspensions depleted in Thy 1.2-positive cells had an enhanced capacity to produce IFN in response to the L1210 cells.
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PMID:Interferon production in mixed cultures of murine leukocytes and syngeneic L1210 leukemia cells. 608 76

Radiation leukemia virus-induced leukemia of a male C57BL/6 mouse, B6RV2, is immunogenic to female BALB/c X C57BL/6 F1 mice. In these mice, B6RV2 tumors regressed after initial growth, and after tumor regression the mice were resistant to repeated inocula of up to 10(8) B6RV2 cells. Serum from these mice reacted with B6RV2 in mixed hemadsorption or protein A assays, and absorption analysis indicated that the antigen was restricted to B6RV2; it could not be detected in normal thymocytes or spleen concanavalin A blasts from different inbred strains, nor in 16 C57BL/6 or BALB/c leukemias. Spleen cells from mice in which the tumor had regressed were cytotoxic to B6RV2 after in vitro stimulation with B6RV2, as shown by 51-chromium release assay. This cytotoxicity was eliminated by pretreatment of the cells with anti-Thy-1.2, anti-Lyt-2.2, anti-Lyt-3.2, and complement, indicating that the effector cells were T-cells. The specificity of T-cell killing of B6RV2 was examined by competitive inhibition assays with unlabeled cells; only B6RV2 inhibited killing, while eight other C57BL/6 leukemias did not inhibit. Thus, the antigen on B6RV2 defined serologically and by cytotoxic T-cells is a unique antigen. However, it was not revealed by antibody-blocking test whether the unique determinant defined serologically was related to that recognized by T-cells; B6RV2 antiserum did not block lytic activity in the absence of added complement, irrespective of whether the target cells were untreated or anti-H-2b-treated B6RV2. H-2Kb antisera, but not H-2Db antisera, blocked lysis. This indicated that the H-2Kb molecule was exclusively involved in recognition of B6RV2 by cytotoxic T-cell.
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PMID:Detection of a unique antigen on radiation leukemia virus-induced leukemia B6RV2. 609 70


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