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Biomedical subjects

K Nooter

Publications and source records attributed to K Nooter.

124 records · Page 7Linked to original sources
PubMed1979

Type-C virus antigen detection in co-cultures of human leukaemic bone marrow and dog cells.

Bone marrow of leukaemic patients, non-leukaemic patients and normal individuals were co-cultivated with the canine cell line A7573. These co-cultures were screened for retrovirus antigens by means of the indirect cytoplasmic immunofluorescence assay (IFA). Rabbit antisera directed against the major structural protein (p30) of woolly monkey (simian) sarcoma leukaemia virus (grown in human lymphoid cells) and Rauscher murine leukaemia virus were used for testing. After 2 months in culture, 6 of 17 co-cultures containing cells from leukaemic patients showed positive staining in the IFA with the anti-simian virus serum. In control dog cells fluorescence was never observed. Five of the six positive cultures were derived from leukaemic children. One of 12 co-cultures of the non-leukaemic group and one of nine normal bone marrow co-cultures were positive with the simian virus antiserum. None of the 38 co-cultures stained positive in the IFA with Rauscher virus antiserum. Absorption of the simian virus antiserum with calf serum or mouse mammary tumour virus had no dramatic effect in the IFA on positive control cells or on cells of a positive co-culture. However, absorption with purified simian virus (grown in rat cells) completely abolished these fluorescence reactions. The results provide evidence that simian sarcoma-leukaemia virus related information was present in the original bone marrow samples and that co-cultivation with permissive mammalian cells enabled the detection of virus footprints.

Adult↗
PubMed1978

Type-C oncovirus isolate from human leukemic bone marrow: further in vitro and in vivo characterization.

Rabbit corneal cells transformed by a putative human type-C helper virus pseudotype of the mouse sarcoma virus produce large amounts of transforming and non-transforming viruses. The virions are antigenically related to the woolly monkey (simian) sarcoma-leukemia type-C oncovirus. Typical sarcoma virus lesions developed in newborn rats injected with virus-producing rabbit cells. Cells producing only the putative type-C helper viruses as a result of exposure to a high dilution of transforming virus stock induce lymphosarcomas after inoculation into newborn rats.

Animals↗
PubMed1978

Rescue of a transforming virus from a spontaneous nonproducing osteosarcoma in BALB/c mice.

Cells from spontaneous osteosarcoma V793 that originated in a 19-month-old female BALB/c mouse were cultured. They did not produce a C-type oncovirus as determined by extracellular reverse transcriptase assay and cytoplasmic immunofluorescence. After cocultivation with Balb/3T3 cells chronically infected with a murine leukemia virus (MuLV), a focus-forming principle that transformed 3T3 cells, secondary BALB/c mouse embryo and WAG/Rij rat embryo fibroblasts were rescued. The transformation could be inhibited by antiserum to MuLV.

Animals↗
PubMed1977

Detection of human C-type "helper" viruses in human leukemic bone marrow with murine sarcoma virus-transformed human and rat non-producer cells.

Bone-marrow cells from two leukemic children were co-cultivated with the leukemic children A 7573. In early passages, C-type oncornaviruses were released as detected by extracellular reverse transcriptase assay. Co-cultivation of the infected canine cells with the non-producing cell lines R-970-5 (human) or K-NRK (rat) both transformed by Kirsten mouse sarcoma virus (MSV) yielded a new pseudotype of MSV that could transform rat embryo, rabbit SIRC and human kidney cells but not mouse embryo cells. The focur formation could be inhibited by an antiserum to the simian sarcoma virus but not by a serum directed against murine leukemia virus. A cell line derived from a focus of transformed cells became a highe virus is related to the simian sarcoma virus. It is concluded that the leukemic bone-marrow cells produce a C-type oncornavirus that can serve as a helper virus to the defective MSV.

Acute Disease↗
PubMed1976

Hormone independent in vitro erythroid colony formation by mouse bone marrow cells.

B.M. cells of RLV-infected BALB/c mice can proliferate in methylcellulose in the absence of E.P., while normal B.M. cells cannot (12). Not only the more primitive BFU-E shows hormone-independency (18). This phenomenon is in favour of the view that the Rauscher virus induced erythroblastosis is a true neoplasia although transplantation experiments failed so far. The experiments in which transformation in vitro of B.M. cells by RLV is established (19) show that the CFU-E can serve as a target for the virus. Treatment of normal mice with CFA leads to a rapid increase in CFU-E in the bone marrow (18). Splenomegaly of RLV-infected mice is enhanced by CFA-treatment probably due to an increase in targets. Transfection with proviral DNA also can transform the CFU-E of BALB-c mice. This approach allows in vitro studies on the resistence of mouse strains to RLV in vitro. The studies are of interest for the human disease in two aspects. In vitro transformation assays are needed to study the oncogenic potential of putative human leukemia viruses. Furthermore the studies have yielded some new insight in the pathogenesis of virally induced erythroblastosis. This might serve as a model for e.g. acute myeloid leukemia in man.

Anemia↗
PubMed1976

In vitro studies on the enhancement of Rauscher virus-induced erythroblastosis by complete Freund's adjuvant in BALB/c mice.

