Monoclonal proliferation of Friend murine leukemia virus-transformed myeloblastic cells occurs early in the leukemogenic process.

Sola, Brigitte; Heard, Jean‐Michel; Fichelson, Serge; Martial, M A; Pozo, Franklin Mayca; Bordereaux, Didier; Gisselbrecht, Sylvie

doi:10.1128/mcb.5.5.1009

Cited by 7 publications

(5 citation statements)

References 32 publications

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“…This observation was surprising because M. dunni cells are known to harbor little endogenous viral information compared with other mouse strains (15). In fact, we observed these bands in all laboratory mouse strains tested so far, including AKV-negative strains and SC1 fibroblasts from wild mice (22). Because this band was not found in DNAs from other species (hamsters, rats, minks, dogs, or humans), it can be concluded that this endogenous F-MuLV-related viral sequence has been conserved along the mouse speciation but remains limited to this species (unpublished data).…”

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confidence: 77%

Genetic analysis of myeloproliferative leukemia virus, a novel acute leukemogenic replication-defective retrovirus

Penciolelli¹,

Wendling²,

Robert-Lézénès³

et al. 1987

J Virol

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The myeloproliferative leukemia virus (MPLV) is a new acute leukemogenic, nonsarcomatogenic retroviral complex that is generated during the in vivo passage of a molecularly cloned Friend ecotropic helper virus. Examination of viral RNA expression in MPLV-producing cells revealed the presence of two distinct molecular species that hybridized with a long terminal repeat or an ecotropic env-specific probe but not with a xenotropic mink cell focus-forming virus env-specific probe derived from a spleen focus-forming virus: an 8.2-kilobase species corresponding to a full-length Friend murine leukemia virus (F-MuLV) and a deleted species with a genomic size of 7.4 kilobases. This deleted virus was biologically cloned by limiting dilutions and single cell cloning in Mus dunni fibroblasts. Three nonproducer clones with normal morphologies and containing one single integrated copy of the deleted virus were superinfected with F-MuLV, Moloney murine leukemia virus, Gross murine leukemia virus, mink cell focus-forming virus (HIX), or the amphotropic 1504 murine leukemia virus. All pseudotypes caused macroscopic and microscopic abnormalities in mice that were similar to those seen in the parental stock. A comparison of the physical maps of F-MuLV and MPLV, which was deduced from the restriction enzyme digests of unintegrated proviral DNAs, indicated that the MPLV-defective genome (i) is probably derived from F-MuLV, (ii) has conserved the F-MuLV gag and pol regions, and (iii) is deleted and rearranged in the env region in a manner that is clearly distinct from that of Friend or Rauscher spleen focus-forming viruses.

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mentioning

confidence: 77%

Genetic analysis of myeloproliferative leukemia virus, a novel acute leukemogenic replication-defective retrovirus

Penciolelli¹,

Wendling²,

Robert-Lézénès³

et al. 1987

J Virol

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“…Their results also indicated that the events leading to malignant transformation resulted in the emergence of one or a small number of tumor cell clones. Sola et al (25) analyzed the integration sites of F-MuLV in myeloblastic cell lines that were transformed by F-MuLV alone and also concluded a monoclonal origin of these cells.…”

Section: Discussionmentioning

confidence: 99%

Multistage Friend erythroleukemia: independent origin of tumor clones with normal or rearranged p53 cellular oncogenes

Chow¹,

Ben‐David²,

Bernstein³

et al. 1987

J Virol

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The erythroleukemia induced by Friend virus complex in adult mice is a multistage malignancy characterized by the emergence, late in the disease, of tumorigenic cell clones. We have previously shown that a significant proportion of these clones have unique rearrangements in their cellular p53 oncogene. The clonal relationships among Friend tumor cells isolated in the late stages of Friend erythroleukemia were analyzed by examining the unique integration site of Friend murine leukemia virus and the unique rearrangement in their cellular p53 oncogene. The majority of clones isolated from individual mice infected with Friend virus were clonally related as judged by the site of Friend muriiie leukemia virus integration. However, Southern gel analysis of DNA from individual Friend cell clones indicated that all of the clones with a normal p53 gene from the same mice were clonally related, but were unrelated to the Friend cell lines with a rearranged p53 gene. These results suggest that Friend tumor cells with rearrangements in their p53 gene arise as the result of a unique transformation event, rather than by progression from already existing tumor cells with a normal p53 gene. They also suggest that such rearrangements in the p53 gene confer a strong selective advantage to these cells in vivo.

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“…We have previously reported that the in vitro generation of murine myeloblastic leukemic cells from F-MuLVinfected bone marrow cells is a multistep process (Heard et al, 1984). This process is characterized by the initial proliferation of clonal CSF-dependent cell lines (FDCL) (Sola et al, 1985) which further acquire the capacity of autonomous growth (ACL) and tumorigenicity.…”

Section: Discussionmentioning

confidence: 99%

“…In the in vitro myeloblastic leukemogenic process, the early clonal expansion of factor-dependent cells (Sola et al, 1985) implies a n uncoupling between cell differentiation and proliferation (Sachs, 1980). These cells having lost their differentiation ability still remain under exogenous CSF control for their survival and growth.…”

Section: Discussionmentioning

confidence: 99%

The in vitro autocrine secretion of CSFs alone does not account for the longterm growth of murine myeloid leukemic cells in suspension cultures

Fichelson

Heard

Lévy

1985

Journal Cellular Physiology

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To investigate the mechanisms supporting the in vitro longterm growth of murine leukemic myeloblastic cells, factor-dependent and autonomous myeloblastic cells have been examined for their CSF responsiveness, CSF secretion, and autostimulation of growth. Purified CSF-1, GM-CSF, and IL-3 stimulated cloning and proliferation of both autonomous (ACL) and factor-dependent cell lines (FDCL), and were unable to induce differentiation of these cells. Sensitivities to CSFs were similar for ACL, FDCL and normal bone marrow cells. Most of the cell lines secreted CSFs, stimulating colony formation from normal bone marrow cells in bilayer agar cultures. The number of induced granulo-macrophagic colonies was similar in the presence of either ACL or FDCL. The ability to stimulate their own proliferation was similar for both ACL and FDCL in a longterm suspension culture assay as well as in a shortterm cloning assay. These results strongly suggest that the autocrine secretion of CSF-related activities are not sufficient to fully account for the in vitro longterm proliferation of virus-transformed myelomonocytic cells.

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Monoclonal proliferation of Friend murine leukemia virus-transformed myeloblastic cells occurs early in the leukemogenic process.

Cited by 7 publications

References 32 publications

Genetic analysis of myeloproliferative leukemia virus, a novel acute leukemogenic replication-defective retrovirus

Genetic analysis of myeloproliferative leukemia virus, a novel acute leukemogenic replication-defective retrovirus

Multistage Friend erythroleukemia: independent origin of tumor clones with normal or rearranged p53 cellular oncogenes

The in vitro autocrine secretion of CSFs alone does not account for the longterm growth of murine myeloid leukemic cells in suspension cultures

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