Gene/Protein Disease Symptom Drug Enzyme Compound
Pivot Concepts:   Target Concepts:
Query: UMLS:C0023418 (leukemia)
 93,477 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Anomalous appearance of TL (thymus-leukemia) antigens is a characteristic feature of radiation-induced leukemias of C57bl/6 mice. We now report that thymocytes of irradiated C57BL/6 mice express TL antigens long before the development of overt leukemia. Thus, TL is a marker for preleukemic changes occurring during radiation leukemogenesis. Low levels of murine leukemia virus (MuLV)-related antigens are also detected on preleukemic thymocytes. Comparative tests on individual mice show no direct correlation between TL and MuLV antigen expression.
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PMID:Preleukemic expression of TL antigens in x-irradiated C57BL/6 mice. 19 1

A resistance locus to leukemogenesis in mice by A-RadLV (a variant of the radiation leukemia virus) is described. This locus, Rrv-1, was mapped to subregions I-A, I-B, and I-J of the H-2 complex. It is suggested that Rrv-1 may be in complementation with a second locus to the right of it, between Rrv-1 and H-2D. This localization and the complementation of the two loci for resistance are characteristics similar to Ir genes, and indicate a possible relationship between the genetic regulation of immune responsiveness and susceptibility to leukemia.
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PMID:Resistance genes to murine leukemia in the I immune response gene region of the H-2 complex. 19 97

Two cases of acute myeloblastic leukemia were observed in a young 22 year old woman, then two years later, in her brother aged 16 years. The elder brother had died previously probably from the same disease. The very rare families in which more than two members had the same type of leukemia show the possible intervention of a hereditary factor in leukemogenesis.
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PMID:[Familial leukemia]. 19 13

The effect of serum from 12 cats with lymphosarcoma induced by feline leukemia virus (FeLV) on the response of normal cat peripheral blood lymphocytes to phytomitogen-induced blastogenesis was studied. The majority of FeLV sera, when tested at a concentration of 20% of the incubation medium, caused a 40 to 70% reduction in the mean blastogenic response to concanavalin A compared to the response obtained with a similar concentration of normal feline serum. Results with pokeweed mitogen were similar, but the depression in blastogenesis was less than with concanavalin A. Further studies showed that the blastogenic inhibitory activity of FeLV serum (a) was heat labile at 56 degrees for 30 min, (b) could not be overcome by greater concentrations of mitogens, (c) was proportional to the concentration of FeLV serum in the incubation medium, and (d) could not be demonstrated when lymphocytes were preincubated in FeLV serum followed by washing and reincubating in normal feline serum. The results suggested that a substance present in the serum of FeLV-infected cats contributes to altered immunological reactivity during leukemogenesis in the cat.
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PMID:Inhibition of normal lymphocyte mitogenic reactivity by serum from feline leukemia virus-infected cats. 19 25

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

Four biologically distinct groups of endogenous murine leukemia virus (MuLV) have been isolated from AKR mice. These viruses included (i) ecotopic XC+ MuLV that occur in high titer in normal tissues and serum of AKR mice throughout their life span, (ii) ecotropic XC- MuLV that are produced in high titers by leukemia cells, (iii) xenotropic MuLV that are readily demonstrable only in aged mice, and (iv) polytropic MuLV thatarise in the thymuses of aged mice as a consequence of genetic recombination between ecotropic and xenotropic MuLV. Virus of each of these biological classes were assayed in AKR mice for their ability to accelerate the occurrence of spontaneous leukemia. Certain isolates of ecotropic XC- MuLV and polytropic MuLV were found to have high oncogenic activity. These viruses induced 100% leukemias within 90 days of inoculation. In contrast, ecotropic XC+ MuLV that were obtained from AKR embryo fibroblasts and xenotropic MuLV that were obtained from the lymphoid tissues of aged AKR mice did not demonstrate oncogenic activity. These findings demonstrate fundamental differences between XC- and XC+ ecotropic MuLV that are found in leukemic and normal tissues, respectively. Furthermore, these findings point to the role of ecotropic XC- and polytropic MuLV in the spontaneous leukemogenesis of AKR mice.
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PMID:Oncogenicity of AKR endogenous leukemia viruses. 21 Dec 48

