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)

During the period January 1975 to August 1977, alkaline phosphatase levels in 30 patients with osteogenic sarcoma were closely followed in an attempt to determine if these measurements had clinical value in predicting the course of patients with this disease. Of 17 patients with elevated preoperative alkaline phosphatase levels, 12 recurred. Of 13 patients with normal preoperative alkaline phosphatase levels, only 4 recurred (p less than .05). Thus, alkaline phosphatase levels that were elevated preoperatively were correlated with poor prognosis. A similar correlation between postoperative alkaline phosphatase levels and prognosis could not be made.
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PMID:Prognostic significance of alkaline phosphatase measurements in patients with osteogenic sarcoma receiving chemotherapy. 28 47

Levels of alkaline phosphatase were measured in the primary tumor of 26 patients with osteosarcoma. One of seven patients with a tissue alkaline phosphatase level less than 0.6 microM/min/mg developed pulmonary metastases. In contrast, 16 or 17 patients with a tissue alkaline phosphatase level greater than 0.6 microM/min/mg developed pulmonary metastases. It thus appears that tissue alkaline phosphatase levels of primary osteosarcomas are strongly correlated with prognosis (p less than .01).
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PMID:Alkaline phosphatase levels in osteosarcoma tissue are related to prognosis. 29 11

Light microscopic, histochemical and ultrastructural studies of a transplantable mouse osteosarcoma were carried out. The osteosarcoma grew in CBA mice after injection of cultured cells derived from a Dunn osteosarcoma. The tumour differed from the original Dunn osteosarcoma with respect to metastatic potential and structural features. The transplantable tumour was an anaplastic, richly vascularized fibroblastic osteosarcoma with alkaline phosphatase activity and rather sparse osteoid formation, resulting in death of the animals within 6 to 8 weeks. Virus particles were found intracellularly, mainly localized to cisterns of rough endoplasmic reticulum, and extracellularly often close to plasma membranes and collagen fibres. Sign suggestive of formation of collagen fibres by tumour cells were observed. A possible viral influence upon the tumour was suggested also by its growth behaviour in vitro. The results indicate that this new transplantable tumour, obtained in an allogenic system, represents a clonal derivative of the original Dunn osteosarcoma.
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PMID:Transplantable osteosarcoma in mice. Structural characterization of a transplantable osteosarcoma obtained in an allogenic system. 29 21

Malignant degeneration of fibrous dysplasia is rare. It occurs with similar frequency at all ages and in both sexes. It is more frequent in cases of polyostotic than in monostotic fibrous dysplasia. In cases of fibrous dysplasia that do show malignant degeneration it is common to find that a high level of alkaline phosphatase persists in the serum, even in adults. Previous radiotherapeutic treatment appears to me a predisposing factor. Osteosarcoma is the most frequent neoplasm, followed at some distance by fibrosarcoma and chondrosarcoma. The tumour is most often localised in the femur; it is not unusual to find it in the tibia, maxilla and mandible. The treatment and prognosis are the same as those of the involved malignant neoplasm.
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PMID:Malignant degeneration in fibrous dysplasia (presentation of 6 cases and review of the literature). 29 46

Histological and biochemical changes during calcitonin treatment have been studied in 15 patients with Paget's disease of bone. For each patient, osteoclast counts were made by the same observer on serial needle biopsies of diseased bone from the posterosuperior iliac spine. Serial estimations were also made of the serum alkaline phosphatase and urinary hydroxyproline excretion. A total of 66 biopsies was examined (ranging from two to seven per patient). Osteoclast populations and the biochemical measurements were log normally distributed. During calcitonin treatment there was a statistically significant decrease in: (1) the total osteoclast count per square millimetre; (2) the number per square millimetre of osteoclasts in resorption cavities on the trabecular surface; (3) the relative proportion of osteoclasts sited in resorption cavities compared with total osteoclasts; (4) the serum alkaline phosphatase level; (5) 24-hour urinary hydroxyproline excretion. On stopping treatment there was a statistically significant increase in all of these histological and biochemical values except that the proportion of osteoclasts in resorption cavities remained low. The trabecular cement line pattern remained abnormal during and after treatment in all biopsies examined, and complete suppression of osteoclast activity was not observed. One of the patients developed a Paget's osteosarcoma while on calcitonin therapy.
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PMID:Effect of calcitonin treatment on osteoclast counts in Paget's disease of bone. 74 91

