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Query: UMLS:C0029463 (osteosarcoma)
 16,637 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Various agents have caused osteosarcoma in several experimental animal systems. These agents or initiators may be classified as chemicals, radiation, viruses, and miscellaneous. Zinc beryllium silicate with beryllium oxide in rabbits and FBJ virus in mice are two such initiating agents. The relevance of these animal experiments to the human situation is not known, but recent reports regarding a transmissible agent obtained from human osteosarcoma tissue suggest that a virus may be implicated. There is a theoretic indication that the various etiologic agents, including viruses, may affect the DNA of normal cells in such a way that further evolution and differentiation through several cell divisions may result in the clinical appearance of cancer.
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PMID:The etiology of osteosarcoma. A review of current considerations. 5 Aug 94

Serological analysis of the reverse transcriptase (RTase), purified from human osteosarcoma tissue, has shown that it is antigenically related to DNA polymerases from BEV and from RD-114. No cross-reactivity of the osteosarcoma RTase was observed with RTases purified from AMV, RLV, SiSV, GaLV and from human spleen of a patient with myelofibrosis.
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PMID:Serological characterization of a purified reverse transcriptase from osteosarcoma of a child. 9 61

Nine patients with osteogenic sarcoma and one patient with epitheloid sarcoma of bone undergoing treatment with high-dose methotrexate (MTX) therapy were studied immunologically. The following peripheral blood lymphocyte parameters were evaluated: 1-8 days after the intravenous infusion of 7.5 g MTX followed by leucovorin rescue: absolute count/mm3, the stimulatory response to the mitogens, phythemagglutinin (PHA) and pokeweed (PW) and the reactivity in the mixed lymphocyte culture (MLC). The response to PHA remained unaffected during the observation period, whereas the response to PW decreased on the 2nd and 4th day after treatment. The MLC response was inhibited between the 1st and the 4th day. The inhibition manifested itself first in the patients plasma and was demonstrable 48 hours later in the lymphocyte itself. The responsiveness regained normal or even reacted supranormal values about 7 days after treatment. Lymphocyte function remained essentially unaltered after several cycles of treatment. Absolute lymphocyte counts, however, tended to decrease. The MTX sensitive period in vitro lasts from the 2nd to the 6th day of the MLC, which is the period of intense RNA and DNA synthesis. We conclude that high-dose MTX therapy for osteogenic sarcoma leaves the patient without major permanent damage to cellular immune function.
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PMID:[Cellular immunity during and after high-dose methotrexate therapy in patients with osteosarcoma (author's transl)]. 14 98

Biological studies on FBJ osteosarcoma virus in tissue cultures have led to the isolation of murine sarcoma virus. Characteristic type C-MuLV particles were observed in bone tumors induced by the SD-MSV-M-virus in vitro and in vivo. The SD-MSV-M virus also induced bone tumors in rats of all strains tested, and it has a similar tumor-inducing property in hamsters. Immunoelectronmicroscopic studies showed that envelope antigens of MSV-SD virus in rat bone tumors can be distinguished from those found in hamster bone tumor cells. In tissue cultures of MSV-SD rat bone tumors, two separate cell lines have been established: one of them releases both MSV and MuLV and the other produces MuL virus only. The MuLV in this cell line acts as helper. The different interactions appear to support the concept of control mechanisms for the partial expression of genes which are responsible for neoplastic properties, virus replication, and synthesis of gs-antigens. Biochemical studies on structural rearrangement and subunit composition of RNA released from MSV-SD virus, have shown that there are two forms of the native genome RNA differing in their sedimentation coeffiiecients and in subunit composition. In human osteosarcoma tissue culture, type-C viruslike particles are found. In cocultures derived from human osteosarcoma with cells taken from the bone marrow or peripheral blood of patients with different types of leukemia, certain morphological changes are observed which resemble those induced in animal cells by RNA tumor viruses. In osteosarcomas where no cytoplasmic antigen could be proved by an immunofluorescence test, the antigen could be produced by cocultivation with antigen-positive leukemic bone marrow cells. Whole human embryo cells treated with fluid from leukemia bone marrow cultures showed the presence of the cytoplasmic antigen when tested with positive sera, but they showed no morphologic changes. In high molecular weight RNA species, sedimentation coefficients ranging from 62S to 68S are demonstrated by molecular hybridization techniques. In cross-hybridization experiments, annealing values were observed only with complementary DNA products synthesized from sarcoma viruses. Three particularly high molecular weight RNA species released from human sarcoma cell cultures showed no cross-hybridization with either the DNA product of Rauscher leukemia virus or that of Gross leukemia virus.
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PMID:Morphological, biological, immunological and biochemical studies on bone tumors of animals and man. 18 70

The virus-specific nucleotide sequences in the RNA and DNA of a Kirsten mouse sarcoma virus (Ki-MSV)-transformed non-producer human osteosarcoma cell clone and two subclones of these cells that reverted to a normal phenotype have been analysed by hybridization of sarcoma virus-specific complementary DNA (cDNA) to cellular RNA or DNA. Whereas the transformed clone had acquired de novo Ki-MSV sequences in the RNA and DNA of the cells, both the revertant cell lines seemed to have lost most or all of this information from the cellular nucleic acids. The DNA from the revertant cells lacked the sequences represented either in the Ki-MSV-specific cDNA or in the total cDNA of the leukaemia-sarcoma virus complex. Thus, the reversion of the virus-transformed human cells to normal morphology is associated with the loss of most or all of the proviral sequences from the cellular DNA.
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PMID:Reversion of Kirsten sarcoma virus transformed human cells: elimination of the sarcoma virus nucleotide sequences. 22 28

