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

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

Osteosarcomas formed in antilymphocyte serum (ALS)-treated hamsters when 2x10(6) TE-85 human osteosarcoma cells (maintained in tissue culture) infected with M-MSV (RD-114) virus were injected adjacent to the femur or the scapula; undifferentiated sarcomas formed when 1 x 10(6) cells were injected subcutaneously. Tumors were palpable 10 to 14 days after the cells were injected and grew progressively until the animals died (mean survival time was 30 days). All animals had pulmonary metastases. Neither the subcutaneous sarcomas nor the metastases contained bone or osteoid; however, the osteosarcomas adjacent ot the femur and scapula contained collagen, osteoid and calcified bone when observed by light and electron microscopy. These results indicate that the TE-85-M-MSV cell-ALS hamster system is an animal model for the study of osteosarcomas of human cell origin.
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PMID:An animal model for human osteosarcoma. 26 8

New Zealand White rabbits were immunized with whole-cell suspensions of TE-85 cells (from a human osteosarcoma) maintained in tissue culture. RNA was extracted from the lymphoid tissues of the immunized animals. Normal human peripheral blood lymphocytes were pretreated with both the whole-cell immune RNA (IRNA) and the Sephadex column-eluted fractions of the whole-cell IRNA. Significant stimulation of the cytotoxic effect of the lymphocytes was observed following whole-cell IRNA pretreatment and pretreatment with peak III fractions eluted from the column. This increase in inhibition was observed whether the target cells were TE-85 (the immunizing cells), L.M. and M.Mc. (two unrelated osteosarcoma primary cell cultures), or TE-85-M-MSV cells (a cell line capable of producing a human osteosarcoma in immunosuppressed hamsters). No inhibition was observed when cells from other types of human tumors were used as target cells. The results suggested that the transferred immunity was directed against tumor-specific osteosarcoma antigens.
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PMID:Effect of xenogeneic immune RNA on normal human lymphocytes against human osteosarcoma cells in vitro. 26 78

Human osteosarcoma (HOS) clonal cells transformed in vitro by N-methyl-N'-nitro-N-nitrosoguanidine (MNNG) were characterized, and compared to non-producer HOS cells transformed by Kirsten murine sarcoma virus (Ki-MSV). The MNNG- and virus-transformed cells grew in the aggregate form above an agar base, grew in soft agar, and had a high fibrinolytic activity. When inoculated into nude mice, all the chemically or virally altered cells produced tumors or tumor nodules. When transplanted into ATS-treated hamsters, the cells transformed by MNNG (0.01 mug/ml) and Ki-MSV produced tumors but MNNG (0.1 mug/ml) transformed cells did not produce tumors. The control HOS cells did not grow in the aggregate form but formed colonies in soft agar, and had low fibrinolytic activity and no capacity to form tumors in nude mice and ATS-treated hamsters. However, one of the control clonal lines had a high level of fibrinolytic activity. Cellular aggregation properties of human transformed cells did appear to correlate with tumorigenicity in nude mice.
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PMID:Characterization of human cells transformed in vitro by N-methyl-N'-nitro-N-nitrosoguanidine. 26 98

Moloney murine sarcoma virus (M-MSV) was injected directly into the fetuses of Sprague-Dawley rats during the late stage of gestation and into the neonates within 24 hours after birth. Ninety rats developed 188 neoplastic lesions during the 8-week period of observation. Nearly all of the neoplasms were of mesenchymal derivation. Sixty percent of these neoplasms revealed more complex histologic features than those previously reported for neoplasms induced in rodents with M-MSV and were designated "malignant mesenchymoma" which developed preferentially in the proximal parts of the extremities, distant from the inoculation site. Rhabdomyosarcoma and osteosarcoma which developed in a pure form at the various sites were the next most common tumor type. Osteosarcoma developing in a pure form and as a component of malignant mesenchymoma in the humerus and femur was comparable to that of juxtacortical osteosarcoma of man; The development of excessive bones were observed in the forelimb and/or hind leg, suggesting a type of skeletal malformation. The reaction to M-MSV merits attention as a model for the study of an osteosarcoma and malignant mesenchymoma as well as rhabdomyosarcoma and also for the study of viral teratogenesis in man, as "rubella syndrome".
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PMID:Pathology of neoplasms and other lesions induced in rats with Moloney murine sarcoma virus. 26 56

