scholarly journals BALB- and Harvey-murine sarcoma virus transformation of a novel lymphoid progenitor cell.

1982 ◽  
Vol 156 (3) ◽  
pp. 873-887 ◽  
Author(s):  
J H Pierce ◽  
S A Aaronson
Keyword(s):  
Progenitor Cell ◽  
Leukemia Virus ◽  
Lymphoid Cells ◽  
Terminal Deoxynucleotidyl Transferase ◽  
Continuous Cell Lines ◽  
Early Stages ◽  
Sarcoma Virus ◽  
Murine Sarcoma

BALB- and Harvey-murine sarcoma viruses (MSV) comprise a family of retroviruses whose mouse- and rat-derived onc genes are closely related. These viruses induce sarcomas and erythroleukemias in susceptible animals. An in vitro colony assay that detects transformation of lymphoid cells by Abelson-murine leukemia virus was used to demonstrate that BALB- and Harvey-MSV transform a novel hematopoietic cell both in culture and in vivo. Bone marrow colony formation was sarcoma virus dependent, followed single-hit kinetics, and required the presence of mercaptoethanol in the agar medium. BALB- and Harvey-MSV-induced colonies could be established in culture as continuous cell lines that demonstrated unrestricted self-renewal capacity and leukemogenicity in vivo. The cells had a blast cell morphology and lacked detectable markers of mature cells within the myeloid or erythroid series. They also lacked detectable immunoglobulin mu chain or Thy-1 antigen, markers normally associated with committed cells of the B and T lymphoid lineages, respectively. However, the transformants contained very high levels of terminal deoxynucleotidyl transferase (TdT), an enzyme believed to be specific to early stages within the lymphoid differentiation pathway. This phenotype distinguishes these BALB- and Harvey-MSV transformants from any previously reported hematopoietic targets of transforming retroviruses, including the pre-B lymphoid cell transformed by Abelson-MuLV under identical assay conditions. These newly identified lymphoid progenitor cell transformants may provide an important means of studying early stages of lymphoid ontogeny and the possible role of TdT in lymphoid development.

In Vivo and In Vitro Studies on the Morphogenesis of Tumors Induced by Murine Sarcoma Virus (Harvey) 2

1973 ◽  
Vol 51 (5) ◽  
pp. 1541-1549 ◽  
Author(s):  
W. R. Thomas ◽  
E. J. Aw ◽  
J. M. Papadimitriou ◽  
P. J. Simons
Keyword(s):  
In Vitro Studies ◽  
Murine Sarcoma Virus ◽  
Sarcoma Virus ◽  
Murine Sarcoma

scholarly journals The effect of helper virus on Abelson virus-induced transformation of lymphoid cells.

1978 ◽  
Vol 147 (4) ◽  
pp. 1126-1141 ◽  
Author(s):  
N Rosenberg ◽  
D Baltimore
Keyword(s):  
Bone Marrow Cells ◽  
Cell Transformation ◽  
Leukemia Virus ◽  
Fibroblast Cell ◽  
Helper Virus ◽  
Lymphoid Cells ◽  
Mouse Bone Marrow ◽  
Abelson Virus

Abelson murine leukemia virus (A-MuLV)-transformed fibroblast nonproducer cells were used to prepare A-MuLV stocks containing a number of different helper viruses. The oncogenicity of the A-MuLV stocks was tested by animal inoculation and their ability to transform normal mouse bone marrow cells was measured in vitro. All of the A-MuLV stocks transformed fibroblast cells efficiently. However, only A-MuLV stocks prepared with helper viruses that are highly oncogenic were efficient in vivo and in vitro in hematopoietic cell transformation. In addition, inefficient helpers did not establish a stable infection in lymphoid nonproducer cells. Thus, helper virus has a more central role in lymphoid cell transformation than in fibroblast cell transformation.

scholarly journals Decreased susceptibility to calpains of v-FosFBR but not of v-FosFBJ or v-JunASV17 retroviral proteins compared with their cellular counterparts

1997 ◽  
Vol 323 (3) ◽  
pp. 685-692 ◽  
Author(s):  
Ann-Muriel STEFF ◽  
Serge CARILLO ◽  
Magali PARIAT ◽  
Marc PIECHACZYK
Keyword(s):  
Cysteine Proteases ◽  
Calcium Dependent ◽  
Peptide Motifs ◽  
Interesting Possibility ◽  
Murine Sarcoma Virus ◽  
Sarcoma Virus ◽  
Infected Cells ◽  
Murine Sarcoma

