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)

Forty-nine cases of primary tumors of the mandible have been reviewed. The anatomic location, pathologic features, sites of metastases, survival rates, and treatment methods were evaluated. Lesions studied included ameloblastoma, osteogenic sarcoma, reticulum cell sarcoma, fibrosarcoma, chondrosarcoma, myxosarcoma, epidermoid carcinoma, adenocarcinoma, and giant cell sarcoma. An in-depth discussion of primary osteogenic sarcoma of the mandible is presented. Because of upper cervical lymph node metastases in two cases of osteogenic sarcoma of the mandible, an upper neck dissection should be considered in the primary treatment. Also presented in this study are the first reported cases or primary myxosarcoma of the mandible and giant cell sarcoma of the mandible. Recent methods of treatment of ablative resection of the mandible followed by immediate or delayed repair are discussed. A revised technic for mandibular replacement which has met with success in six of seven cases is presented.
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PMID:Primary tumors of the mandible. A study of 49 cases. 79 Sep 85

Spontaneous pneumothorax is an uncommon complication of lung metastatic disease. In most of the cases reported until today, the primary disease was a sarcoma (osteogenic sarcoma, soft tissue sarcoma, hemangioendotheliosarcoma, and Ewing's sarcoma). An exceptional case of spontaneous pneumothorax in a patient suffering from carcinoma of the breast with lung metastases, is herein presented. The pneumothorax developed immediately after regression of lung metastases during administration of combined chemotherapy. Some etiological factors, as well as the rarity of this complication and its treatment, are also discussed.
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PMID:Spontaneous pneumothorax complicating lung metastases from carcinoma of the breast. 83 Mar 15

After inoculating newborn W/Fu rats with adenovirus type 9, 27 of 27 females developed mammary fibroadenomas with a latency period of 14-25 weeks. No tumors were observed after inoculation with adenovirus type 5 or in males with the type 9 inoculation. After persistence of the tumors for 3-14 months, malignant transformation of the stroma resulted in different types of sarcoma in three rats: fibrosarcoma, round-cell liposarcoma, osteosarcoma and malignant mesenchymoma. In another animal the stroma of a fibroadenoma was highly cellular, suggesting a transition into fibrosarcoma. Malignant transformation of the epithelial component was not observed. Tumor cells contained adenovirus type 9-specific T-antigen, and rats with transplanted tumors were immunized to T-antigen. Mammary fibroadenomas without signs of malignant transformation developed in eight of nine female rats inoculated with adenovirus type 9 at an adult age. Neonatal thymectomy and total body x-irradiation neither significantly shortened the induction time of adenovirus 9-induced fibroadenomas nor increased the frequency of malignant transformation in females. One lipoma and one highly differentiated liposarcoma, however, appeared in two male rats. The results provide an example of the progression of a virus-induced benign tumor into a malignant neoplasm.
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PMID:Studies on adenovirus type 9-induced mammary fibroadenomas in rats and their malignant transformation. 87 51

The bone inducing factor derived from BF osteosarcoma was purified in the following manner. Step 1. The sarcoma, grown in CBA mice, was excised and lyophilized. Step 2. The powder was washed with chilled acetone. Step 3. The acetone-treated powder was then homogenized with chilled distilled water. Step 4. Washing with 0.15M KCl. Step 5. The precipitate was incubated in in 0.2 N NH2OH, pH7.0, for 48 H at 25 degrees. After Step 5, the bone-forming activity showed a slight increase; however, the factor remained insoluble. The properties of the factor were as follows. The factor is relatively relatively heat stable; the osteogenic activity survived the treatment at 75 degrees for 15 min or at 55 degrees for 19 h. The activity was easily lost by mechanical shaking. Incubation with DNase, RNase, neuraminidase, chondroitinase ABC and beta-galactosidase left the osteogenic activity intact, but treatment with either pronase or collagnease destroyed this activity. The results suggest that the factor may be a protein. The activity was seen with the lyophilized BF osteosarcoma cells (without matrix), and it is probable that the factor was exclusively synthesized in the cells. The bone formation, observed across a millipore filter when living BF osteosarcoma enclosed in a millipore chamber was implanted in mice, suggests the synthesis and secretion of the factor from the cells.
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PMID:Studies on a factor responsible for new bone formation from osteosarcoma in mice. 105 58

