Identification of a transforming virus from a lymphoma of a mouse infected with a wild mouse retrovirus.
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Biomedical subjects
T N Fredrickson
Publications and source records attributed to T N Fredrickson.
Magnal steroid hormone receptors during egg formation in the domestic hen.
Levels of magnal estrogen and progesterone receptors during egg formation in the hen were determined. Hens were sacrificed at various times after ovulation and magnal receptor levels were determined by tritiated hormone binding assays. A coincident increase in nuclear estrogen receptor and decrease in cytosol estrogen receptor 2 to 4 h postoviposition was suggestive of in vivo receptor translocation. At 12 to 16 h postoviposition cytosol progesterone receptor increased 2-fold and subsequently declined during the time of preovulatory progesterone surge (8 h to 6 h prior to expected ovulation). These data suggest that changes in circulating levels of estrogen and progesterone, associated with ovulation, are coordinated with oviductal function. This is reflected by fluxes of their respective oviductal receptors.
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Spontaneous tumors of NFS mice congenic for ecotropic murine leukemia virus induction loci.
NFS/N mice congenic for ecotropic murine leukemia virus (MuLV) induction loci from AKR and C58 mice ("NFS V-congenics") were evaluated for the development of spontaneous neoplasms in comparison to such development in virus-negative NFS/N mice. Congenic mice developed thymic lymphomas, whereas NFS/N did not. However, the frequency of thymic lymphomas was reduced, and the latent period for their development was prolonged in NFS V-congenics as compared to that in AKR/N or C58/Lw mice. In addition, the frequencies of nonthymic lymphomas and myelogenous leukemias were increased more than threefold in the congenics over NFS/N. The increased frequencies of hematopoietic neoplasms in congenic animals were related to early expression of high systemic levels of ecotropic MuLV.
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Histologic and cell surface antigen studies of hematopoietic tumors induced by Cas-Br-M murine leukemia virus.
Cas-Br-M, a cloned ecotropic murine leukemia virus (MuLV) of wild mouse origin that induces both neurogenic hindlimb paralysis and lymphomas, was injected into NFS/N inbred mice neonatally. Then the mice were observed for the development of neurologic disease and tumors. All mice manifested neurologic abnormalities by 6 months of age, and 58% of the animals died with hematopoietic neoplasms. The tumors included T- and B-cell lymphomas, lymphoblastic lymphoma, erythroleukemias, myelogenous leukemias, and a megakaryocytic leukemia. Cas-Br-M thus appeared to be unique among ecotropic MuLV in inducing a wide spectrum of hematopoietic tumors.
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A unique series of lymphomas related to the Ly-1+ lineage of B lymphocyte differentiation.
Six new B lineage lymphomas of NFS mice established in primary tissue culture were examined for a number of phenotypic, functional, virologic, and molecular genetic characteristics. Two of the tumors and their cloned derivatives bore surface markers characteristic of B cells, whereas four tumors resembled pre-B cells. One of the B cell and two of the pre-B cell lymphomas had rearrangements of both heavy and light chain immunoglobulin genes, confirming their designation as B-lineage lymphomas. All the tumors but one were Ly-1+, indicating that Ly-1 may be expressed by some pre-B cells as well as some B cells. In addition, one pre-B cell lymphoma was Mac-1+. MCF murine leukemia viruses obtained from two of the tumors did not accelerate development of B-lineage lymphomas in NFS mice.
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Susceptibility to Friend helper virus leukemias in CXB recombinant inbred mice.
The seven CXB recombinant inbred strains were tested for susceptibility to Friend helper virus (F-MuLV) hematopoietic neoplasms. BALB/c and CXB-H mice develop erythroblastosis after neonatal inoculation with F-MuLV, while C57BL/6 and the six other RI strains develop lymphoma and myelogenous leukemia. This strain distribution pattern is different from that for H-2, Gpd-1 (linked to Fv-1), Fv-2, Rfv-3, and Cv (linked to Rmcf) but the same as that for Bv, the endogenous ecotropic virus of C57BL/6. However, analysis of crosses segregating Bv show that resistance to F-MuLV erythroblastosis is not linked to Bv. Disease-free survival is shortest for BALB/c mice, intermediate for CXB-H and CXB-J, and longest for C57BL/6 and the other RI strains. We conclude: (a) the major C57BL/6 gene for resistance to F-MuLV erythroblastosis is different from previously identified Friend virus restriction loci; (b) latency for F-MuLV leukemias is controlled by more than one gene; and (c) latency and susceptibility to F-MuLV erythroblastosis are not inherited concordantly in the CXB-RI strains.
