Showing papers on "Friend leukemia published in 1981"

Amplification of the metallothionein-I gene in cadmium-resistant mouse cells

Abstract: Friend leukemia cells resistant to cadmium toxicity were selected. More than 70% of total cysteine incorporation in these cells was into the metal-binding protein, metallothionein. We used cDNA and genomic DNA clones containing the metallothionein-I gene to measure the concentration of its mRNA, the rate of gene transcription, and the number of genes. On a per cell basis, optimally induced, cadmium-resistant cells have a 14-fold more metallothionein-I mRNA, a 6-fold higher rate of metallothionein-I gene transcription, and 6-fold more metallothionein-I genes than do nonresistant cells. Metaphase spreads revealed that the resistant cells are nearly tetraploid and contain, on the average, three very small chromosomes that are absent from non-resistant Friend cells.

Clonal analysis of early and late stages of erythroleukemia induced by molecular clones of integrated spleen focus-forming virus

Abstract: The integrated proviral DNA of the polycythemia-inducing isolate of Friend spleen focus-forming virus (SFFVp) has been identified in rat cell clones nonproductively infected with this replication-defective erythroleukemia virus and cloned in phage lambda vectors. These lambda SFFVp recombinants, lambda SFFVp502 and lambda SFFVp542, contain endonuclease EcoRI inserts of size 7.4 and 8.2 kilobases, respectively, and include full copies of the SFFVp genome, along with host flanking sequences. Infectivity of the cloned SFFVp genomes was tested by a two-step DNA transfer procedure involving transfection of the cloned DNA into 3T3 mouse fibroblasts or cotransfer of the cloned DNA into thymidine kinase-deficient 3T3 cells together with the cloned thymidine kinase gene of herpes simplex virus, followed by rescue of the transferred DNA by superinfection with a helper virus. Inoculation of the rescued virus into adult mice resulted in the appearance of spleen foci, rapid splenomegaly, and polycythemia. Early after infection, spleen cell populations contained large numbers of cells capable of forming small erythroid colonies in vitro (CFU-E) in the absence of erythropoietin. Late after infection, these mice contained cells capable of forming macroscopic colonies (CFU-FV) in vitro. These data indicate that molecular clones of SFFVp, in conjunction with a helper virus, induce the appearance of hemopoietic colony-forming cells characteristic of both the early and late stages of Friend leukemia.

Friend leukemia as a multiple-step disease.

Abstract: The results presented here indicate that erythroleukemia induced by Friend virus evolve by multistage processes. The early phase of Friend disease is characterized by a rapid increase in the number of erythroblastic cells with limited proliferative capacity. The second phase is associated with the appearance of malignant cells with extensive proliferative capacity and autonomous growth. Friend leukemia appears to be a valuable model for studying the sequence of modifications occurring in cells progressing from a normal state to a preneoplastic and finally a highly malignant one.

Inducibility of spleen focus-forming virus by BrdUrd is controlled by the differentiated state of the cell

Abstract: All Friend cells--except thymidine kinase (ATP:thymidine 5'-phosphotransferase, EC 2.7.1.21)-deficient mutants--are highly inducible for the release of biologically active spleen focus-forming virus (SFFV) after exposure to BrdUrd. We studied SFFV production in somatic cell hybrids made between Friend leukemia cells (FLC) and cells expressing various differentiation programs. High inducibility of SFFV and release of constitutive Friend virus (FV) and SFFV are eliminated in all hybrids in which the potential for erythroid differentiation is suppressed. FV release and its induction by BrdUrd are unchanged in hybrids that maintain the expression of erythroid differentiation.

The effect of hexamethylene‐bis‐acetamide on multiparameter analysis of friend leukemia cells

Abstract: Friend leukemia cells were induced to differentiate by hexamethylene-bis-acetamide (HMBA). The relationship between cell growth cell volume distribution, fluorescence intensity and fluorescence anisotropy of the membrane probe 1,6 diphenyl 1,3,5 hexatriene (DPH) was analyzed in differentiated and undifferentiated cells with the aid of the fluorescence activated cell sorter (FACS II). The induction of a differentiated state was associated with a decrease in cell volume and an increase of fluorescence anisotrophy. The inhibition of this induction by dexamethasone prevented the decrease of cell volume without affecting the increase of fluorescence anisotropy. We conclude therefore that the high degree of anisotropy is not correlated to the differentiated state nor with the volume of the cells.

Normal and Friend Virus Specific Cell Compartments in Friend Leukemia Characterized by their Sensitivity to Actinomycin D in vivo

Abstract: DBA/2 mice were infected with the polycythemia inducing Friend Virus (F-MuLV-P) and treated with different doses of Actinomycin D (Act D) when the whole erythroid cell system, as measured by the CFU-E technique with and without addition of erythropoietin (Ep), had been transformed into Ep-independence. During and after this therapy the different stem cell pools CFU-S, CFU-C, BFU-E and CFU-E (with and without Ep) were studied and their sensitivity to Act D in bone marrow and spleen was compared to that of normal mice, recently published by other authors. There seemed to be no difference in the Act D sensitivity between normal erythropoiesis and Ep-independent erythropoiesis caused by F-MuLV-P. Furthermore a cell called ICPC (infectious centers producing cell) was studied. This cell system, detected by spleen colony formation due to high local virus production in an unirradiated host, proved to be Act D sensitive in the spleen but not in the marrow. When the erythroid cell system regenerated after Act D chemotherapy, all erythroid colony growth was Ep-independent. This means that Act D did not induce normal erythropoiesis as seen with hydroxyurea treatment.