Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0029463 (osteosarcoma)
 16,637 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

The transformed cells that arise from among the hamster epithelial and mesenchymal cells exposed to SV40 in vitro are, as a rule, fibroblastoid and pleomorphic rather than epithelioid. Moreover, the neoplasms that these transformed cells induce in the allogeneic host are spindle cell sarcomas and pleomorphic sarcomas rather than carcinomas. Since this phenomenon may result from cellular dedifferentiation in culture, to the extent that the anaplastic morphology and lack of specialized function can no longer suggest the cell or origin, we investigated the fate of the differentiated state of cells of three types of SV40-induced hamster tumors before and after serial passage in vitro. The tumors evaluated were three reticulum cell sarcomas, three osteogenic sarcomas, and two lymphosarcomas of B-cell origin. Our data demonstrate that reticulum cell sarcoma cells lose their morphological differentiation soon after the original tumors are dissociated into cell suspensions but preserve their phagocytic activity throughout their in vitro passage. Osteogenic sarcoma cells lose their differentiated phenotype and their capacity to form osteoid during but not before their serial passage in culture. Lymphosarcoma cells preserve their lymphoid morphology and their ability to produce immunoglobulin even after many in vitro passages. These results indicate that, in many types of SV40-induced tumors, neoplastic cell dedifferentiation, following serial passage in culture, is responsible to a great extent for the emergence of new cell phenotypes lacking in morphological and functional features characteristic of the cells originally transformed by SV40.
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PMID:Loss or persistence of the differentiated state of simian virus 40-induced hamster tumor cells before and after serial passage in culture. 18 42

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

The growth inhibitory effect of human leukocyte and fibroblast interferons was tested in vitro. The effect of fibroblast interferon was more pronounced on osteosarcoma cells and the effect of leukocyte interferon was more pronounced on lymphoid cells. This suggests that the capacity of interferon to inhibit cell growth is, in some measure, tissue specific.
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PMID:Is interferon tissue specific?- Effect of human leukocyte and fibroblast interferons on the growth of lymphoblastoid and osteosarcoma cell lines. 26 37

Parabiosis of rats permits one partner to survive 1000 R X-radiation if the other is shielded. This dose to the previously shielded partner after intervals of 5, 10 or 30 days tests the ability of the first irradiated partner to recover and, in turn, support the second. The effectiveness of this can be measured by the late effects induced in the pair. Lifespan was shortened by 100--150 days following a 5-day interval, by 30 days following a 10-day interval and not shortened following a 30-day interval. The incidence of leukaemia was about 6 per cent in each group, close to that in control pairs. Shortening the interval between the irradiations decreased the average age of death from leukaemia. No solid lymphoid tumours were induced in the doubly irradiated pairs. The incidence of osteogenic sarcoma was 1.6 per cent in controls and 12.9 per cent in the pairs with both partners irradiated.
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PMID:Late effects of successive massive doses of radiation on parabiont rat pairs. 30 53

The production of a cytotoxic factor synthesized by human haemic killer cells growing in vitro is described. The factor can be found extra- and intra-cellularly. It is released from the cells by an apocrine form of secretion, illustrated by light and electron micrographs. The culture fluid from 14C-labelled killer cells reveals numerous radioactive bands following SDS-gel electrophoresis. The killing factor is precipitated by 30 to 60% saturation of ammonium sulphate. Cultures of human rhabdomyosarcoma and osteosarcoma cells are more susceptible to the killer cells than normal human dermal or lung fibroblasts. During contact or killer with target cells a higher level of cytotoxic activity can be detected in the culture fluid. The cell-killing activity is completely inactivated by 30 min at 60 degrees C, but it is not absorbed by target cells during 1 h of incubation. The cytotoxic factor is unlikely to be an interferon since it did not prevent the replication of a wide range of viruses and only a low level of interferon could be detected in the culture medium. The introduction of Strep. faecalis into cultures of killer cells caused their transformation into immunoblast-like cells, indicating their lymphoid origin. The cells did not phagocytose the microorganism. When the humoral factor was injected into fibro-sarcoma-bearing mice approximately 50% survived, whereas all control animals died.
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PMID:A humoral cytotoxic substance produced by a human killer cell line. 41 8

