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Query: UMLS:C0598766 (leukemogenesis)
 4,065 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Repeated percutaneous applications of 7,12-dimethylbenz(a)anthracene on weaning DBA/2 and ST/a mice induced 100% leukemias with short latency periods. Endogenous C-type viruses were activated during the treatment as evidenced by (a) increased expression of the murine leukemia virus major core protein, p30, in blood and spleens and (b) increased frequency of detection of ecotropic virus by cocultivation of the splenocytes with SC-1 cells. The treatment did not affect p30 expression in several nonlymphoid organs, and detection of xenotropic viruses in the splenocytes was decreased. Virus expression did not correlate with the progression of disease in that (a) high p30 levels were generally found in mice with relatively low spleen weights and (b) p30 levels had no obvious connection to survival of the individual. 7,12-Dimethylbenz(a)anthracene treatment had little influence on p30 expression in spleens and blood from C3H and BALB/c mice, which are less sensitive to 7,12-dimethylbenz(a)anthracene-induced leukemogenesis. The results indicate an association of C-type virus activation with chemical induction of leukemia but do not necessarily imply an etiological role of the virus in the disease.
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PMID:Activation of C-type virus during chemically induced leukemogenesis in mice. 20 89

Ultrastructural, enzyme histochemical (acide phosphatase, adenosine triphosphatase, neutral 5'-nucleotidase) and immunohistochemical (cytokeratins with monoclonal antibodies BH11 and BC3) features of the thymus cortical epithelial cells of leukemic DBA/2 inbred mice have been studied. In the leukemic mice epithelial cells appeared possessing some ultrastructural and histochemical features of cell activation. Lympho-epithelial complexes, composed mainly of BH11 and BC3 immunoreactive cells and of lymphoid cells were subcapsulary and subseptally found. It is discussed on the eventual involvement of the lympho-epithelial complexes in the intrathymic leukemogenesis during lymphoid leukemia.
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PMID:Structural and histochemical features of cortical thymic epithelial cells in mice with chemically-induced lymphoid leukemia. 324 59

The relationship between immunodepression and leukemogenesis induced by a murine retro-virus. PLLV-T2, was studied in different strains of mice. Cellular immunity, using as parameters both allograft rejection and graft versus host reaction, was not affected during the early phase of leukemia development. As for humoral immunity, determined by the response to xenogeneic red blood cells and to lipopolysaccharides, no direct relationship between the immunodepression caused by the retrovirus and leukemogenesis could be encountered: in certain strains, such as DBA/2, with susceptibility to leukemogenesis similar to that of BALB/c, no decrease in the immune response was registered during the early phase of the disease. The results obtained demonstrate that immunodepression is not a necessary condition for the clinical appearance of this viral-induced leukemia indicating that humoral and/or cellular immunity would not play an important role as surveillance mechanism against this neoplasia.
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PMID:[Lack of relationship between viral leukemogenesis and immunosuppression in the mouse]. 610 Oct 65

Glycolipid-bound sialic acid levels were elevated 2 to 4-fold in the sera of two strains of mice bearing thymic lymphoma produced either spontaneously (AKR/J) or due to chemical carcinogenesis [Swiss mice injected with 5-(3,3-dimethyl-1-triazeno)imidazole-4-carboximide]. The serum glycolipid-bound sialic acid level reflected the tumor burden of the AKR/J mice during the early stages of leukemogenesis. Furthermore, the elevation was found to coincide with the ontogenesis of thymic lymphoma and not to be simply an age-dependent phenomenon. TLC analysis of Florisil column-purified gangliosides from the sera of AKR/J and Swiss mice suggested presence of gangliosides with mobilities very close to GM2 and GM3 standards respectively. On the premise that the elevated glycolipid levels in circulation might interfere with normal lymphocyte functions, the immunoinhibitory properties of exogenously added mixed gangliosides were examined on tests of in vitro correlates of the immune response. Gangliosides inhibited concanavalin A and lipopolysaccharide-induced [3H]-thymidine, [14C]-leucine and [3H]-lysine uptake by normal AKR/J mouse thymocytes and spleen cells. Mixed gangliosides also suppressed the two-way mixed lymphocyte reaction of AKR/J X Swiss and AKR/J X DBA/2 spleen cells. These and other results strongly suggest a general immunologically relevant role for gangliosides in the ontogeny of thymic lymphoma of mice.
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PMID:Murine leukemia. Proposed role for gangliosides in immune suppression. 621 63

