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

Adult wild mice (LC) from a natural colony with a high incidence of spontaneous lymphomas had free infectious virus in their seara (average 10(3.5) infectious units/ml) and parenchymal organs (average 10(5.2) infectious units/g tissue). They did not have detectable levels of free virus-specific antibodies that could be demonstrated by virus neutralization or immunofluorescence at higher than a 1:10 dilution. Only 5 of 28 animals had free antibodies detectable by radioimmunoprecipitation assay, and tissues of 4 mice also had nondetectable levels of virus determined by infectivity assay. Formalized vaccine from the indigenous virus did not induce production of virus-neutralizing antibodies or protect against naturally occurring disease. The animals with persistent leukemia virus infection, however, elicited good humoral immune responses to virus-unrelated antigen.
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PMID:Inefficient humoral immune response of lymphoma-prone wild mice to persistent leukemia virus infection. 18 95

334C murine leukemia virus, which induces a high incidence of lymphatic leukemias (80-90%) in susceptible mice following a long latency period, was found to cause a severe in vivo suppression of direct plaque-forming cells from the spleen, following antigenic stimulation with sheep red blood cells. Neonatally infected inbred BALB/c and outbred Ha/ICR Swiss mice, which develop a sustained viremia, were highly susceptible to the immunosuppressive effect of this virus as early as 1 week after virus infection, long before any detectable histologic evidence of leukemia development. Ha/ICR Swiss mice, which are highly resistant to the leukemogenic potential of this virus following infection in adult life, were highly resistant to its immunosuppressive action; only a moderate and transient suppression, without viremia, occurred 2 weeks after virus infection. In marked contrast, BALB/c mice were highly susceptible to the immunosuppressive action of 334C murine leukemia virus following infection in adult life; a severe and sustained suppression was observed as early as 1 week after virus infection and was followed by a sustained viremia, beginning at 2 weeks, with a 55-60% incidence of leukemia observed over a period of 1 year. Infectious virus was essential to produce theimmunosuppressive effect; heat-inactivated (56 degrees C/30 min) and attenuated (4 degrees C/4 1/2 mo) virus preparations were ineffective. The plaque-forming response of spleen cells from lethally irradiated syngeneic adult BALB/c mice was markedly suppressed following reconstitution with thymus-dependent (T) or thymus-independent (B) cells from the thymus and bone marrow, respectively, of virus-infected mice, in combination with each other, or with the appropriate cell populations from normal mice.
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PMID:Immunosuppression in mice after inoculation with 334C, a murine lymphatic leukemia-inducing virus. 19 Apr 12

Studies carried out over the past four decades on factors controlling the susceptibility to viral leukemias in mice have shown the existence of specific controlling gene loci. Evidence from a number of studies using various mouse strains and different leukemia viruses has shown that the controlling genes may act either directly or indirectly. "In vitro" experiments have shown controlling effects directed by the prospective target cells themselves in which effective virus infection and/or and/or replication is inhibitied. From "in vivo" experiments it is also evident that susceptibility may be controlled through indirect means mediated by immune relationships and other factors involved in the basic regulations of hematopoiesis. The present paper presents a brief review of the various genes known to control susceptibility and resistance to murine leukemia viruses. Certain conflicts in the literature relating to the naming of particular specific genes by different laboratories is also discussed, and some minor revisions in nomenclature designed to resolve some of the existing confusion are proposed.
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PMID:Genetic influence in murine viral leukemogenesis. 19 Nov 15

Monoclonal immunoglobulins (Eg) are detected in the serum of 7/29 patients treated for leukemia (6 cases) or lymphoma (1 case). All of them developped cytomegalovirus (CMV) infection. The 7 patients were children or young adults; 6/7 were in complete remission of the hematological disease. They completed chemotherapy before the onset of the viral infection and had received blood components. The monoclonal Ig are IgG (6 cases) and IgM (1 case), In 2 sera there are two M components. The level of the peak was under 1 g/100 ml (5 cases) and reached 1.5 and 1.7 g/100 ml in the 2 other sera. Polyclonal Ig are normal except in one case where there is moderate hypo-Ig; Plasmocytic infiltration was observed in none of the 7 patients. Evidence of CMV infection was confirmed by viremia and/or significant rise of complement fixing antibodies. In four cases, the monoclonal Ig disappeared in less than 6 months. The significance of the monoclonal Ig associated with CMV infection is discussed.
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PMID:[Monoclonal immunoglobulins, cytomegalovirus infection and malignant observations blood diseases]. 19 34