A lymphocyte proliferation assay (LPA) for cellular immune responses to osteosarcoma antigens is described and applied to an examination of peripheral blood lymphocytes (PBL) taken from osteosarcoma patients. The antigen preparations were derived from 3 M KC1 solubilized osteosarcoma, taken from a limited number of patients. Lymphocytes from most tumor-bearing patients were stimulated to significant proliferation when cultured in normal human serum. Such stimulation was observed whether or not the lymphoid cells were preincubated 24 hours at 37 degrees C prior to addition of antigen. Patients whose lesion had been resected and who were without evidence of disease for 5-70 months had diminished proliferative responses. Lymphocytes from normal subjects, from patients having other types of sarcoma, and patients having carcinomas rarely responded to the soluble osteosarcoma antigens. When responsive PBL taken from tumor-bearing patients were cultured in autologous serum, the proliferative responses were abrogated or blocked. Serial assays made in the course of bearing this tumor under a variety of therapeutic regimens, including an immunotherapy protocol, suggest that the LPA may be useful in monitoring clinical progress of the disease and possibly in other immunotherapy protocols for osteosarcoma.
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PMID:Specific antigen stimulated lymphocyte proliferation in osteosarcoma. 106 27

We isolated four monoclonal antibodies (MAbs), M38, M101, M104, and C33, which were capable of inhibiting syncytium formation induced in a human T-cell line, MOLT-4-#8, by coculture with human T-cell leukemia virus type 1 (HTLV-1)-positive human T-cell lines. The MAbs had, however, no inhibitory activity on syncytium formation induced in a human osteosarcoma line, HOS, by HTLV-1-positive T-cell lines. They also did not inhibit syncytium formation induced in MOLT-4-#8 by human immunodeficiency virus type 1-positive MOLT-4. All MAbs reacted with various human cell lines of lymphoid and nonlymphoid origins, including HTLV-1-positive T-cell lines. Furthermore, they all reacted with a murine A9 clone containing human chromosome 11 fragment q23-pter. Two MAbs, M104 and C33, immunoprecipitated a membrane antigen with the same molecular size. The antigen (henceforth called C33 antigen) was about 40 to 55 kDa in HTLV-1-negative Jurkat, CEM, MOLT-4, and normal peripheral blood CD4-positive human T cells and about 40 to 75 kDa in HTLV-1-positive C91/PL, TCL-Kan, MT-2, and in fresh HTLV-1-transformed CD4-positive human T-cell lines. Pulse-chase experiments revealed that C33 antigen was synthesized as a 35-kDa precursor that was then processed to 41 to 50 kDa in MOLT-4 and to 44 to 70 kDa in C91/PL. In the presence of tunicamycin, a 28-kDa protein was synthesized. The conversion from 35 kDa to 41 to 50 kDa in MOLT-4 and to 44 to 70 kDa in C91/PL was inhibited by monensin. Treatment with N-glycanase alone, but not with sialidase and O-glycanase in combination, completely removed the sugar moiety of C33 antigen from both HTLV-1-negative Jurkat and HTLV-1-positive C91/PL. Therefore, C33 antigen has only N-linked carbohydrates, the modification of which appears to be substantially altered in the presence of the HTLV-1 genome.
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PMID:Identification of membrane antigen C33 recognized by monoclonal antibodies inhibitory to human T-cell leukemia virus type 1 (HTLV-1)-induced syncytium formation: altered glycosylation of C33 antigen in HTLV-1-positive T cells. 173 99