Male mice of strain GR develop T-cell leukemia at a low frequency late in life. These leukemia cells contain large amounts of mouse mammary tumor virus (MMTV) RNA and MMTV proteins in a precursor form (Nusse et al., J. Virol. 32:251-258, 1979). We used restriction enzyme analysis and molecular hybridization to identify MMTV proviruses in the DNA of these leukemia cells. GR leukemia cells contained additional integrated MMTV proviruses at various sites in the genome. This amplification of MMTV proviruses in GR leukemia cells is not restricted to one particular endogenous MMTV provirus of strain GR. The number and location of the extra MMTV proviruses present in transplants of GR leukemia cells did not change upon serial transplantation of the leukemia cells. Acquisition of MMTV proviruses was also found in a similar leukemia, L1210 of the DBA/2 mouse strain, but not in three other leukemias, SL2 of DBA/2, BW5147 of AKR, and a spontaneous thymoma of BALB/c. The two main classes of MMTV RNA, 35S and 24S, were present in the cytoplasmic RNA of GR leukemia cells, indicating that the aberrant processing of MMTV precursor proteins is not due to anomolously sized RNAs. We could not detect extra RNAs in GR leukemia cells which would represent read-through transcripts of cellular genes adjacent to the extra MMTV proviruses, initiated by a promoter signal in the right MMTV long terminal repeat sequence. These data suggest that acquisition of MMTV proviruses may coincide with the onset of leukemogenesis in GR male mice.
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PMID:Acquisition of proviral DNA of mouse mammary tumor virus in thymic leukemia cells from GR mice. 629 63

DBA/1, DBA/2, CBA/N, and CBA/Ca mice carry a gene which specifically restricts infectivity of mink cell focus-forming (MCF) murine leukemia viruses. The gene, designated Rmcfr, is dominant or semidominant and maps to chromosome 5; it is closely linked to the morphologic marker gene Hm. The Rmcf gene may be of much use as a means of determining the role of MCF viruses in various forms of leukemogenesis.
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PMID:A mouse gene on chromosome 5 that restricts infectivity of mink cell focus-forming recombinant murine leukemia viruses. 630 33

Leukemias induced by neonatal inoculations of several mouse strains with different strains of Friend murine leukemia helper virus (F-MuLV) were followed for time of disease onset, cytochemical analysis of predominant cell types in leukemic organs, and expression of infectious mink cell focus-inducing (MCF) viruses detected by mink cell foci or MCF-specific monoclonal antibodies. Most BALB.B and IRW mice had a rapidly appearing, severe anemia and hepatosplenomegaly consisting of erythroid cells. MCF viruses were usually isolated from enlarged spleens of IRW mice. In contrast, C57BL/10 mice had a lower incidence of disease and much slower course. Splenomegaly and lymphadenopathy with mild anemia were seen, and the predominant cell types were either myeloid (chloroleukemia) or lymphoid. MCF viruses were never isolated from this mouse strain. (C57BL/10 X IRW)F1 mice were intermediate in latency, but all mice had disease by 8 months. Myeloid, lymphoid, and some mixed leukemias with an erythroid component were observed, but in no case did we see the severe anemia or pure erythroid involvement typical of IRW and BALB.B mice. MCF viruses were, however, isolated from 22% of these mice regardless of leukemia cell type. DBA/2 mice had a disease pattern similar to the (C57BL/10 X IRW)F1 mice, and MCF viruses were isolated from three of six mice tested. Inoculation of IRW mice with the low virulence B3 strain of F-MuLV produced disease with a longer latency than F-MuLV 57, but similar cell types were transformed by both viruses. In vitro cell lines were derived from 14 mice, and most were tumorigenic in vivo. Three lines released infectious MCF virus, and three others expressed MCF-specific cell surface antigens but did not release virus. Eight lines expressed no MCF infectious virus or viral antigens. Several lines released infectious xenotropic viruses and/or expressed xenotropic MuLV cell surface antigens recognized by monoclonal antibodies reactive with xenotropic viruses. The lack of MCF expression in many primary leukemic tissues as well as in in vitro derived leukemia cell lines of C57BL/10 and (B10 X IRW)F1 mice suggested that MCF virus generation and expression may not be required for leukemogenesis in some mouse strains or in some hemopoietic lineages.
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PMID:Effect of murine host genotype on MCF virus expression, latency, and leukemia cell type of leukemias induced by Friend murine leukemia helper virus. 630 93