The c-Fos and c-Jun transcription factors are rapidly turned over in vivo. One of the multiple pathways responsible for their breakdown is probably initiated by calpains, which are cytoplasmic calcium-dependent cysteine proteases. The c-fos gene has been transduced by two murine oncogenic retroviruses called Finkel-Biskis-Jenkins murine sarcoma virus (FBJ-MSV) and Finkel-Biskis-Reilly murine sarcoma virus (FBR-MSV); c-jun has been transduced by the chicken avian sarcoma virus 17 (ASV17) retrovirus. Using an in vitro degradation assay, we show that the mutated v-FosFBR, but not v-FosFBJ or v-JunASV17, is resistant to calpains. This property raises the interesting possibility that decreased sensitivity to calpains might contribute to the tumorigenic potential of FBR-MSV by allowing greater accumulation of the protein that it encodes in infected cells. It has also been demonstrated that resistance to cleavage by calpains does not result from mutations that have accumulated in the Fos moiety of the viral protein but rather from the addition of atypical peptide motifs at its both ends. This observation raises the interesting possibility that homologous regions in viral and cellular Fos either display slightly different conformations or are differentially accessible to interacting proteins.

scholarly journals Expression patterns of c-myb and of v-myb induced myeloid-1 (mim-1) gene during the development of the chick embryo

Development ◽  
1992 ◽  
Vol 114 (1) ◽  
pp. 125-133 ◽  
Author(s):  
C. Queva ◽  
S.A. Ness ◽  
F.A. Grasser ◽  
T. Graf ◽  
B. Vandenbunder ◽  
...  
Keyword(s):  
Chick Embryo ◽  
Leukemia Virus ◽  
Expression Patterns ◽  
Lymphoid Cells ◽  
Bursa Of Fabricius ◽  
Transient Transfection Assay ◽  
The Relationship ◽  
Hemopoietic Progenitor

The v-myb oncogene of the acute avian leukemia virus E26 encodes a transcription factor that directly regulates the promyelocyte-specific mim-1 gene (Ness, S.A., Marknell, A. and Graf, T. Cell, 59, 1115–1125). We have investigated the relationship between the c-myb proto-oncogene and the transcription of the mim-1 gene both in vitro and in vivo. We demonstrate that the c-myb protein can transactivate the transcription of mim-1 in a transient transfection assay. In the chick embryo, we confirm that mim-1 is specifically expressed during granulopoiesis and we show that the expression of c-myb and mim-1 are perfectly correlated in the granulocytic spleen and pancreas. However we suggest that mim-1 is efficiently transcribed in the absence of c-myb in the yolk sac and in the promyelocytes at the onset of the colonization of the bursa of Fabricius. On the other hand c-myb transcripts detected in the early hemopoietic progenitor cells, in lymphoid cells and in proliferative epithelia are never associated with mim-1 transcription. We conclude that the granulocyte-specific mim-1 gene is regulated by c-myb-dependent and c-myb-independent mechanisms depending upon the environment in which granulocytic precursor cells differentiate.

scholarly journals Ectopic expression of murine TPO receptor (c-mpl) in mice is pathogenic and induces erythroblastic proliferation

Blood ◽  
1996 ◽  
Vol 88 (5) ◽  
pp. 1656-1665 ◽  
Author(s):  
L Cocault ◽  
D Bouscary ◽  
C Le Bousse Kerdiles ◽  
D Clay ◽  
F Picard ◽  
...  
Keyword(s):  
Progenitor Cell ◽  
Leukemia Virus ◽  
Ectopic Expression ◽  
Hematopoietic Progenitor Cell ◽  
Severe Thrombocytopenia ◽  
Colony Forming Unit ◽  
Adult Mice ◽  
Cell Assays

c-mpl, the cellular homologue of the v-mpl oncogene transduced in the myeloproliferative leukemia virus (MPLV), encodes the receptor for thrombopoietin, a cytokine involved in the proliferation and differentiation of cells of the megakaryocytic lineage. Here, we show that a retrovirus containing murine c-mpl cDNA (HSFmmpl) is pathogenic in vivo when inoculated in adult mice. All mice developed hepatosplenomegaly and died within 9 to 12 weeks after infection. Histological analysis showed that spleen, liver, and peripheral blood were invaded by erythroblasts at every stage of differentiation. In contrast to the myeloproliferative syndrome induced by MPLV, we did not observe an infiltration of these organs with cells from the granulocytic lineage nor a thrombocytosis. In fact, the platelet count of HSFmmpl mice progressively decreased and a severe thrombocytopenia was observed late in the course of the disease. Further characterization of the target progenitor of HSFmmpl virus in the spleen and bone marrow of diseased animals was accomplished using in vitro clonogenic progenitor cell assays. This analysis indicated that both late and early erythroid compartment (colony-forming unit- erythroid and burst-forming unit-erythroid) were largely increased in the spleens. The colony-forming unit-granulocyte-macrophage compartment was also increased but to a lesser extent. This study shows for the first time that ectopic expression of a member of the cytokine receptor superfamily promotes hematopoietic progenitor cell proliferation and could play a role in leukemogenesis.

