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)

Interleukin-1 (IL-1) is probably an important lymphokine mediator of inflammation and bone resorption. IL-1 derived from mononuclear cells, a melanoma cell line (MM96 cells), and recombinant human IL-1 (rHuIL-1 beta) increased in vitro bone resorption, as measured by the release of 45Ca from cultured mouse calvariae. The 50% maximum active resorption was observed with 0.125 ng/ml or approximately 10(-11) M rHuIL-1 beta. The resorptive action of IL-1 was not entirely dependent on prostaglandin mediation, since its effect was evident when prostaglandin synthesis was inhibited in the cultures by indomethacin. IL-1-induced resorption has been shown to be inhibited by 10(-5) M 3-amino-1-hydroxypropylidene-1-1-bisphosphonate (APD). This inhibition was partially reversed by increasing doses of IL-1. In vitro toxicity studies showed that at concentrations of 10(-4) M, APD inhibited the growth of cultured MM96, murine myelomonocytic P388D1, and rat osteosarcoma UMR 106 cells, but not other mast and lymphoid cell lines. These in vitro observations may have relevance to the use of APD in bone and joint diseases in which inflammation and bone resorption are prominent.
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PMID:Aminobisphosphonate inhibition of interleukin-1-induced bone resorption in mouse calvariae. 326 Jan 1

Tumor metastasis may be facilitated by interaction of tumor cells with platelets. It is not known, however, whether solid tumors which have predisposition to pulmonary metastasis affect platelets differently than lymphoid tumors, which rarely spread to lungs. We therefore examined the effects of cultured osteogenic sarcoma (MG-63, U2-OS), as well as leukemia (NALM-16, LAZ-221, K-562) and lymphoma (RAJI, MOlt 4) cells, on human platelet aggregation. Human osteogenic sarcoma (MG-63) cells alone induced platelet aggregation, whereas U2-OS cells induced platelet aggregation only after preincubation of platelets with subthreshold concentrations of epinephrine. In contrast, neither leukemia nor lymphoma cells affected platelet aggregation. These observations suggest that the platelet proaggregatory potential of tumor cells is variable and that the platelet stimulatory effects of osteogenic sarcoma cells may relate to their high risk of pulmonary metastasis.
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PMID:Effect of human tumor cells on platelet aggregation: potential relevance to pattern of metastasis. 347 52

Primary malignant bone tumors, osteosarcomas (9 cases), and Ewing's sarcomas (10 cases) were examined for their reactivities with monoclonal and polyclonal antibodies against filamentous proteins and cell membrane determinants of the lymphoid and macrophage marker series. The reactivity of antibodies was studied on snap-frozen tissue probes by using a triple layer immunoperoxidase method. Osteosarcomas were positive for vimentin and, in part, for HLA-DR. Other types of intermediate-sized filaments were not detected in tumour cells. In a small number of cases (2/9) tumour cells were reactive with antibodies of the macrophage series (Leu M2). In Ewing's sarcomas, vimentin and HLA-DR was also demonstrated. It was particularly interesting that Leu M2 staining was found in the majority of cases (8/10). The staining pattern supports the assumption that this peculiar tumour is of mesenchymal (monocyte/macrophage) histogenesis. It was evident from the present study that, in primary osteogenic tumors, none of the examined tumour "markers" were as distinctive as they are for bone metastases. Nevertheless, the reactivity of Ewing's sarcoma cells with monoclonal antibodies of the Leu M2 type throws some highlights on the, as yet, obscure histogenesis of the neoplasm and may be of diagnostic value in conjunction with the known light and electron microscope features of the tumour.
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PMID:Osteosarcomas and Ewing's sarcomas. Comparative immunocytochemical investigation of filamentous proteins and cell membrane determinants. 392 63

FBJ osteosarcoma virus (FBJ-MSV) isolated originally from a spontaneously arising osteosarcoma in a CF1 mouse is the only known naturally occurring murine sarcoma virus (MSV). It is unique among strains of MSV in producing primarily sarcomata in mice. The capacity of tumour cells transformed in vivo by this agent to elicit specific transplantation immunity in syngeneic hosts was investigated. A low level of resistance (10(4)-10(5) cells) was consistently induced by implantation of x-irradiated (15,000 rad) tumours or surgical excision of developing subcutaneous grafts. By contrast intraperitoneal inoculation of virus containing cellfree extracts of FBJ-MSV sarcomata was a far less effective immunization procedure. Confirmatory evidence for the antigenicity of these neoplasms was obtained in tests in which preincubation of tumour cells with lymphoid cells from specifically immune donors inhibited in vivo outgrowth of the FBJ-MSV cells in untreated syngeneic recipients. The induction of host resistance to FBJ-MSV cells by immunization with identical and independently-induced FBJ-MSV tumours established that FBJ-MSV cells possess common cell surface antigenic specificities in a manner analogous to those of experimental neoplasms induced by other oncogenic DNA and RNA viruses. Since FBJ-MSV cells release infectious virus it was not possible in this system to establish whether the tumour-rejection antigen was cellular or virion in nature. The antigenic weakness of FBJ-MSV cells in syngeneic hosts is comparable with that of virus-induced murine leukaemias of the Gross (G) or "wild" type subgroup to which category FBJ-MSV also belongs. These features suggest that FBJ-MSV exemplifies naturally occurring sarcomagenic viruses more closely than those of the Friend-Moloney-Rauscher-Graffi (FMRGr) subgroup which in general induce highly antigenic neoplasms.
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PMID:Tumour-associated transplantation antigens of neoplasms induced by a naturally occurring murine sarcoma virus (FBJ-MSV). 451 7

