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Friend leukemia

About: Friend leukemia is a research topic. Over the lifetime, 319 publications have been published within this topic receiving 7463 citations.


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Journal ArticleDOI
01 Jul 1975-Virology
TL;DR: Mice could be protected against Friend leukemia virus-induced leukemia by inoculation with the major viral glycoprotein GP71 or its antiserum.

96 citations

Journal Article
TL;DR: It is concluded that elevation of RNase activity within the lymphocyte represents an early event in oncogenic viral infection within these two tumor models.
Abstract: The ribonuclease activity of peripheral lymphocytes from Balb/c mice was studied at various intervals subsequent to infection of mice by oncornavirus. Lymphocytes from mice infected with Friend leukemia virus possessed elevation of RNase activity within 8 days subsequent to infection. Balb/c mice infected with Moloney sarcoma virus demonstrated an analogous elevation of RNase activity with 7-9 days postinfection. Diminishment of cellular RNase activity occurred in the Friend leukemia model concomitant to the occurrence of significant numbers of erythroblasts in the peripheral blood, while ribonuclease activity in lymphocytes from mice infected with Molney sarcoma virus returned to normal 1-2 weeks subsequent to host rejection of tumor. It is concluded that elevation of RNase activity within the lymphocyte represents an early event in oncogenic viral infection within these two tumor models. The possible meaning of elevation of RNase activity is a target (the lymphocyte) not predestined to undergo neoplastic transformation is discussed.

95 citations

Journal ArticleDOI
TL;DR: Findings indicate that 8-substituted analogues of guanosine and 2'-deoxyguanosine have the potential to terminate leukemia cell proliferation through conversion to end-stage differentiated cells.
Abstract: A variety of 8-substituted guanosine and 2'-deoxyguanosine derivatives were synthesized and tested as inducers of the differentiation of Friend murine erythroleukemia cells in culture. The most active agents in the guanosine series were 8-substituted-N(CH3)2, -NHCH3, -NH2, -OH, and -SO2CH3, which caused 68, 42, 34, 33, and 30% of erythroleukemia cells to attain benzidine positivity, a functional measure of maturation, at concentrations of 5, 1, 0.4, 5, and 5 mM, respectively. The 8-OH derivative of the 2'-deoxyguanosine series produced comparable activity, causing 62% benzidine-positive cells at a level of 0.2 mM. These findings indicate that 8-substituted analogues of guanosine and 2'-deoxyguanosine have the potential to terminate leukemia cell proliferation through conversion to end-stage differentiated cells.

89 citations

Journal ArticleDOI
TL;DR: The hypothesis thatPU.1 interferes with the commitment of erythroblasts to differentiate and that chemicals that reduce PU.1 expression reinstate the erythropoietic program is supported.
Abstract: Both viral and cellular genes have been directly implicated in pathogenesis of Friend viral erythroleukemia. The virus-encoded gp55 glycoprotein binds to erythropoietin receptors to cause mitogenesis and differentiation of erythroblasts. However, if the provirus integrates adjacent to the gene for the PU.1 transcription factor, the cell loses its commitment to terminally differentiate and becomes immortal, as indicated by its transplantability and by its potential for indefinite growth in culture (C. Spiro, B. Gliniak, and D. Kabat, J. Virol. 63:4434-4437, 1989; R. Paul, S. Schuetze, S. L. Kozak, and D. Kabat, J. Virol. 65:464-467, 1991). To test the implications of these results, we produced polyclonal antiserum to bacterially synthesized PU.1, and we used it to analyze PU.1 expression throughout leukemic progression and during chemically induced differentiation of Friend erythroleukemia (F-MEL) cell lines. This antiserum identified three electrophoretically distinct PU.1 components in extracts of F-MEL cells and demonstrated their nuclear localization. Although PU.1 proteins are abundant in F-MEL cells, they are absent or present in only trace amounts in normal erythroblasts or in differentiating erythroblasts from the preleukemic stage of Friend disease. Furthermore, chemicals (dimethyl sulfoxide or N,N'-hexamethylenebisacetamide) that overcome the blocked differentiation of F-MEL cells induce rapid declines of PU.1 mRNA and PU.1 proteins. The elimination of PU.1 proteins coincides with recommitment to the program of erythroid differentiation and with loss of immortality. These results support the hypothesis that PU.1 interferes with the commitment of erythroblasts to differentiate and that chemicals that reduce PU.1 expression reinstate the erythropoietic program.

83 citations

Journal Article
TL;DR: Inhibitors of DNA and RNA synthesis such as adriamycin, mitomycin C, and hydroxyurea:mithramycin were synergistic in stimulating erythroid differentiation.
Abstract: Summary The induction of erythroid differentiation in the T3-CI2 clone of Friend leukemia cells by dimethyl sulfoxide is accompanied by reduction in viral RNA-dependent DNA polymerase activity with increased cellular δ-aminolevulinic acid synthetase activity and hemoglobin synthesis. These cells were treated with a variety of compounds to determine whether other drugs are capable of inducing erythroid differentiation. While several hormones, inhibitors of RNA synthesis, organic solvents, inhibitors of DNA polymerase, sulfhydryl inhibitors, and inducers of δ-aminolevulinic acid synthetase administered singly did not stimulate hemoglobin synthesis like dimethyl sulfoxide, inhibitors of DNA and RNA synthesis such as adriamycin, mitomycin C, and hydroxyurea:mithramycin were synergistic in stimulating erythroid differentiation.

81 citations


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Performance
Metrics
No. of papers in the topic in previous years
YearPapers
20213
20192
20161
20151
20143
20121