Murine interferon inhibited the growth of a continuous line of osteogenic sarcoma (OGS) cells in tissue culture. Inhibition of tumor cell growth by interferon was demonstrated by: a) decreased colony formation in soft agar, b) suppression of clone formation in liquid medium, and c) reduction of tumor cell counts in monolayer cultures. This inhibition of cell growth was further documented by suppression of [3H]thymidine uptake by OGS cells exposed to interferon, which suggested inhibition of DNA synthesis of tumor cells. Exposure of tumor cells for 4 hours, 24 hours, and 2,3,4,6, and 8 days demonstrated greater activity with prolonged exposure to interferon. Inhibition of cell growth was significantly greater for OGS cells than for normal mouse embryo fibroblasts. Finally, the antitumor activity of the interferon preparation could be reversed by anti-interferon antibody.
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PMID:Antitumor activity of interferon against murine osteogenic sarcoma cells in vitro. 27 70

Analysis of time-lapse cinematographic film permitted the construction of pedigrees from 88 well oxygenated cells of a mouse osteosarcoma (MOS). These cells have been chronically treated with various concentrations of the hypoxic cell sensitizer misonidazole (MIS) over periods of up to 96 h. At concentrations of 0.5 and 7 mM there is a 2--3 h increase in cell-cycle time. Concentrations of 2 mM show an intermitotic time delay of 7.6--10.3 h. At 4 mM cells divided only once. With increasing drug concentration there was an increase in the number of abnormal mitoses. These results were compared with cloning efficiency (PE) experiments. PE at 0.5 mM is 80%, at 1 mM 40 and at 2 mM is reduced to 4%. Cells treated with 2mM MIS over a period of 28.6 h resume their normal cycle when the drug is washed from the culture. This may indicate that DNA is not a major target for MIS. It is concluded that this hypoxic cell sensitizer is also toxic for MOS cells in well oxygenated conditions.
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PMID:Influence of the hypoxic cell sensitizer misonidazole on the proliferation of well-oxygenated cells in vitro during prolonged exposure. 29 53

DNA metabolism in bone marrow cells was measured under high-dose Methotrexate/Leucovorin adjuvant chemotherapy of a patient with primary amputation of his right leg because of osteogenic sarcoma. The biochemical data showed that there was no rescue effect of Leucovorin after 200 mg/kg Methotrexate. Corresponding to this "biochemical failure" of the rescue effect the patient died from the complications of a long and very severe bone marrow suppression. To improve the safety of this therapeutic regimen the intravenous injection and in some cases a higher dose of Leucovorin is recommended.
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PMID:[High-dose methotrexate/leucovorin adjuvant chemotherapy of osteogenic sarcoma: biochemical effects in DNA-synthesis of bone marrow cells (author's transl)]. 30 51

Anthracyclines, such as daunorubicin (DNR), rubidazone (RBD) and adriamycin (ADR) are intercalating drugs used in cancer chemotherapy. They inhibit synthesis of DNA and RNA, break DNA and inhibit mitochondrial oxidative chain. Their antitumoral experimental activities depend upon type of drug, tumor and route of administration. After i.v. administration, the drug is present in all tissues except central nervous system. Its disappearance from the plasma is biphasic with a long terminal half life, justifying intermittent chemotherapy. Anthracyclines metabolism occurs mainly in liver micrososomes, and 90% metabolites are excreted in the bile. The main toxicity is cardiac, as a congestive heart failure which appears when a cumulated drug dose is overcome. In man only, a few derivatives have been studied, compounds with activity and no cardiotoxicity are still in research. Action of malignancies depends on type of derivative. We use DNR since 1967, it is a remarkable active drug in induction treatment of AML, it is the only active drug on acute promyelocytic leukemia, and it increases number of remissions in all of adult patients and severe forms of children ALL. Adriamycin (ADR) is active on solid tumors (osteosarcoma, breast and thyroid cancers) and lymphomas. With rubidazone (RBD) we obtain 2/3 of remissions in acute monoblastic leukemia, and it is easier to use than DNR and equally active on AML. RBD is also active on severe cases of lymphomas (lymphosarcomas and Hodgkin's disease). A new compound DEA 14 DNR seems interesting: experimental antitumor activity is high (compared to DNR, RBD and ADR) and it appears to possess activity on solid tumors in man.
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PMID:[Survey of anthracyclines derivatives in haematology (author's transl)]. 67 74

Recent evidence suggests that endocrine factors play an important role in the natural history of osteosarcoma. The occurrence of this tumor in the metaphysis of rapidly growing adolescents, coupled with increased female survival led to the investigation of the effects of various hormones on cultured osteosarcoma cells. The in vitro effects of physiologic concentrations of human growth hormone, 17beta estradiol, and progesterone on cultured osteosarcoma cells and chondrocytes are presented. Growth hormone significantly enhances 3H-thymidine incorporation in osteosarcoma cells and chondrocytes, in the presence of human serum. The use of other sera, culture media, or heat inactivation of the human serum abolishes this effect. Estradiol and progesterone, alone, or in combination produce significant suppression of DNA synthesis in cultured tumor cells. Several sera contain a heat-labile factor which has the capacity to block the suppressive effect of estradiol. This factor could be overcome by increasing the concentration of hormone, or by heat-inactivation of the serum. The use of hormone therapy in the treatment of osteosarcoma has never been reported, despite its demonstrated value in certain other malignancies. In light of these observations and considering the poor prognosis in this disease it seems reasonable to initiate a study of adjunctive hormone therapy in osteosarcama.
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PMID:Hormone suppression of DNA synthesis in cultured chondrocyte and osteosarcoma cell line. 105 8


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