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A new gene that controls the type of leukemia induced by Friend murine leukemia virus.
NB tropic Friend murine leukemia virus (F-MuLV) replicates equally well in BALB/c and C57BL mice inoculated as neonates but causes almost exclusively erythroblastosis in BALB/c mice and nonerythroid (lymphoid and myelogenous) leukemias in C57BL mice. The C57BL resistance to erythroblastosis appears to be controlled by a single dominant gene in first and second backcrosses to BALB/c. This resistance to erythroblastosis is distinct from other genes known to affect susceptibility to Friend virus including Fv-1, Fv-2, H-2, Rfv-3, Fv-4, and Rmcf. We suggest the name Fhe for the new gene controlling susceptibility to Friend helper virus erythroblastosis.
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Murine erythropoietin in ascitic fluid.
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Animals↗
Colony stimulating activity in sera of erythroleukemic mice (RLV-A).
RLV-A serum activity was measured by the agar colony assay to determine the effect of this erythroid dyscrasia on the granulopoietic humoral regulator, colony stimulating factor (CSF). In general, the sera of early, midstage and terminal animals not given endotoxin had high cluster forming properties compared to normal sera. The sera of early, midstage, and terminal mice treated with endotoxin had only a fraction of the colony forming ability of serum obtained from normal endotoxin-treated mice (EMS) with the earliest stages of the disease showing least activity followed by a rise in activity paralleling normal EMS, as the disease progressed. Sera from RLV-A endotoxin treated mice retained ability to stimulate cluster growth especially when compared to the slight activity displayed by normal endotoxin treated mouse sera.
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The effects of endotoxin on CFU-C clonogenic capacity of marrow and spleen cells from RLV-A infected mice.
Bacterial endotoxin was used as a granulopoietic stressor in the RLV-A infected mouse as a means of studying the marrow and spleen CFU-C response to this agent. A control group of phenylhydrazine (PHZ)-treated mice was also employed to induce a reduction in hematocrit levels equivalent to that observed in the early and mid-stage of the disease course and was used to determine whether the cloning observed was a manifestation of RLV-A disease or could be attributed solely to the resulting anemia. Both RLV-A infected and PHZ marrow from mice maintained at a hematocrit of 40% exhibited similar but higher than normal clonogenic capacities, whereas RLV-A (hematocrit 40%) spleen had an expanded number of CFU-C's when compared to PHZ treated (hematocrit 40%) mice. Examination of spleens of endotoxin-treated RLV-A (hematocrit 30%) infected mice indicated a 6 to 7-fold increase in splenic CFU-C numbers compared to endotoxin-treated normal mice. PHZ plus endotoxin-treated normal animals (hematocrit 30%) had splenic CFU-C values which were approximately half those of RLV-A infected (hematocrit 30%) endotoxin-treated animals. Results of this experiment suggest a fully operable but greater than normal CFU-C storage pool in the RLV-A infected mouse spleen which does not seem to be due entirely to the anemia.
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Increased serum erythropoietin activity in rats following intrarenal injection of nickel subsulfide.
To investigate the pathophysiologic mechanisms of nicekl-induced erythrocytosis, serum erythropoietin activities were measured in (a) pooled serum from rats at 2 wk after intrarenal injection of alpha Ni3S2 (5 mg/rat), and (b) pooled serum from control rats at 2 wk after intrarenal injection of sterile NaCl vehicle (0.4 ml/rat). A sensitive erythropoietin bioassay was employed, which entailed repetitive administration of test serums to post-hypoxic polycythemic mice in divided doses (12 s.c. injections of 0.5 ml of serum at 6 hr intervals for 3 da; total dose = 6 ml of serum/mouse). The erythropoietin detection limit was congruent to 20 I.U./liter of serum. In mice which received pooled serum from alpha Ni3S2-treated rats, erythrocyte 59Fe-uptake averaged 28% (S.D. +/- 5) (vs 3.7 +/- 1.1% in control rats; P less than 0.001). Based upon a 7-point calibration plot, the erythropoietin activity in pooled serum from alpha Ni3S2-treated rats averaged 130 I.U./liter (S.D. +/- 18) (vs 27 +/- 6 I.U./liter in control rats; P less than 0.001). In vitro addition of Ni(II) to rat serum (100 microgram/liter) had no effect upon serum erythropoietin activity. This study demonstrates that induction of erythrocytosis in rats by intrarenal injection of alpha Ni3S2 is mediated by increased serum erythropoietin activity.
