Friend Leukemia

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John Lenard - One of the best experts on this subject based on the ideXlab platform.

  • antiretroviral activities of hypericin and rose bengal photodynamic effects on Friend Leukemia virus infection of mice
    Antiviral Research, 1993
    Co-Authors: Nancy R Stevenson, John Lenard
    Abstract:

    Abstract The ability of hypericin to protect mice from splenomegaly resulting from infection with Friend Leukemia virus (FLV) was re-examined in light of recent evidence showing that light is absolutely required for this drug's antiviral activity. FLV-induced splenomegaly was not prevented or ameliorated in mice injected with 100 μg hypericin, either mixed with the FLV inoculum or administered 1 day p.i., either under normal laboratory light or in the dark. These results contradict previous findings. Both hypericin and rose bengal, however, inactivated the FLV inoculum at low doses (

Jeanjacques Farhi - One of the best experts on this subject based on the ideXlab platform.

  • comparative uptake of adriamycin and daunorubicin in sensitive and resistant Friend Leukemia cells measured by flow cytometry
    Cytometry, 2005
    Co-Authors: Haim Tapiero, Alain Fourcade, P Vaigot, Jeanjacques Farhi
    Abstract:

    Based on the fluorescence properties of adriamycin (ADM) and daunorubicin (DNR), uptake in sensitive and resistant Friend Leukemia cells (FLC) was studied with the aid of the fluorescence activated cell sorter (FACS II). A quantitative cell by cell fluorescence intensity analysis showed a differential affinity of FLC to ADM and DNR. The cellular uptake of these two drugs was temperature dependent and was not hindered by sodium azide treatment; incorporation into isolated nuclei was not temperature dependent, nor hindered by sodium azide. Friend Leukemia cell variants resistant to adriamycin (ADM-RFLC) and to daunorubicin (DNR-RFLC) were developed. The rate of uptake of ADM and DNR across the plasma membrane of these two cell variants was lower than in sensitive cells. Although these cells were crossresistant to both ADM and DNR, the drug-induced fluorescence intensity was distributed differently in the corresponding resistant cell variants. We suggest therefore that resistance is the consequence of changes induced in the plasma membrane components. These changes may differ according to which drug is used.

Nancy R Stevenson - One of the best experts on this subject based on the ideXlab platform.

  • antiretroviral activities of hypericin and rose bengal photodynamic effects on Friend Leukemia virus infection of mice
    Antiviral Research, 1993
    Co-Authors: Nancy R Stevenson, John Lenard
    Abstract:

    Abstract The ability of hypericin to protect mice from splenomegaly resulting from infection with Friend Leukemia virus (FLV) was re-examined in light of recent evidence showing that light is absolutely required for this drug's antiviral activity. FLV-induced splenomegaly was not prevented or ameliorated in mice injected with 100 μg hypericin, either mixed with the FLV inoculum or administered 1 day p.i., either under normal laboratory light or in the dark. These results contradict previous findings. Both hypericin and rose bengal, however, inactivated the FLV inoculum at low doses (

Haim Tapiero - One of the best experts on this subject based on the ideXlab platform.

  • comparative uptake of adriamycin and daunorubicin in sensitive and resistant Friend Leukemia cells measured by flow cytometry
    Cytometry, 2005
    Co-Authors: Haim Tapiero, Alain Fourcade, P Vaigot, Jeanjacques Farhi
    Abstract:

    Based on the fluorescence properties of adriamycin (ADM) and daunorubicin (DNR), uptake in sensitive and resistant Friend Leukemia cells (FLC) was studied with the aid of the fluorescence activated cell sorter (FACS II). A quantitative cell by cell fluorescence intensity analysis showed a differential affinity of FLC to ADM and DNR. The cellular uptake of these two drugs was temperature dependent and was not hindered by sodium azide treatment; incorporation into isolated nuclei was not temperature dependent, nor hindered by sodium azide. Friend Leukemia cell variants resistant to adriamycin (ADM-RFLC) and to daunorubicin (DNR-RFLC) were developed. The rate of uptake of ADM and DNR across the plasma membrane of these two cell variants was lower than in sensitive cells. Although these cells were crossresistant to both ADM and DNR, the drug-induced fluorescence intensity was distributed differently in the corresponding resistant cell variants. We suggest therefore that resistance is the consequence of changes induced in the plasma membrane components. These changes may differ according to which drug is used.

Isinsu Kuzu - One of the best experts on this subject based on the ideXlab platform.

  • Friend Leukemia virus integration-1 (FLI-1) expression in gastrointestinal stromal tumors.
    The Turkish journal of gastroenterology, 2009
    Co-Authors: Gulsah Kaygusuz, Isinsu Kuzu
    Abstract:

    Friend Leukemia virus integration-1 expression has been shown in a variety of tumors, including vascular tumors, desmoplastic small round cell tumor, Merkel cell carcinoma, and lymphoblastic lymphoma, in addition to Ewing's sarcoma/primitive neuroectodermal tumor. The aim of the current study was to examine Friend Leukemia virus integration-1 protein expression in a series of gastrointestinal stromal tumors and also to assess if Friend Leukemia virus integration-1 has any role in the disease process. It is the first study analyzing Friend Leukemia virus integration-1 expression in gastrointestinal stromal tumors in the English literature. A tissue microarray block containing 52 cases of gastrointestinal stromal tumors was done. Immunohistochemical analysis was performed for Friend Leukemia virus integration-1 polyclonal antibody. Immunohistochemically, Friend Leukemia virus integration-1 was negative in all cases. Friend Leukemia virus integration-1 can be expressed in a variety of tumors, and is helpful in making the diagnosis of Ewing's sarcoma/primitive neuroectodermal tumor. We think that this protein is not expressed in gastrointestinal stromal tumors and it is not a part of the pathogenesis of this disease.