Inoculation of complete Freund's adjuvant (CFA) into BALB/c mice either before or after infection with Rauscher murine leukemia virus (MuLV-R) led to an acceleration of the disease as determined by spleen weight. Treatment with CFA also induced a higher number of spleen erythroblast foci and, in the bone marrow, erythropoietin-independent cells that produced erythroid colonies in vitro. CFA induced in the bone marrow not only an increase in myeloid progenitor cells that can produce colonies in agar, but an ever larger increase in the number of erythroid colony-forming cells. Virus-induced erythroblastosis was probably enhanced by CFA due to the production of many target cells. The more primitive burst-forming cell, which produced large colonies of erythroid cells after 10 days in culture, was also physiologically transformed in MuLV-R-infected mice; bursts could be formed by cells of such animals in the absence of erythropoietin.

Animals↗
PubMed1976

In vitro growth characteristics of virally transformed murine myeloid cells.

Bone marrow from normal BALB/c mice, mice with myeloid leukemia induced by Soule myeloid leukemia virus, and mice with virally induced mammary carcinoma was cultured in semisolid agar. Bone marrow from either leukemic or mammary tumor-bearing mice produces more clones in vitro in the presence of a specific colony-stimulating factor. However, in all cases, the myeloid progenitor cells have similar requirements for the colony-stimulating factor. The optimum condition for growth in all instances is 7% fetal calf serum + 7% horse serum + 7% tryptose phosphate broth. Decrease in the concentration of these three constituents has a less drastic effect on in vitro proliferation of bone marrow cells from leukemic mice. Some cells from Soule virus-induced leukemias even grew in the absence of serum. The combination of suboptimal amounts of serum and colony-stimulating factor is used as a tool for detecting cells with altered growth characteristics in bone marrow of leukemic mice. During the progression of the leukemia, there is an increase in the amount of transformed colony-forming cells per 5 X 10(4) bone marrow cells. The increase is already noticeable 4 weeks after inoculation, when no clinical signs of the leukemia are present, and reaches a maximum of about 20%.

Animals↗
PubMed1975

Cytopathogenic XC assay for bone marrow from mice infected with murine leukemia viruses.

Virus production "in vitro" by bone marrow cells of murine leukemia virus-infected BALB/c mice was determined with a modified reverse XC cell assay. Bone marrow of mice infected by either Rauscher leukemia virus or Soulé myeloid leukemia virus was cocultivated with XC cells and quantification was done by counting syncytia. During the development of both erythroblastosis and myeloid leukemia, the number of syncytia induced by cocultivation increased. High numbers of syncytia were especially obtained with myeloid leukemia cells; the phenomenon was evident as early as one month following inoculation with virus and before the onset of conspicuous clinical signs of disease.

Animals↗
PubMed1975

Hormone-independent in vitro erythroid colony formation by bone marrow cells from Rauscher virus-infected mice.

Bone marrow cells from BALB/c mice infected with Rauscher erythroblastosis virus produced five to twenty-five times more erythroid colonies in vitro in the absence of erythropoietin (EP) as compared to normal cells. A good correlation existed between the state of the disease and the number of hormone-independent erythroid colony-forming cells (CFU-E). A significant number of hormone-independent CFU-E was found as early as 3 days after infection. A linear relationship existed between the number of cells plated and the number of erythroid colonies formed in vitro. Addition of EP did not enhance colony formation, even at low cell concentrations. Feeder layer experiments demonstrated that EP-independent colony formation was not due to the production of endogenous EP. Repeated injections of phenylhydrazine into normal mice did not lead to the loss of EP responsiveness in vitro; this indicated that the hormone independency induced by the virus was not due to continuous erythropoietic stimulation in vivo. Besides hormone independency, the CFU-E from infected mice required less serum in the culture medium. Normal erythroid colonies regressed after 4 days of culture, but EP-independent colonies from infected mice persisted for more than 2 weeks. These three phenomena may be regarded as indicative for a physiologic transformation.

Animals↗
PubMed1975

Attempts to transform murine hemopoietic cells by Rauscher leukemia virus.

Primary Rauscher leukemia virus (RLV)-induced myeloid leukemias can produce many small clones in agar in the absence of a factor needed for the proliferation of normal myeloid cells. It seems that leukemic cells can more efficiently utilize the small amount of colony-stimulating factor (CSF) that is produced by them. At optimal stimulation by exogenous CSF, leukemic cells exhibit a poorer rate of proliferation than normal bone marrow cells. Hemopoietic cells can replicate the virus after infection in vitro. In some experiments, infection of normal bone marrow cells leads to the production of some cells with the same growth pattern as cells from primary leukemias.

Animals↗
PubMed1975

Cell density-dependent growth in agar of bone marrow cells from tumor-bearing BALB/c mice in the absence of a colony-stimulating factor.

Bone marrow cells from BALB/c mice with myeloid leukemia, lymphosarcoma, erythroblastosis, or mammary tumor produce small clusters in semisolid agar cultures in the absence of specific colony-stimulating factor. This spontaneous growth is observed only when high cell numbers (5 x 10 5 cells/ml) are plated. The phenomenon was encountered only when mice had an elevated number of mature or immature granulocytes in the peripheral blood. Removal of the adherent cells from the bone marrow did not abolish spontaneous growth, indicating that this colony-stimulating factor independency is not due to a high number of colony-stimulating cells in the bone marrow cells. This excluded the possibility that the spontaneous growth was due to a high endogenous stimulating activity of the bone marrow from tumor-bearing mice.

Agar↗