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)

Tumors were induced in 46 of 52 female Sprague-Dawley rats by gastric intubation of 5 mg of DMBA, dissolved in 1 ml of sesame oil, given weekly for 5 weeks. From 4 weeks after the final dose tumors were recorded and measured. Bilateral ovariectomy was done 3 days before sacrifice and assay. Excised tumors were immediately immersed in ice-cold Tris-EDTA buffer. Sections were prepared for histological examination. The assay was done by sucrose density centrifugation after administration of (2,4,6,7-tritiated)-estradiol-17beta in vivo 3 minutes before killing, and/or in vitro. For specific estrogen-binding proteins the capacity to bind (tritiated)-estradiol-17beta was not related to the growth characteristics, time of appearance, or time between ovariectomy and assay. Different tumors had estrogen-binding capacities unrelated to the percentage of neoplastic cells in the tumor, amount of inflammation, mast cell infiltration, or presence of fluid-filled cysts. The number of mitoses and the lipid content of the tumors were correlated with the estrogen-binding capacity in that it was lower in tumors with many mitoses and in those with much lipid in the epithelial cells. Of 19 adenocarcinomas, 6 did not regress after ovariectomy. In 5 of the regressed tumors a new growth phase was seen, beginning 2 months after ovariectomy. Tumors encountered, other than mammary adenocarcinomas, were an extraosseous osteosarcoma, fibroadenomas, and zymbal-gland tumors.
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PMID:Morphology, growth characteristics and oestrogen-binding capacity of DMBA-induced mammary tumours from ovariectomized rats. 40 32

We have previously shown that thrombospondin (TSP) is synthesized and secreted by human MG-63 osteosarcoma cells. In this study, the secretion and cell surface expression of TSP by two different human osteosarcoma cell lines (MG-63 and TE-85) as well as the involvement of TSP in the platelet-aggregating activity of these tumor cells were studied. Using a sandwich enzyme-linked immunosorbent assay, MG-63 cells secreted 3-fold as much TSP as TE-85 cells at 48 h (0.17 +/- 0.01 (SD) versus 0.06 +/- 0.006 micrograms/10(6) cells, P = 0.007). Binding of exogenous 125I-TSP to MG-63 and TE-85 cells in monolayer indicated that binding was time and concentration dependent, saturable, and inhibited by excess cold TSP. However, despite a similar affinity, MG-63 cells had 10-fold more TSP-binding sites than TE-85 cells (402,394 +/- 130,346 versus 36,748 +/- 7,708 TSP-binding sites/cell; P = 0.002). Similar binding differences of 125I-TSP were observed with both osteosarcoma cell lines in suspension. A fluorescence-activated cell-sorting analysis was used in conjunction with an anti-TSP polyclonal antibody, and binding of endogenous TSP to MG-63 and TE-85 cells in suspension was investigated. Addition of an anti-TSP antibody to MG-63 and TE-85 cells in suspension increased the mean fluorescence intensity 50-fold when compared to an irrelevant antibody. Moreover, the fluorescence intensity of MG-63 cells with an anti-TSP polyclonal antibody was increased by 40% when compared to TE-85 cells. Since TSP was expressed on the surface of osteosarcoma cells, the involvement of this glycoprotein in the platelet-aggregating activity of MG-63 and TE-85 cells was therefore investigated using an anti-TSP polyclonal antibody and two monoclonal antibodies (P10 and MA-II), the epitopes of which lie within the Mr 140,000 non-heparin-binding fragment and the Mr 25,000 heparin-binding fragment of TSP, respectively. Preincubation of MG-63 cells (1 x 10(6) cells/ml) with either an anti-TSP polyclonal antibody (100 micrograms/ml) or monoclonal antibody P10 (15 micrograms/ml) inhibited by 80% other platelet-aggregating activity of these tumor cells, while anti-TSP monoclonal antibody MA-II (15 micrograms/ml) had no effect. In sharp contrast, the anti-TSP polyclonal antibody (100 micrograms/ml) only exhibited a slight inhibitory effect on platelet aggregation induced by TE-85 cells when using a low concentration of tumor cells (0.6 x 10(6) cells/ml).(ABSTRACT TRUNCATED AT 400 WORDS)
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PMID:Thrombospondin binds to the surface of human osteosarcoma cells and mediates platelet-osteosarcoma cell interaction. 170 97

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

The bone scan features of different types of sacral tumors in 16 patients were assessed. Four out of five patients with chordoma, the most common sacral tumor, demonstrated either reduced uptake or normal distribution of isotope at the site of this midline tumor. Plasmacytoma, which is not usually central, also caused reduced uptake on the bone scan. Ewing's sarcoma gave no consistent pattern. All other tumors caused increased uptake except for one unusual case of osteogenic sarcoma. Bone scintigraphy can be very useful in the assessment of sacral tumors. A midline sacral tumor that is cold on the bone scan is very likely to be a chordoma.
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PMID:Scintigraphic features of primary sacral tumors. 371 78