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Chromosomal evidence for the transplantability of the Shay chloroleukemia.
Chloroma cells, which were shown to contain the X and Y chromosomes, were used to induce Shay chloroleukemia (SCL) in female recipients. Karyotype analyses of leukemic myeloblasts which appeared in the peripheral blood of the female recipients during blast crisis demonstrated invariably the presence of the X and Y chromosomes. These results directly demonstrate that transmission of SCL is the result of donor cell colonization and therefore SCL can be considered a true transplantable leukemia. Reports by other workers of viral association with this disease are discussed in light of our results.
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Measurement of erythropoietin in chloroleukemic rats.
Erythropoietin (Ep) levels were measured in Shay chloroleukemic rats at various stages of anemia. Serum Ep was shown to increase logarithmically as the anemia became more severe. This increase in Ep levels was similar to that observed in normal rats subjected to acute blood loss. Significant levels of Ep were also demonstrated in ascitic fluid extracted from the peritoneal cavity of leukemic rats. These results indicate that the anemia of this disease is not due to a diminished production of Ep.
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Failure of mice infected with Rauscher leukemia virus (RLV-A) to develop splenic colonies.
A progressive increase occurs in the CFU-S/10(6) spleen cells with the development of RLV-A-induced erythroleukemia. In addition, alteration of the spleen by the RLV-A appears to prevent the seeding and development of spleen colonies in infected mice.
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The interaction of erythropoietin with fetal liver cells. I. Measurement of proliferation by tritiated thymidine incorporation.
Erythropoietin stimulates the erythropoietin responsive cell to undergo DNA synthesis and subsequent mitosis. To define further the physiology of this effect, a liquid suspension microculture utilizing mouse fetal liver cells was developed. Tritiated thymidine incorporation into erythroid precursors was found to parallel radiolabeled iron incorporation with peak DNA synthesis occurring after 24 hours of culture. Both tritiated thymidine and iron incorporation were dependent on erythropoietin concentration. The responsiveness to erythropoietin decreased when erythropoietin was withheld and this diminishment in reactivity paralleled a morphological differentiation of the cells. This observation, together with the finding that erythropoietin activity could be removed by absorption with large numbers of cells, suggests the proliferation induced by erythropoietin depends on a specific stage in the differentiation of the red blood cell and may be mediated through a specific cellular receptor.
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The interaction of erythropoietin with fetal liver cells. II. Inhibition of the erythropoietin effect by interferon.
To investigate the effect of interferon on the proliferation of normal erythroid precursor cells, various interferon preparations were added to mouse fetal liver cells cultured in a liquid microculture system. The effect of interferon was studied using cellular tritiated thymidine incorporation both in the presence and in the absence of erythropoietin. Interferon was found to suppress cellular tritiated thymidine incorporation. The suppression was directly related to the antiviral activity and was not found when control preparations were used. The mechanism of suppression seemed to involve a direct effect on the cells which was dependent of erythropoietin. These studies suggest that the viral inhibitory effects of interferon may also be accompanied by effects on normal cellular proliferation.
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In vitro evaluation of granulocyte differentiation of diffusion chamber inocula.
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Animals↗
In vitro granulocytic stem cell clonogenic capacity of marrow and spleen cells from mice infected with Rauscher leukemia virus.
Bone marrow and spleen cells from early, midstage, and terminal Rauscher leukemia virus (RLV-A)-infected erythroleukemic mice were assessed for granulocyte stem cell (CFU-c) clongenic capacity in the semisolid agar culture assay. It was found that marrow CFU-c concentrations exceeded normal in early stages of this erythroid disease but returned to near normal values during mid- and terminal phases. Splenic CFU-c concentrations, on the other hand, were generally higher than control values for all stages of the disease. These results are discussed with reference to the pathogenesis of RLV-A disease.
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