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 susceptibility to two tissue culture cell lines established from (BALB/cx DBA/2)F1 (CDF1) mice to murine leukemia viruses (MLVs) was compared with those of various cell lines. While embryo cells of CDF1 mice were resistant to both N- and B- tropic MLVs, one cell line was susceptible to N-tropic MLV and the other to B-tropic MLV. So the cell lines of CDF1 mice had not the same susceptibility to MLVs as CDF1 embryo cells had. Cell lines established from N- and B-type inbred mice had kept their original susceptibility to MLVs. These results suggested the phenotype of some F1 hybrid mouse cells tended to change into either parental type after establishment as cell lines.
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PMID:Cell lines established from (BALB/cx DBA/2)F1 mice which show parent type susceptibility to murine leukemia viruses. 18 Mar 14

Specific rabbit antisera to the major glycoproteins of Friend leukemia virus (gp71) and the mouse mammary tumor virus (gp52) were utilized to study the surfaces of C3H-, DBA-, BALB/c-, and C57BL-transformed and normal cells by immunoelectron microscopy. Antiserum to gp71 showed reactivity with all of the mouse cells tested regardless of strain, virus production, or state of transformation. In cells producing murine leukemia virus, budding viruses and other areas of the cell surface were consistently labeled with gp71 antiserum. A gp52-like antigen was likewise detected on both cell surfaces and virions of C3H and DBA cells producing the mammary tumor virus. Budding virions with surface spikes but with crescent-shaped nucleoids in C3H/HeJ cells were labeled specifically with gp52 antiserum. The antigen localized with anti-gp52 serum was detected in low concentration on the surface of nonvirus-producing cultures of a C57BL/6 sarcoma induced by the Schmidt-Ruppin D strain of Rous avian sarcoma virus (SRD-2), a BALB/c bone marrow culture (JLS-V9), and a normal BALB/c fibroblast culture (BALB/cF). Other cell cultures transformed by either C-type virus or methylcholanthrene failed to demonstrate gp52 antigen. Both gp52- and gp71-like antigens were found to be expressed simultaneously in C3H/HeJ, C3H-MT, DBA-MT, SRD-2 (transformed) and BALB/cF, JLS-V9, and C3H-1 (normal) cultures. Expression of gp52 antigen in the absence of gp71 was not detected in any of the cultures examined. These findings demonstrate the ubiquitous expression of gp71 in a wide variety of normal and transformed mouse cells while gp52 tends to be expressed predominantly in cells from mice with high mammary tumor incidence (C3H) and DBA), but only to a minor extent in cells from low mammary tumor incidence strains (BALB/c and C57BL).
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PMID:Detection of the major glycoproteins of Friend leukemia virus (gp71) and the murine mammary tumor virus (gp52) on the surface of mouse cells. 18 44

The major core protein, p30, of mouse C-type viruses was quantitated radioimmunologically in lymphoid organs and blood from inbred strains of mice. The concentration of p30 in thymus and spleen had a weak and moderate correlation, respectively, to leukemia frequency. In contrast, the concentration of p30 in blood from mice with a high incidence of leukemia (strains AKR and C58) was 100-fold increased at 2 months of age compared with 10 strains with a low incidence of the disease. The SJL mice, which have a high incidence of reticulum cell neoplasms, showed generally elevated, but variable, values. The high concentration in AKR blood developed during the first weeks of life. Approximately one-third of the DBA/2 mice had elevated levels after 4 to 5 months, whereas the values from mice of the 129 strain were low irrespective in their age. The major part of p30 appeared to be associated with the erythrocytes. The concentration of p30 in the blood seems to reflect the presence of replicating virus in mice. It identifies among the inbred strains a high leukemia group one-half year prior to disease.
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PMID:C-type virus protein p30 in blood from inbred mice correlates with their later incidence of leukemia. 19 98

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

Allogenic, semisyngeneic and syngeneic sera of animals immunized with ML-positive leukemia L1210 cells, besides anti-ML antibodies, contain antibodies which react with Gross cellular surface antigen. ML antigen and Gross cellular surface antigen were shown by the immunoferritin test in electron microscopy, and by the blocking test, to be situated on different parts of the cell surface. No budding viral particles were found on the areas occupied by these antigens. By distinguishing the ML antigen identified on the surface of leukemia L1210 cells from the Gross cellular antigen, it was shown that the MTV present in leukemias of DBA/2 mice has no leukemogenic properties. Demonstration of core and envelope antigens of the MTV and Gross MuLV, besides C particles and intracytoplasmatic A particles, which are precursors of B particles, is proof of existence of genomes of both viruses in leukemia L1210 cells. The ability of leukemia L1210 cells to absorb activity from the anti-ML sera and reaction between anti-ML sera and isolated B particles of the MTV in immunoprecipitation, indicate probable existence of an antigenic component of the MTV within the ML antigen.
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PMID:Serological identification of viral and virus-related antigens on DBA/2 mouse leukemia lymphocytes. 22 Sep 30