We studied the transformation of epithelial, diploid cell lines (RL-33 and RL-34) derived from W rat liver by the Kirsten murine sarcoma virus. On days 4-5 after virus infection, the epithelial cells began to pile up focally, forming small projections and releasing round cells from the foci. The epithelial cells grew in chains or as islets and grew in suspension above the cells attached to the bottom of the flasks when the cultures reached the confluent stage. The virus titration pattern was "one-hit." Three classes of transformed cells were isolated with respect to virus release and antigen expression: 1) virus producer, 2) non-producer, and 3) sarcoma-positive, leukemia-negative cells. When transplanted sc into newborn rats, the transformed cells produced sarcomas. The transformed cells formed within 1-3 days larger aggregates than those of their normal counterpart cells when suspended in liquid growth medium above an agar base. Aggregate properties (size, viability, and proliferation) of transformed cells correlated with growth in soft agar and tumorigenicity. RNA-dependent DNA polymerase and type C virus particles were readily induced in the normal rat liver epithelial cells after exposure to 5-iodo-2'-deoxyuridine.
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PMID:Transformation of rat liver epithelial cells by Kirsten murine sarcoma virus. 19 67

Resistance to neoplasia caused by radiation-induced leukemia virus (RadLV) is mediated by gene(s) in the H-2D region of the major histocompatibility complex. The previous observation that rapid increases in cellular synthesis and cell-surface expression of H-2 antigens are detectable immediately after virus inoculation has suggested that altered expression of H-2 antigens may play a significant role in the mechanism(s) of host defense to virus infection. This concept is supported by the following observations. First, cell-mediated immunity against RadLV transformed or infected cells can be detected with ease when H-2-positive target cells are used in the cell-mediated lympholysis (CML) assay. (Although RadLV transformed cells obtained from overtly leukemic animals and maintained in tissue culture are H-2 negative, these cells can regain their H-2 phenotype by in vivo passage in normal animals. The H-2-negative cells are poor targets in a CML assay.) Second, resistant mice develop greater numbers of effectors when infected with RadLV than do susceptible mice. Third, injection of normal (uninfected) thymocytes into syngeneic recipients of resistant or susceptible H-2 type does not stimulate a CML response. However, injection of RadLV infected thymocytes from resistant mice produces a vigorous CMI response, and such thymocytes elicit the strongest response at a time when both H-2 and viral antigen expression is elevated. By contrast, injection of infected thymocytes from susceptible mice, which express viral antigens, but low levels of H-2 antigens, does not stimulate a CML reaction. These findings may explain the easier induction of leukemia found by many investigators when virus is inoculated into neonatal mice and the preferential thymus tropism of some oncogenic type-C RNA virus. Cells expressing very low levels of H-2, such as thymocytes, may serve as permissive targets for virus infection because they lack an important component (H-2 antigens) of the dual or altered recognition signal required to trigger a defensive host immune response.
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PMID:A role for elevated H-2 antigen expression in resistance to neoplasia caused by radiation-induced leukemia virus. Enhancement of effective tumor surveillance by killer lymphocytes. 21 30

Strain XVII mice with Graffi virus induced leukemia of various hematological types showed a pronounced thrombocytopenia which was severe in erythroblastic leukemia and weaker in lymphatic ones. The thrombocytic reactions shortly following Friend and Rauscher virus applications and occurred 3 weeks after birth in AKR mice are not found in Graffi virus system. A significant preleukemic thrombocytopenia did appear only 8 weeks after Graffi virus infection. The origin of both the preleukemic and the secondary thrombocytic reactions are discussed. (XVII X AKR) F1 hybrids, neonatally treated with N-nitroso-N-methylurea (NMU), resulted also in a decline in the number of thrombocytes after manifestation of leukemia. In contrast to the expection following NMU treatment a preleukemic thrombocytopenia appeared as in viral leukemogenesis too. The possibility of a co-operation of oncogenic viruses in chemical carcinogenesis is considered.
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PMID:[Thrombocytic reactions in experimentally induced neoplasms (author's transl)]. 22 14