Antigens associated with cells transformed in vivo by FBJ virus, a wild type murine sarcoma virus (MSV) complex originating from a spontaneously arising osteosarcoma in a CF1 mouse, have been partially characterized by complement fixation (CF). Using rat antisera against antigens specified by Gross leukaemia virus (GLV) the group specific (gs) antigen of C-type RNA murine tumour viruses was demonstrated in FBJ tumours as well as in GLV rat leukaemias, AKR lymphomata and sarcomata induced by MSV-H (Harvey), an MSV isolate of Friend-Moloney-Rauscher (FMR) subgroup specificity. Using mouse antisera against antigens present in FBJ cells the Gross (G) or wild type specificity of FBJ tumours was demonstrated by cross reactivity with antigens expressed on normal AKR lymphoid tissues and leukaemias. These antigens were absent from MSV-H induced sarcomata and in reciprocal tests mouse antisera to MSV-H failed to react with antigens present in FBJ tumour cells. No distinction between cellular and virion antigens expressed by FBJ cells was possible by CF although evidence for a cellular antigen with G specificity was obtained in tests using aged C57B1 antiserum containing a naturally occurring G antibody lacking significant virus neutralizing capacity. However, the likelihood that mouse FBJ antisera contain antibodies to type specific viral envelope antigens (VEA) as well as cellular antigen is discussed.
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PMID:Antigens of tumours induced by naturally occurring murine sarcoma virus (MSV-FBJ). I. Detection of group and type specific antigens by complement fixation. 482 Sep 43

A variety of solid and hematological human tumors and normal human bone marrow specimens were assayed for colony formation in a short-term soft-agar culture system. The effect of human fibroblast, lymphoid, and myeloid interferons on inhibition of colony formation was assessed. The effect of interferon on colony formation formed a continuum from complete inhibition to stimulation of growth. Of 40 evaluable tumor specimens, 18 showed at least a 70% inhibition of colony formation in the presence of interferon, at concentrations of 1000 units/ml or less. Four specimens (acute myelogenous leukemia, osteogenic sarcoma, neuroblastoma, ovarian carcinoma) showed at least 3-fold stimulation of colony formation with interferon. Two of 12 normal bone marrow specimens grown with colony-stimulating, factor-conditioned media showed greater than 70% colony inhibition with interferon. A dose-response relationship was seen in all tumor specimens tested. While fibroblast interferon was the most active in this system, all interferons showed the same magnitude and direction of activity. Continuous exposure and 1-hr incubation of tumor cells with interferon were identical in terms of colony inhibition. These data support the ability of this assay system to select tumors responsive in vitro to interferon, suggest the optimal species and concentration for inhibition or stimulation of growth, and support a direct role of interferon in the regulation of cell growth independent of other immunoregulatory actions of interferon. Such information may prove useful for predicting response in vivo to interferon in Phase II trials.
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PMID:Effect of fibroblast, lymphoid, and myeloid interferons on human tumor colony formation in vitro. 616 Sep 5

Two murine IgG2Ak monoclonal antibodies (703D4, 704A 1) were produced and characterized after immunization with a human large cell lung cancer line (NCI-H 157). These antibodies detect different epitopes on 31 kilodalton [35S]methionine incorporating protein(s). Radiobinding and immunohistochemical studies show these antibodies bind to most (11/13) human non-small cell lung cancer (adenocarcinoma, epidermoid, and large cell), but not to small cell lung cancer (0/11) tumors tested. The epitopes these antibodies recognized are also expressed on human melanomas (7/8), two other tumors (osteogenic sarcoma, renal cell carcinoma), but not on many other human tumors (breast, colon, neuroblastoma, lymphoid), and not on a panel of normal adult human tissues. Because the antigen(s) are preserved after fixation and because of their ability to distinguish lung cancer types from each other and normal tissues, they should be of clinical, as well as of biologic interest.
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PMID:Monoclonal antibodies that distinguish non-small cell from small cell lung cancer. 630 2

