The coenrichment of stem cells, prothymocytes, and stromal elements with ecotropic retrovirus-producing cells from the bone marrow of leukemia-prone AKR mice

Buckheit, Robert W.; Kurtzberg, Joanne; Bolognesi, Dani P.; Weinhold, Kent J.

doi:10.1016/0042-6822(88)90475-8

Cited by 9 publications

(3 citation statements)

References 18 publications

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“…We further demonstrated lifelong susceptibility of the rat bone marrow for at least transient FB29 infection and associated alterations. This contrasted with the situation for MuLV-induced leukemogenesis in AKR mice (Buckheit et al, 1987(Buckheit et al, , 1988 and in mice inoculated with Moloney MuLV (Belli and Fan, 1994), respectively. In both cases, early postnatal infection of the bone marrow with MuLV has been proposed to be crucial for the development of leukemia in mice.…”

Section: Figcontrasting

confidence: 57%

Suppression of Rat Bone Marrow Cells by Friend Murine Leukemia Virus Envelope Proteins

et al. 1998

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In a retroviral rat model, we have investigated the nontransforming effects of murine leukemia virus FB29 on the bone marrow. Upon intraperitoneal inoculation with murine leukemia virus FB29 of either neonatal or adult rats, bone marrow cells became massively infected within the first 12 days postinoculation. In neonatally inoculated rats, a persistent productive bone marrow infection was established, whereas in rats inoculated as adults, no infected bone marrow cells could be detected beyond 12 days postinoculation. Retroviral infection was most likely cleared by an antiviral immune response (Hein et al., 1995, Virology 211, 408-417). Exposure to virus irreversibly decreased numbers of bone marrow cells staining with monoclonal antibody OX7 by 10-30%. Reduction of OX7+ bone marrow cells by 20% was also observed in vitro, after bone marrow cells from uninfected adult rats had been co-incubated with virus. FB29-envelope proteins were sufficient alone to reduce numbers of OX7+ bone marrow cells, both in vivo and in vitro. According to results on incorporation of propidium iodide, decreased numbers of OX7+ cells were due to cell death. By flow cytometric analyses OX7+ bone marrow cells as well as monocytes/macrophages were identified to be major target cells for infection with FB29 within the bone marrow. Thus, the mechanism(s) responsible for death of OX7+ bone marrow cells might be due to direct toxicity of viral envelope proteins and/or to interactions of viral envelope proteins with cells of the monocytic lineage.

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Section: Figcontrasting

confidence: 57%

Suppression of Rat Bone Marrow Cells by Friend Murine Leukemia Virus Envelope Proteins

et al. 1998

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“…This led to the hypothesis that the virus might originally infect an immature T-cell or a HPC to form a ICSC/ILSC which then continues to differentiate post-infection, initially in the bone marrow and then in the thymus [67,94]. Because T-lymphocytes develop in the thymus from bone marrow-derived immature precursors (pro-thymocytes), it has been proposed by several investigators that a bone marrow-thymus axis plays an important role in the development of T-cell lymphoma by M-MuLV [93,95-97]. Although the identity of the initial target cell for M-MuLV infection is still unknown, a two-stage leukemogenesis model for the development of M-MuLV-induced leukemia has been proposed [67].…”

Section: Retroviruses and Leukemogenesis: The "Two-hit" Hypothesismentioning

confidence: 99%

Hematopoietic stem cells and retroviral infection

et al. 2010

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Retroviral induced malignancies serve as ideal models to help us better understand the molecular mechanisms associated with the initiation and progression of leukemogenesis. Numerous retroviruses including AEV, FLV, M-MuLV and HTLV-1 have the ability to infect hematopoietic stem and progenitor cells, resulting in the deregulation of normal hematopoiesis and the development of leukemia/lymphoma. Research over the last few decades has elucidated similarities between retroviral-induced leukemogenesis, initiated by deregulation of innate hematopoietic stem cell traits, and the cancer stem cell hypothesis. Ongoing research in some of these models may provide a better understanding of the processes of normal hematopoiesis and cancer stem cells. Research on retroviral induced leukemias and lymphomas may identify the molecular events which trigger the initial cellular transformation and subsequent maintenance of hematologic malignancies, including the generation of cancer stem cells. This review focuses on the role of retroviral infection in hematopoietic stem cells and the initiation, maintenance and progression of hematological malignancies.

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“…This population corresponded to light-density cells shown to be preferentially infected by naturally occurring retroviruses in wild mice (Buckheit et aL, 1988). Reconstitution experiments in primates have shown that these light-density cells were up to 20-fold enriched for stem cells (G. Wagemaker, personal communication).…”

Section: Introductionmentioning

confidence: 95%

Cryopreserved Primate Bone Marrow Cells Can Be Used for Retroviral-Mediated Gene Transfer

Wieder

1991

Human Gene Therapy

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Retroviral-mediated gene transfer into Rhesus monkey bone marrow cells, which were cryopreserved, stored, and then transduced at the time of thawing, was studied for potential application in gene therapy protocols. Albumin density gradient fractionation was used to define subpopulations of cryopreserved cells transduced by a murine retroviral vector. The transfer of the bacterial neomycin phosphotransferase gene into Rhesus monkey bone marrow that was cryopreserved and thawed was found to be preferential in a light-density population enriched for granulocyte-macrophage colony-forming units (CFU-GM). These results are similar to results obtained with freshly harvested bone marrow in which this population is enriched for CD34 antigen-positive cells, as well as for cells that were undergoing cell division. This method may be useful in enriching for transduced precursors in future gene transfer experiments in primates.

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The coenrichment of stem cells, prothymocytes, and stromal elements with ecotropic retrovirus-producing cells from the bone marrow of leukemia-prone AKR mice

Cited by 9 publications

References 18 publications

Suppression of Rat Bone Marrow Cells by Friend Murine Leukemia Virus Envelope Proteins

Suppression of Rat Bone Marrow Cells by Friend Murine Leukemia Virus Envelope Proteins

Hematopoietic stem cells and retroviral infection

Cryopreserved Primate Bone Marrow Cells Can Be Used for Retroviral-Mediated Gene Transfer

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