Susceptibility to SV40 virus infection has been suggested as an in vitro marker of predisposition to leukaemia and possibly other cancers in man. To evaluate this relationship, sporadic as well as familial cases of acute non-lymphocytic leukaemia were tested. Among skin fibroblast lines from 22 patients without family history of leukaemia, eight had values above the 95% confidence limit for the normal control population. In four leukaemia-prone families, elevated T-antigen expression was found in all four patients tested and in three-quarters of 36 blood relatives. In addition, elevated values were found in two of three cases of acute myelogenous leukaemia associated with constitutional cytogenetic anomalies, and in all three cases with preleukaemic haematologic disorders. Since SV40 T-antigen expression was elevated in most persons prone to acute non-lymphocytic leukaemia, as well as over one-third of sporadic cases, heritable risk factors may be involved in both groups.
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PMID:SV40 T-antigen expression in acute non-lymphocytic leukaemia. 23 Aug 55

Leukemia viruses can be activated from within murine hosts by immunological reactions against foreign histocompatibility antigens both during graft versus host reactions (GVHR) and host versus graft reactions (HVGR). Presence of both lymphocyte-mediated graft rejection reactions and immuno suppression appears necessary for maximal virus activation and replication in vitro, although viruses can be activated by mixed lymphocyte reactions (MLR) alone in vitro. During HVGR, viruses are first detectable in lymph nodes draining the graft site, and later reach maximal titers in the spleen. Mice infected with murine leukemia virus (MuLV) as neonates or carrying MuLV secondary to milk transmission (carriers) also develop complex autoaggressive responses. By a sensitive in vitro microcytotoxicity assay, neoplastic or pre-neoplastic thymocytes from carrier mice were found to react vigorously against normal uninfected syngeneic embryonic fibroblasts, whereas they reacted much less vigorously with similarly prepared but MuLV-infected fibroblasts. Thymocytes from uninfected animals did not react with infected or uninfected fibroblasts. Peripheral lymphocytes from carriers reacted against MuLV infected fibroblasts, but not against uninfected fibroblasts, a pattern indistinguishable from deliberately-immunized mice. It is proposed that responses analogous to GVHR are also important in the pathogenesis of leukemia following exogenous leukemia virus infection.
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PMID:Autoaggressive reactions and leukemia virus infections: interrelated events in their pathogenesis. 24 Mar 53

Hydroxyurea (HU), given ip four times, each time at 500 mg/kg in 6-hour intervals, was used to treat DBA/2 mice with Friend murine leukemia virus-induced polycythemia (F-MuLV-P). In these mice a new cell type, found after virus infection, gave rise to erythropoietic colonies in vitro without addition of erythropoietin (Ep) and completely replaced Ep-dependent normal erythropoietic colonies in vitro. The colony-forming units in the spleen (CFUs), the colony-forming units in culture (CFUc), and the erythropoietic colony-forming units (CFUE) were studied. Two days after treatment, CFUs were reduced to about 20% in controls and F-MuLV-P-infected animals, and CFUc were reduced to 6-11% in controls and F-MuLV-P-infected animals. CFUE were not detectable. At day 4 after the first HU dose, when CFUs has regenerated to about normal levels, a sharp rise in Ep-dependent CFUE was seen in the marrow; this rise was not present before HU treatment. The subsequent fall at day 7 coincided with a regeneration of CFUE in the spleen, but in the spleen these CFUE were all Ep-independent. Possibly, the normal Ep-dependent CFUE during regeneration in the marrow might have derived from previously resting CFUs that were not killed by HU. The subsequent conversion to Ep independency could have been due to reinfection by F-MuLV-P persisting in the animal.
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PMID:Hematopoietic stem cells in Friend murine leukemia virus-infected mice undergoing chemotherapy: remission and relapse of erythropoietin-independent erythropoiesis induced by hydroxyurea. 28 82


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