Beagle dogs were given subcutaneous implants of plutonium in their forepaws to mimic hand wounds received by workers accidentally contaminated with plutonium. Ten dogs received 9.46 +/- 0.43 mu Ci of plutonium oxide, and eight dogs received 1.25 +/- 0.60 mu Ci of plutonium nitrate. Surviving dogs were sacrificed at 8 and 5 yr, respectively, after exposure, and radionanalyses were performed on the injection site, regional lymph nodes, liver, spleen and bone. Histopathologic and autoradiographic examinations were performed on injection sites, regional lymph nodes, livers, spleens, kidneys and grossly observed lesions. The injected paws sequestered 21 and 16%, respectively, of the injected activity from plutonium oxide and plutonium nitrate in hypocellular scar tissue. The highest concentrations of translocated radionuclides were found in the regional lymph nodes. Histopathologic and autoradiographic examinations of regional lymph nodes showed that the alpha activity was largely sequestered by scar tissue that replaced lymphoid parenchyma in the plutonium-oxide-injected dogs. In the plutonium-nitrate-injected dogs, activity was widely distributed in relatively intact regional lymph nodes. The liver had the next highest concentration for both radionuclides; activity was present as alpha stars. The spleen had the next highest concentration for plutonium-oxide-injected dogs, although concentrations in the spleen were lower than the skeleton in the plutonium-nitrate-injected dogs. Osteosarcomas and hepatomas were present in one dog injected with plutonium oxide. There does not appear to be any unique risk for dogs related to the subcutaneous route of exposure to plutonium.
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PMID:Plutonium-induced wounds in beagles. 646 50

Wistar rats treated with cyclophosphamide, total lymphoid irradiation (TLI), and/or cyclosporin A (CSA) develop a state of immune suppression permitting the growth of tumor xenografts. Experiments were carried out on this newly developed model to investigate the growth patterns of a mouse osteosarcoma and a human colon adenocarcinoma. The combination of cyclophosphamide and CSA permitted a limited period of growth of the mouse osteosarcoma with a tumor take rate of 66%. No takes were observed with the human adenocarcinoma. The combination of cyclophosphamide and TLI resulted in a period of immunosuppression followed by recovery of the immune status. During the period of immunosuppression, tumor xenografts showed a 100% take rate. The most efficient immunosuppression was achieved by a combination of cyclophosphamide, TLI and CSA administered on alternate days. Wistar rats subjected to this treatment showed prolonged tolerance to mouse osteosarcoma and human adenocarcinoma xenografts. There was no alteration in the tumor doubling time or histological morphology of the xenografts in the adapted host as compared with those in the donor tumors. The tumor growth curve showed a pattern of initial growth, a period of stagnation, followed by a steady but slower growth phase. The significance of the results and the advantages of the rat model described in this paper for human tumor xenotransplantation are discussed.
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PMID:Growth pattern of tumor xenografts in Wistar rats after treatment with cyclophosphamide, total lymphoid irradiation and/or cyclosporin A. 657 7

The immunogenicity of a virus-induced rat osteosarcoma was studied utilizing the lymphocyte microcytoxicity test. Lymphocytes from "progressor" animals (in which the tumour progressed and metastasized) demonstrated an ability to kill osteosarcoma cells in vitro, while serum from these animals abrogated or blocked the cell-mediated cytotoxicity. Lymphocytes from "regressor" animals (in which tumours failed to develop or regressed spontaneously) also showed cytolytic activity against osteosarcoma cells in vitro, but their serum failed to block the lymphocyte-mediated cytolysis. Both progressor and regressor animals demonstrated the presence of humoral cytotoxic antibodies to tumour antigens on the basis of the ability of their serum to kill tumour cells in vitro. In an attempt to alter the fatal course of the disease in progressor animals, immunoprophylaxis and immunotherapy of the osteosarcoma in F1 hybrid rats war carried out by injecting them with parentalor, third party, allogeneic lymphoid cells. Injection of parental spleen lymphocytes into F1 hybrids produced a transient graft versus host reaction (GVHR), and prolonged the survival of the animals when lymphocytes were injected three days before, seven days after and on the day of tumour induction. Injection of allogeneic, third party lymphoid cells produced no detectable GVHR and prolonged the survival of F1 hybrids with osteosarcoma only when injected on the day of tumour induction. The prolonged survival of the groups treated with parental lymphoid cells was a result of stimulation of the host's immunological mechanisms during a transient GVHR, whereas the prolongation of survival in the group given allogeneic cells was most likely the result of a direct action of the donor lymphocytes on tumour cells, and not connected to a GVHR.
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PMID:The biology, pathology and immunology of a virus induced rat osteosarcoma. II. Immunological studies. 693 50


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