Flow microfluorometry was used to assess levels of xenotropic murine leukemia virus envelope-related cell-surface antigens (XenCSA) expressed on lymphocytes of mice derived from crosses between C57BL/6 (B6) and DBA/2 (D2); 24 recombinant inbred strains (BXD RIs) and 62 backcross mice were studied. The results suggest that XenCSA expression is affected by more than one gene but that the predominant influence is exerted by a single semidominant gene apparently located on chromosome 4 at or in close proximity to the Fv-1 locus. Studies of spontaneous virus production in B6D2F1 X D2 mice suggest that this locus may also affect production by spleen cells of xenotropic MuLV registering in a fluorescent antibody assay of mink lung cells.
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PMID:Expression of xenotropic murine leukemia viruses as cell-surface gp70 in genetic crosses between strains DBA/2 and C57BL/6. 22 12

A temperature-sensitive strain of Sendai virus, HVJ-pi, showed little or no cytopathic effect and led to establishment of carrier cultures in several cell lines. By the use of this characteristic, L1210 leukemia cells persistently infected with HVJ-pi (L1210/c--HVJ-pi) was established, almost all of which were positively stained with fluorescent HVJ antibody. They are viable and grow almost equally as uninfected L1210 leukemia cells in vitro. Athymic nude mice (BALB/c, nu/nu), deficient of T-cells, died from intraperitoneal inoculation of L1210/c--HVJ-pi cells as well as by uninfected L1210 leukemia cells. However, viable L1210/c--HVJ-pi cells showed lower transplantability in normal syngeneic mice. This immunological mechanism of rejection was explained by the modification of cell surface membrane due to HVJ-pi infection. The mice which survived the inoculation of 10(5) L1210/c--HVJ-pi cells were able to reject 10(5) uninfected L1210 leukemia cells challenged subsequently. The induction of immune resistance was more prominent in (C57BL/6 x DBA/2)F1 mice or (BALB/c x DBA/2)F1 mice than in DBA/2 mice.
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PMID:Induction of tumor resistance in mice by L1210 leukemia cells persistently infected with HVJ (Sendai virus). 22 53

BW 5147 leukemia in AKR mice has been successfully treated by adoptive immunotherapy using allogeneic spleen cells from C57BL/6J mice. Graft-versus-host reaction was prevented by treatment with spleen cells from a second allogeneic strain (CBA, H-2 identical with AKR), followed by cycloposphamide and syngeneic spleen cells. Successful treatment of leukemia without graft-versus-host reaction is dependent upon a close relationship at the H-2 locus between the second allogeneic donor and the host AKR mice, since cells from a non-H-2 identical donor (DBA/2) do not increase survival. The doses of cyclophosphamide and of C57BL/6J spleen cells are also parameters of critical importance in successful treatment.
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PMID:Graft versus leukemia without fatal graft-versus-host disease in AKR mice. 23 89

We examined L1210 murine leukemia growth rate and survival of host male DBA/2J mice fed a diet rich in either polyunsaturated fat (16% sunflower oil) or saturated fat (16% coconut oil). The survival of mice that received transplants of L1210 leukemia cells was longer among the animals that had ingested a diet rich in the saturated fat as compared to those fed the more unsaturated fat. In duplicate experiments, the mean survivals of mice fed coconut oil were 200.9 +/- 1.6 and 202.5 +/- 3.4 hours compared to 188.7 +/- 5.3 and 187.6 +/- 3.5 hours for those fed sunflower oil. Tumor growth rate or the rate of DNA synthesis by the leukemia cells did not differ between the two experimental groups. Therefore, the alteration in survival was apparently due to an effect of the diets on the responses of the hosts rather than their effect on tumor size or growth rate.
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PMID:Effect of dietary fat saturation on survival of mice with L1210 leukemia. 27 34

The spleen colony assay was used to examine the effect of thymidine (dThd) on 5-fluorouracil (FUra) cytotoxicity in two transplantable leukemias, AKR (in AKR mice) and L1210 [in (BALB/c x DBA/2)F1 mice], in vivo. A large dose of dThd (10 mg/mouse) could not rescue these cell lines from FUra toxicity. Instead, when dThd was given within 1 hour before FUra, it enhanced FUra cytotoxicity by a factor between 100 and 1,000 in AKR leukemia. That dThd increased the cytotoxicity of FUra only by a factor of 3 in L1210 leukemia suggested a different mechanism of interaction of the two drugs in the two cell lines. Examination in hybrid mice capable of supporting the growth of both leukemias showed the enhancement to be tumor related rather than host related. We also demonstrated a dose-dependent effect of dThd injection 15 minutes before FUra in AKR leukemia. Concerning the kinetics of killing of AKR leukemia colony-forming units (LCFU) following the administration of dThd 15 minutes before FUra, LCFU survival continued to decrease for 24--36 hours following drug administration.
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PMID:In vivo enhancement of 5-fluorouracil cytotoxicity to AKR leukemia cells by thymidine in mice. 27 62


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