T cell leukemias were induced by a single dose of methylnitrosourea (MNU) in DBA/2, C57/Bl/6, NMRI, BDF1, and CBA mice. The latency period in the CBA strain was much longer than in the others. Studies on the pluripotent stem cells in the bone marrow and T cell reactions of thymus and spleen cells showed a toxicity of MNU for these parameters but no significant differences between the strains. The activity of the natural killer (NK) cells in the spleen and peritoneal exudate cells, studied also after additional stimulation by injection of Corynebacterium parvum, was influenced by MNU, but again no relation to leukemogenesis could be established. The first leukemic (transplantable) cells were found in the thymus. The presence of leukemic cells could be responsible for low NK cell activities found in BDF1 and DBA/2 mice late after MNU.
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PMID:Leukemia induction by methylnitrosourea (MNU) in selected mouse strains. Effects of MNU on hemopoietic stem cells, the immune system and natural killer cells. 633 13

Investigations were performed on models of murine leukemogenesis induced by butylnitrosourea or methylnitrosourea in DBA/2, C57B1/6, NMRI, BDF and CBA mice. The latency period in CBA mice was longer than in mice of the other strains. The first transplantable cells appeared mostly in the thymus, and only in two cases in the bone marrow. Methylnitrosourea suppressed the activity of natural killer cells, but not to the same extent as leukemogenic irradiation. Heterogeneity of leukemic T-cell phenotypes with respect to the expression of the ly-1 and ly-2 antigens was detected. At the same time leukemic cells revealed consistent inability to be agglutinated by peanut agglutinine. When hydrocortisone was injected to mice after the carcinogene treatment or within 24 h before it, the leukemogenesis was delayed.
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PMID:[T-cell lymphomagenesis induced by chemical carcinogens in mice]. 633 77

It has previously been shown that DBA/2 mice protected against the development of Friend leukemia virus (FLV)4-induced disease by the passive administration of heterologous antisera directed against disrupted virions or the major viral envelope glycoprotein (gp71) fail to undergo the generalized immunosuppression which characterizes FLV leukemogenesis. In the present studies, the susceptibility of spleen cells from serum-protected mice to the immunosuppressive effects of FLV-infected spleen cells has been examined by means of in vitro assays of antibody production and of natural killing (NK). In contrast to the parallel suppression of both functions in FLV-infected mice and their lack of suppression in serum-protected animals, a dichotomy was observed in the in vitro susceptibility of these activities of spleen cells from serum-protected mice to the suppressive effects of virus-infected splenocytes, implying that more than one mechanism of suppression is operative. Thus, the antibody-producing capability of serum-protected splenocytes was not suppressed by FLV-infected spleen cells, this suppression reflecting the activity of infectious virus, while the NK effector function of serum-protected spleen cells was as susceptible as that of normal splenocytes to suppression by virus-infected spleen cells. This suppression of NK activity is mediated by virus-induced suppressor cells and does not involve free infectious virus, in contrast to suppression of antibody production. These results thus indicate that, while serum therapy inhibits the development of the virus-induced NK suppressor cells found in the spleens of progressively infected mice, splenic NK effectors, which are present, demonstrate full susceptibility to the suppressive effects of such independently generated virus-induced suppressor cells. Preliminary attempts at characterizing these NK suppressors in the spleens of FLV-infected mice indicate that they are not eliminated by treatment with antisera directed against T cells, B cells, macrophages or FLV gp71. However, Percoll fractionation of spleen cells from infected mice has revealed the presence of an expanded (as compared to normal spleen cells) population of cells of density 1.077 which demonstrates high in vitro NK suppressor activity, presumably representing the virus-induced suppressor cells measured in this assay. At the present time, the mechanism of the resistance of serum-protected spleen cells' antibody production to suppression by FLV-infected splenocytes (i.e., by FLV itself) remains undefined.
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PMID:Immunotherapy of murine leukemia. XI. differential susceptibility of spleen cells from serum-protected mice to the in vitro immunosuppressive effects of Friend leukemia virus-infected splenocytes. 654 Jul 57


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