scholarly journals Antiretrovirus Activity of a Novel Class of Acyclic Pyrimidine Nucleoside Phosphonates

2002 ◽  
Vol 46 (7) ◽  
pp. 2185-2193 ◽  
Author(s):  
J. Balzarini ◽  
C. Pannecouque ◽  
E. De Clercq ◽  
S. Aquaro ◽  
C.-F. Perno ◽  
...  
Keyword(s):  
Pyrimidine Nucleotide ◽  
Immunodeficiency Virus ◽  
Murine Sarcoma Virus ◽  
Acyclic Nucleoside Phosphonates ◽  
Sarcoma Virus ◽  
Acyclic Nucleoside ◽  
Murine Sarcoma ◽  
Antiretroviral Activity

ABSTRACT A novel class of acyclic nucleoside phosphonates has been discovered in which the base consists of a pyrimidine preferably containing an amino group at C-2 and C-4 and a 2-(phosphonomethoxy)ethoxy (PMEO) or a 2-(phosphonomethoxy)propoxy (PMPO) group at C-6. The 6-PMEO 2,4-diaminopyrimidine (compound 1) and 6-PMPO 2,4-diaminopyrimidine (compound 11) derivatives showed potent activity against human immunodeficiency virus (HIV) in the laboratory (i.e., CEM and MT-4 cells) and in primary (i.e., peripheral blood lymphocyte and monocyte/macrophage) cell cultures and pronounced activity against Moloney murine sarcoma virus in newborn NMRI mice. Their in vitro and in vivo antiretroviral activity was comparable to that of reference compounds 9-[(2-phosphonomethoxy)ethyl]adenine (adefovir) and (R)-9-[(2-phosphonomethoxy)-propyl]adenine (tenofovir), and the enantiospecificity of (R)- and (S)-PMPO pyrimidine derivatives as regards their antiretroviral activity was identical to that of the classical (R)- and (S)-9-(2-phosphonomethoxy)propyl purine derivatives. The prototype PMEO and PMPO pyrimidine analogues were relatively nontoxic in cell culture and did not markedly interfere with host cell macromolecular (i.e., DNA, RNA, or protein) synthesis. Compounds 1 and 11 should be considered attractive novel pyrimidine nucleotide phosphonate analogues to be further pursued for their potential as antiretroviral agents in the clinical setting.

scholarly journals TUMOR INDUCTION BY MURINE SARCOMA VIRUS IN AKR AND C58 MICE

1974 ◽  
Vol 140 (5) ◽  
pp. 1162-1179 ◽  
Author(s):  
Luigi Chieco-Bianchi ◽  
Alfonso Colombatti ◽  
Dino Collavo ◽  
Fujiro Sendo ◽  
Tadao Aoki ◽  
...  
Keyword(s):  
Leukemia Virus ◽  
Neutralizing Antibody ◽  
Immune Reactivity ◽  
Neoplastic Tissue ◽  
Cell Surface Antigens ◽  
Murine Sarcoma Virus ◽  
Sarcoma Virus ◽  
Murine Sarcoma ◽  
Akr Mice

Adult AKR and C58 mice injected intramuscularly with murine sarcoma virus, Moloney isolate (M-MSV), developed high incidence of nonregressing local tumors. Histologically, these tumors revealed the typical pleomorphism of M-MSV sarcomas; in some cases, however, neoplastic tissue showed a nodular or diffuse growth of monomorphic myoblastlike cells, reminiscent of clonal aggregates. No depression of immune reactivity was found in M-MSV-injected mice as evaluated by direct hemolytic plaque-forming cells against SRBC and by virus-neutralizing antibody production. The MSV recovered from the induced tumors proved to be, by neutralization assay, a Gross (G)-MSV pseudotype. Moreover, tumor cell suspensions absorbed out cytotoxic antibody directed against G-cell surface antigens. Therefore, the conclusion was drawn that MSV with envelope characteristics of endogenous G leukemia virus had formed in vivo through a phenotypic mixing phenomenon. The failure of tumors to regress has been interpreted as mainly due to the partial unresponsiveness of host immune reactivity towards G-MuLV specified antigens. Since MSV-tumors arose in AKR mice after a very long latent period, the possibility was considered that this relative resistance might depend on immunologic mechanisms. In fact, M-MSV-injected AKR mice immunodepressed by goat antimouse lymphocyte serum or rendered partially tolerant by neonatal M-MuLV inoculation developed sarcomas with higher incidence and with a shorter latency. Furthermore, the MSV recovered from these early tumors proved to be the original Moloney pseudotype.

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