Cytotoxic T lymphocytes (CTL) against autologous fresh osteosarcoma cells were generated in mixed lymphocyte tumor culture (MLTC), and then were propagated and maintained for up to 19 days with culture medium containing T cell growth factor (TCGF). CTL generated with MLTC and propagated with TCGF (TCGF-CL) lysed fresh autologous osteosarcoma cells, but not autologous phytohemagglutinin-blastoid lymphocytes. More than 90% of the propagated lymphoblastoid cells were E-rosette forming cells. A subpopulation of TCGF-CL was Leu-2a positive and Leu-3a negative CTL. The cytotoxic activity to the autologous tumor detected by 51Cr release assay was not blocked by cold allogeneic tumor cells from 4 out of 5 patients tested. Human leukocyte antigen and chromosomes of TCGF-CL showed no abnormality.
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PMID:Cytolysis of autologous fresh osteosarcoma cells by human cytotoxic T lymphocytes propagated with T cell growth factor. 660 70

A retrospective examination of the bone scans of 425 pediatric oncology patients was undertaken to determine the incidence of photon-deficient (cold) lesions in this population. Eight patients (1.8%) had cold lesions due to a wide variety of tumors. Of the tumor types, six had not been previously reported to give cold lesions on bone scan. The appearance of the radiograph at the site of the cold lesion was normal in five of the eight patients. All but one of the patients had "hot spots" as well as a cold lesion. Follow-up scans showed resolution of the cold lesions in two cases and a change from cold to hot in one case. A review of the literature revealed eight cases of cold lesions on bone scan due to tumor in pediatric patients. The previous reports included five patients with neuroblastoma and three with osteosarcoma.
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PMID:Cold lesions on bone scan in pediatric neoplasms. 670 10

The adenylate cyclase (ATP pyrophosphate-lyase (cyclizing), EC 4.6.1.1)-stimulating factor from rat osteosarcoma cytosol was purified 600-fold by ion-exchange chromatography. The factor has an apparent Mr of 20000, is cold-labile, but retains activity at -20 degrees C in 10% glycerol. The factor enhanced parathyroid hormone stimulation of adenylate cyclase and restored hormone responsiveness to membranes washed with 0.5 M NaCl. These 'GTP-like' effects were not inhibited by 100 microM GDP-beta-S, which completely abolished the GTP enhancement of both basal and hormone-stimulated adenylate cyclase. Adenylate cyclase activity in the presence of the stimulating factor was linear with time, and showed hyperbolic dependence on factor concentration. The factor also linearized (in double reciprocal plots) the downward-concave Mg2+-dependence of adenylate cyclase, increasing the apparent affinity of the enzyme for Mg2+. The presence of the factor in two clonal osteosarcoma cell lines correlated with parathyroid hormone-stimulatable adenylate cyclase. Factor stimulation was absent while GTP stimulation was retained in the hormone-nonresponsive clone. Factor and hormone sensitivity were restored by in vivo passage. This factor thus may represent a guanyl nucleotide-independent path for cellular regulation of hormone response.
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PMID:Osteosarcoma cytosol factor promotes parathyroid hormone stimulation of adenylate cyclase independent of GTP. 693 11

Two patients with extraosseous osteosarcoma of the gluteal region are presented. In one early case liquifaction of the tumour delayed the diagnosis due to confusion with a cold abscess. In the second patient the tumour developed in a region that had been subjected to post-operative radiotherapy for a uterine carcinoma seven years earlier. In both patients the tumour developed rapidly and with a fatal outcome only a few months after apparently satisfactory local excision.
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PMID:Extraosseous osteosarcoma - two cases. 694 83

Inactivation of the p53 tumor suppressor gene has been implicated in the pathogenesis of numerous human cancers, including osteosarcomas. Appendicular osteosarcomas of the dog appear to be a good model for their human equivalent with regard to biologic behavior, epidemiology and histopathology. We individually screened exons 5-8 of the p53 gene for mutations in 15 canine appendicular osteosarcomas using 'Cold' SSCP to compare the role of this gene in human and canine osteosarcoma tumorigenesis. Seven of the tumors (47%) exhibited point mutations, with one tumor possessing two mutations within different exons. Of these, seven were missense mutations and the eighth was a 'silent' mutation potentially affecting the exon 6-7 splicing region. Five of the missense mutations were located in highly conserved regions IV and V, while another corresponded with the highly conserved codon 220 mutational hotspot located outside the conserved domains. The locations and types of mutations were nearly identical to those reported in human cancer. These findings provide strong evidence of the involvement of p53 mutations in the development of canine appendicular osteosarcomas. Canine osteosarcomas appear to be a promising model for their human equivalent on a clinical, pathologic, and molecular level.
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PMID:Mutation of the p53 tumor suppressor gene in spontaneously occurring osteosarcomas of the dog. 947 14

Induction of WAF1 expression was investigated in human glioblastoma cell lines differing in p53 gene statuses after cold shock treatment. Accumulation of both wild-type (wt) and mutant p53 (mp53) was induced by cold shock at 4 degrees C for 60 min, however, WAF1 accumulation was induced by cold shock in A-172 cells carrying the wtp53 but not in T98G cells carrying the mp53. Inactivation of wtp53 by a dominant negative p53 mutant (p53Trp248) abolished cold shock-induced WAF1 expression in A-172 transfectant cells. Furthermore, no WAF1 expression was induced by cold shock in p53-deficient human osteosarcoma Saos-2 cells. Northern blot analysis showed that the WAF1 but not p53 gene was activated by cold shock only in A-172 cells. These findings suggest that WAF1 expression is cold shock-inducible in human glioblastoma cells, and that this induction may be due to signal transduction mediated by p53 in response to non-genotoxic stress, cold shock.
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PMID:p53-dependent induction of WAF1 by cold shock in human glioblastoma cells. 952 49


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