Xeroradiography, a method of X-ray imaging based upon selenium photoconductivity, was used for the study of experimental osteosarcoma induced by MSV-M virus in rats. Due to the peculiar features of xeroradiographic image (enhancement of details and lowering of the overall contrast) good pictures of osseous structures together with soft tissues were obtained even in very young animals. Serially perfomred xeroradiographies gave a permanent representation of tumor evolution with time. Advantages and drawbacks of this method are discussed, particularly with respect to radiation dosage. Xeroradiography is proposed for the study of the response to antiblastic chemotherapy of experimental bone tumors.
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PMID:Xeroradiographic evaluation of murine osteosarcoma. 27 Aug 62

The TE-85 osteosarcoma cell line has several of the in vitro properties of malignant cells, including colony formation in agar, but has low extracellular fibrinolytic activity and no capacity to form tumors in ATS-treated hamsters. Some TE-85 cells clones (clones 2, 4 and 6) have increased fibrinolytic activity but do not form tumors in hamsters. TE-85 cells infected with mammalian transformation-defective viruses have low (FeLV) or increased (RD-114 virus) levels of fibrinolytic activity and do not form tumors in hamsters. TE-85 cell either nonproductively infected with Ki-MSV or productively infected with M-MSV (RD-114), have fibrinolytic activity and can form tumors in hamsters. The MSV gene(s) but not colony formation in agar or extracellular fibrinolytic activity appears to be capable of rendering TE-85 cells tumorigenic in ATS-treated hamsters.
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PMID:The relationship between tumorigenicity, growth in agar and fibrinolytic activity in a line of human osteosarcoma cells. 108 Jul 52

An activated c-mos oncogene was detected by DNA transfection assay of hamster SHOK cells with DNAs from X-ray-induced mouse osteosarcoma. It was molecularly cloned by the cosmid rescue method and found to form transformed foci of SHOK cells. Genomic DNA sequencing revealed that in this oncogene the N-terminal coding region of the mouse proto-mos gene was deleted and replaced by a hamster-derived sequence in the primary transformant, suggesting that activation was due to the rearrangement during transfection. The gene product was about 37 kDa and was immunoprecipitated with anti-mos antibody from a lysate of a SHOK cell transfectant. This truncated mos (t-mos) gene transformed SHOK cells more effectively than v-mos. A chimeric gene construct of this hamster-derived upstream sequence and normal mouse c-mos also transformed SHOK cells at a lower level, whereas neither t-mos nor the chimeric c-mos gene transformed NIH3T3 cells appreciably. The high transforming efficiency of t-mos in SHOK cells was due not only to truncation of the coding region but also to its integration under a putative promoter sequence derived from the hamster genome. This is the first report of detection of an activated c-mos gene by DNA transfection assay.
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PMID:Oncogenic activation of murine mos protein kinase by DNA rearrangement of its N-terminal coding region. 153 43

A tumour cell line was established from a non-metastatic osteosarcoma which had developed in the right femur after infection of a newborn mouse with FBR osteosarcoma virus (FBR MSV). After 20 cell culture passages and injection of the cells into newborn syngeneic mice, the animals developed fibrosarcomas on the site of injection. Metastatic lung tumours were detected in 50% of the mice. Metastatic tumour growth was preferentially observed in the walls of large blood vessels and in subpleural zones. Large areas of the metastatic tumours resembled mature connective tissue. This model of in vitro progression from a primary non-metastasizing osteosarcoma to a neoplasm with particular metastatic potency, though with a growth pattern similar to fibromatosis may serve as a useful system to study the different steps of metastatic progression, distinct tropism of invasive cells and fibrous maturation of metastatic tumours.
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PMID:Metastatic growth of v-fos-induced osteosarcoma, following in vitro cultivation. 161 Jul 71


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