Sinonasal neoplasms and neoplasm-like proliferations composed of light microscopically poorly differentiated or undifferentiated, small- to medium-sized cells cause considerable diagnostic confusion. Lesions in this category include lymphoepithelioma (undifferentiated carcinoma), olfactory neuroblastoma, small-cell undifferentiated (oat cell) carcinoma, sinonasal undifferentiated carcinoma, malignant melanoma, pituitary adenoma, lymphoid hyperplasia, malignant lymphoma, plasmacytoma, lymphomatoid granulomatosis, rhabdomyosarcoma, mesenchymal chondrosarcoma, small cell osteosarcoma, Ewing's sarcoma, and synovial sarcoma. Many of these lesions can be definitively diagnosed based on light microscopic features alone, but, in some instances, additional techniques such as immunohistochemistry are of value. The authors review the pertinent clinicopathologic features of the above lesions, with emphasis on light microscopic, immunohistochemical, and ultrastructural features of particular utility in differential diagnosis.
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PMID:"Undifferentiated" neoplasms of the sinonasal region: differential diagnosis based on clinical, light microscopic, immunohistochemical, and ultrastructural features. 269 5

We isolated the full length provirus of human T cell leukaemia virus type I (HTLV-I) from MT-2, a lymphoid cell line producing HTLV-I. In three non-lymphoid cell lines (COS7, human osteosarcoma HOS cells, and HeLa) this provirus expressed a trans-acting activity after co-transfection with a recombinant plasmid carrying a bacterial chloramphenicol acetyltransferase gene under the control of a long terminal repeat of HTLV-I provirus. The trans-acting protein p40 was detected by immunoprecipitation in transfected HOS cells. Structural proteins of HTLV-I, the gag and env products, were also formed and processed in the same manner as observed in MT-2 cells. In transfected HeLa cells, the p40 protein was mainly localized in the nucleus, while other structural proteins were detected in the cytoplasm and/or the membrane by indirect immunofluorescence. Syncytium formation was observed in HeLa cells after transfection. These results demonstrated that non-lymphoid cells could produce the major proteins of HTLV-I after DNA transfection of the cloned provirus.
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PMID:Expression of a provirus of human T cell leukaemia virus type I by DNA transfection. 302 87

Human T cell clones cytotoxic for autologous sarcoma cell lines have been developed from patient JM with an osteogenic sarcoma, and from patients EG and RM with malignant fibrohistiocytoma. These clones were derived from the cocultivation of peripheral blood lymphocytes (PBL) with the respective patient's autologous irradiated established tumor cell lines (AIT). After two cycles of stimulation for 5 days in bulk culture, these "educated" lymphocytes were seeded at a density of 1 X 10(6) cells/well in 24-well plates and were cultured in the presence of highly purified natural IL 2 and AIT, the latter serving as a feeder layer. Cell numbers were reduced from the initial seeding density by one log each week until reaching a density of 10(2) cells. These cells were found to be stable in viability and cytotoxic activity, after which limiting dilution was then performed. Within 4 to 6 wk, clones were isolated with unique specificities. These clones were capable of proliferating to a total density of 10(9) cells/ml and maintained their specific cytotoxicity for more than 6 mo. Testing with a panel of target cells of various histotypes, cold-target inhibition assays, and blocking of cytotoxicity with anti-HLA monoclonal antibodies showed that the T cell clones recognize a common sarcoma-associated antigen and that the lysis is HLA restricted. Phenotypically, cytotoxic clones derived from JM were Leu-1+, Leu-2+, and Leu-3-, whereas those derived from EG exhibited either Leu-24 or Leu-3+ markers, the latter phenotype lacking cytotoxicity. RM exhibited mainly Leu-3+ clones with strong cytotoxicity. All were HNK-1- and HLA class II+, with less than 1% of cells of each clone stained by anti-TAC monoclonal antibody. The clones from each patient did not lyse autologous or allogeneic PBL, mitogen-induced T lymphoblasts, normal fibroblasts, cells isolated from benign neoplasms, carcinoma cells, Daudi B lymphoid cells, or K562 cells. With the exception of EG, all clones produced immune interferon in a range from 12 to 50 U/ml. The generation of long-term specific T cell clones can be used to further dissect the cellular immune response to sarcomas. Cytotoxic T cell clones have potential application for tumor immunotherapy.
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PMID:Cellular immune response to human sarcomas: cytotoxic T cell clones reactive with autologous sarcomas. I. Development, phenotype, and specificity. 309 88


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