This is the seventh reported case of soft tissue sarcoma attributed to thorotrast extravasated during the course of an injection for arteriography. An extraskeletal osteosarcoma occurring the cervical region of a 51-year-old man 30 years after a cerebral arteriogram is presented. The other reported cases include a fibrosarcoma, two neurofibrosarcomas, two spindle cell sarcomas, and an extraskeletal chondrosarcoma. The latency period has varied from 5 to 30 years. The thorotrast granules are readily identified in macrophages near or adjacent to the tumor, and the demonstration of alpha tracks on autoradiographs is diagnostic.
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PMID:Thorotrast-induced extraskeletal osteosarcoma of the cervical region. Report of a case. 105 2

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

The local intra-osseous injection of double zinc beryllium silicate into the tibial or femoral epiphysis of a rabbit causes an osteogenic sarcoma in 70 p. 100 of cases. These experimental conditions make it possible to reveal early non specific radiological alterations, later on secondary alterations corresponding to the development of the sarcoma and finally to follow the spontaneous evolution of the tumor. Moreover, this experimental process of induction of an osteogenic sarcoma by means of a local intra-osseous injection is vastly better than an intra-venous injection which causes straight-away multiple visceral lesions.
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PMID:[Experimental production of bone sarcomas in the rabbit by a single local injection of beryllium]. 106 48

Inoculation of Moloney sarcoma virus into the medullary canal of the tibia in newborn Wistar-Lewis rats resulted in an initially localized osteosarcoma which usually metastasized to the lung and resulted in the death of the animal within four to five weeks. Tumor cells were grown in tissue culture and used as target cells in the assay of lymphocyte-mediated cytotoxicity using a microcytotoxicity and a radioisotope labeling method. Lymphocyte-mediated cytotoxicity was demonstrated throughout the course of the clinical disease as well as in a small number of animals which showed spontaneous regression of their tumors. Serum factors which could "block" or augment the cellular response were also identified. This model resembles the spontaneous osteosarcoma of humans in many respects and may be useful for studies of the human disease.
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PMID:A virally induced osteosarcoma in rats. A model for immunological studies of human osteosarcoma. 106 26

An experimental model for osteosarcoma was developed in which, after Moloney murine sarcoma virus was injected into the tibial marrow space of three strains of inbred neonatal rats, a highly malignant neoplasm arose within ten days. This tumor was readily maintained in tissue culture and was transplantable to adult rats. It arose in the metaphyseal marrow of several bones, was locally invasive, metastasized to the lungs, and histologically resembled osteosarcoma.
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PMID:Virus-induced osteosarcoma in rats. 106 27

The immunogenicity of a virus-induced rat osteosarcoma was studied utilizing the lymphocyte microcytotoxicity test. Intratibial injection of murine sarcoma virus (Moloney) resulted in the development of palpable tumors at the injection site which on histopathological examination appeared to be osteosarcomas. In 73 per cent of animals injected these tumors progressed and metastasized to the lungs. Lymphocytes from these "progressor" animals demonstrated an ability to kill osteosarcoma cells in vitro (as quantitated in the microcytotoxicity test) while serum from these animals abrogated or blocked the cell-mediated cytotoxicity. In the remaining animals the tumors either failed to develop or regressed spontaneously. Lymphocytes from these "regressor" animals also demonstrated cytolytic activity against osteosarcoma cells in vitro, but serum failed to block the lymphocyte-mediated cytolysis. Both regressor and progressor groups demonstrated humoral cytotoxic antibodies to tumor antigen on the basis of the ability of their serum to kill tumor cells in vitro.
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PMID:Immunogenicity of virus-induced rat osteosarcoma. 106 28


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