Normal mouse sera were tested for cytotoxic antibody to surface antigens of cultured monolayer cells infected with AKR-derived ecotropic MuLV, xentropic MuLV, or dualtropic MCF 247 MuLV. Antibody to ecotropic MuLV-infected cells was found in a proportion of C57BL/6, C3Hf/Bi, AKR-Fv-1b, and (C3Hf/Bi X AKR)F1 mice, but not AKR or (AKR X C3Hf/Bi)F1 mice. Antibody to xenotropic MuLV-infected cells was virtually restricted to C57BL/6 mice. Antibody to MCF 247-infected cells was found in all strains tested, including AKR mice. Absorption analysis of (C3Hf/Bi x akr)f1 and AKR-Fv-1b sera with selective reactivity for MCF 247-infected cells showed that these sera recognize distinctive antigens on MCF 247-infected cells that are not present on ecotropic or xenotropic MuLV-infected cells. The transplantable AKR spontaneous leukemia AKSL2 was found to be uniquely sensitive to the cytotoxic action of naturally occurring antibody to MCF 247-related antigens and absorption tests with AKSL2 as the target cell and sera from a single AKR-Fv-1b mouse have permitted the definition of a new MuLV-related cell surface antigen, which has been designated G(AKSL2). Thymocytes from young mice of high leukemia-incidence strains (AKR, C58, and PL) express G(AKSL2), whereas thymocytes from 12 other strains do not. In AKR mice, the antigen is expressed in higher amounts on cells from thymus and bone marrow than on spleen cells. All AKR spontaneous leukemias tested express G(AKSL2), as did three MuLV-induced leukemias arising in G(AKSL2)- strains. Five X-ray-induced leukemias of G(AKSL2)- strains were G(AKSL2)-, as were MuLV+ and MuLV- chemically induced sarcomas. In the limited survey conducted to date, natural antibody to G(AKSL2) has been restricted to strains expressing G(AKSL2) in their normal tissues: AKR, AKR congenic mice AKR-Fv-1b and AKR hybrid mice (C3Hf/Bi x akr)f1 and (C57BL/6 X AKR)F1. In vitro G(AKSL2) induction tests involving MuLV infection of cultured monolayer cells showed that 8 of 12 newly isolated dualtropic MuLV shared the property of G(AKSL2) induction with the prototype MCF MuLV, MCF 247. Of the 12 ecotropic MuLV tested, only the N-tropic MuLV isolated from a leukemia originally induced by Passage A Gross virus induced G(AKSL2). The xenotropic and amphotropic MuLV isolates tested lacked G(AKSL2) inducing activity. Recognition of the g(aksl2) system provides a way to trace the origin and natural history of a class of dualtropic MCF MuLV in the mouse and to determine whether natural antibody to G(AKSL2) plays a role in AKR leukemogenesis.
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PMID:G(AKSL2): a new cell surface antigen of the mouse related to the dualtropic mink cell focus-inducing class of murine leukemia virus detected by naturally occurring antibody. 21 64

The effect of leupeptin on the induction of lymphoblastic leukemia in ICR/JCL female mice by N-nitrosobutylurea (NBU) was investigated. NBU was given as a 0.02% solution in drinking water for 10 weeks. A 0.1% concentration of leupeptin was given in the diet. Group A was fed on the leupeptin diet from the beginning, Group B received it after the end of NBU treatment, and Group C was fed on a leupeptin-free control diet throughout. The average periods in the appearance of leukemia in groups A, B, and C were 115+/-50, 112+/-43, and 100+/-17 days (mean+/-SD), respectively, and there was a significant difference between groups A and B and Group C at P less than 0.001. In regard to this point, leupeptin might have the effect of retarding the rpocess of leukemogenesis. However, leupeptin showed no effect on the incidence and histopathological finding of leukemia.
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PMID:Effect of leupeptin on induction of lymphoblastic leukemia in mice by N-nitrosobutylurea. 26 41

A limited number of biologically active materials were examined for their relative ability to selectively inhibit the replication of Gross or Rauscher murine leukemia virus (MLV) in Swiss mouse embryo cells by means of the UV-XC plaque-reduction assay. Among the compounds demonstrating significant antiviral activity against Gross MLV in vitro were 1-(4-fluorobenzyloxy) adenosine (FBAR), polyadenylic acid [poly(A)], the carbocyclic analogue of 6-methylthiopurine ribonucleoside (C-MeMPR), 3-(2,4-dinitrophenylhydrazonemethyl)rifamycin SV (AF/DNFI), and phosphonoacetic acid (PAA). Five compounds that exhibited significant antiviral activity against MLV in vitro were tested for similar activity against Rauscher MLV in vivo. Three of these selected compounds, pyrazofurin (pyrazomycin), ribavirin (Virazole), and 9-beta-D-arabinofuranosyladenine (ara-A), produced a significant (50%-100%) inhibition of virus-induced splenomegaly development in mice, whereas the other two candidate inhibitors, 3-deazauridine (deazaUR) and rifamycin SV, the other two candidate inhibitors, 3-deazauridine (deazaUR) and rifamycin SV, failed to demonstrate any in vivo activity in this 21-day leukemogenesis assay. The administration of an inhibitor of adenosine deaminase (Co-vidarabine) in combination with ara-A resulted in an enhanced antiviral response in both infected cell cultures and animals. Co-vidarabine also increased the potency of ara-AMP against Gross MLV in vitro, indicating the probable dephosphorylation of the compound to ara-A and its subsequent deamination to ara-H in this system.
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PMID:Selective inhibition of RNA tumor virus replication in vitro and evaluation of candidate antiviral agents in vivo. 28 Jan 46

Friend leukemia virus induces erythroblastic leukemia in genetically susceptible BALB/c mice. FLV-containing leukemic cells markedly depressed the humoral immune response to SRBC in the appropriate mouse strain. Both immunosuppression and leukemogenesis were readily transmitted by cell-free virus-containing homogenates of the FLV leukemic splenocytes into normal BALB/c mice. In the present study it was found that both Friend leukemic splenocytes as well as virus containing extracts from the leukemic cells were neutralized by heating and by specific antisera. Suppressive activity passed through a 0.45 mu filter but not a 300,000 MW filter and could be pelleted at 100,000 x g. They were also highly resistant to inactivation by irradiation. Mice given leukemic splenocytes after irradiation with up to 32.000 rads still developed leukemia. Addition of either normal or irradiated FLV-leukemic cells to normal spleen cell cultures in vitro markedly suppressed antibody formation. At least 32,000 rads were required to significantly impair the immuno-suppressive activity of the FLV-leukemic cells. Thus, virus per se appears to be directly responsible for suppression of antibody formation to FLV.
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PMID:Factors from lymphoid cell tumor affecting immune responses. 39 42


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