To establish that alkaline phosphatase (AP) was released by osteosarcoma cells, we measured this enzyme in C3H/HeJ mice with im-implanted osteosarcoma and in in vitro cultures of neoplastic cells subjected to short-term incubation. We found that 10(5) osteosarcoma cells synthesized a significant amount of AP in vitro in 30 minutes at 37 degrees C. A good correlation existed between pulmonary metastatic tumors and the AP values. Serum AP measurements indicated approximate sizes of disseminated and localized tumors, but could not monitor early localized tumors.
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PMID:Monitoring of murine osteosarcoma by serial alkaline phosphatase determinations. 106 57

Electron microscopic study of osteogenic sarcomas has revealed association of the product of the reaction for alkaline phosphatase with membranous structures. The structural and function polymorphism of osteogenic sarcoma cells is also shown.
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PMID:Localization of alkaline phosphatase in subcellular structures of human osteogenic sarcomas. 107 44

A through-knee amputation for suspected osteogenic sarcoma was performed on a patient with Paget's disease of the tibia. Plasma alkaline phosphatase (AP) activity fell to normal values, apparently as a single exponential function of time, with a half-life of 1.7 days. The daily turnover of bone-derived plasma AP was estimated to be approximately 200 I.U. from the Pagetic tibia and 20 I.U. from the rest of the skeleton.
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PMID:An estimate of the turnover rate of bone-derived plasma alkaline phosphatase in Paget's disease. 117 95

The UMR 106-06 rat osteosarcoma osteoblast-like cell line possesses calcitonin (CT) receptors in addition to expressing PTH receptors and a highly osteoblast-like phenotype, and may represent an intermediate developmental stage between early osteoblast precursors and mature osteoblasts. Therefore, we examined the effects of CT and PTH on second messenger generation and osteoblastic function in these cells. In UMR-106-06 cells, 10-1000 nM CT produced a dose-dependent stimulation of intracellular free calcium concentration ([Ca2+]i), which reached a plateau between 2-3 min. This stimulatory effect was abolished in the absence of extracellular Ca2+ ([Ca2+]o) and was mimicked by forskolin and (Bu)2cAMP. One hundred nanomolar CT also produced a slight but significant increase in inositol triphosphate production (13%, P less than 0.05) but did not produce a rapid, transient increase in [Ca2+]i. In contrast, PTH produced a rapid, transient increase in [Ca2+]i, which reached a maximum within 30 sec. This stimulatory effect of PTH on [Ca2+]i signal was dose-dependent and accompanied by a parallel stimulation of inositol triphosphate production. PTH, forskolin, and (Bu)2cAMP all produced a marked dose-related suppression of both DNA and collagen synthesis, which paralleled their stimulatory effects on intracellular cAMP levels. In marked contrast, CT only minimally reduced DNA and collagen synthesis despite producing comparable increases in intracellular cAMP. One hundred nanomolar CT also stimulated alkaline phosphatase specific activity by 33% (P less than 0.05). Thus, CT stimulates cAMP, [Ca2+]i, and inositol phosphate second messengers in UMR 106-06 cells. However, in contrast to other agents which elevate intracellular cAMP levels, CT does not suppress DNA synthesis. These results suggest that the linkage of CT receptor second messengers to effects on cell function differ from those of PTH and/or that CT may produce additional second messenger(s) which antagonize the antiproliferative effect of increased cAMP levels in UMR-106-06 cells.
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PMID:Effects of calcitonin on 3',5'-cyclic adenosine monophosphate and calcium second messenger generation and osteoblast function in UMR 106-06 osteoblast-like cells. 130 38

Injections of parathyroid hormone (PTH) result in increased bone formation in several species. Work in our laboratory and others has shown a stimulation of bone cell proliferation and growth factor production by PTH. Our purpose was to study the effects of PTH on a human bone cell line using TE-85 human osteosarcoma cells as a model. After 24 h treatment, PTH caused an increase in cell proliferation as measured by cell counts and [3H]-thymidine incorporation. Proliferation was not inhibited by an anti-transforming growth factor beta (TGF beta) antibody which could abolish stimulation by exogenous TGF beta. PTH did not stimulate cAMP production, alkaline phosphatase activity or production of insulin-like growth factors I or II (IGF-I or IGF-II) in TE-85 cells. Although basal TE-85 proliferation was slowed by incubation with the calcium channel blocking agent verapamil, PTH still caused an increase in growth rate. We conclude that PTH directly stimulates TE-85 proliferation via a mechanism not involving increased adenylate cyclase activity or increased secretion of IGF-I, IGF-II or TGF beta and may stimulate bone formation in vivo by activating some other mitogenic signal to increase bone cell proliferation.
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PMID:PTH stimulates the proliferation of TE-85 human osteosarcoma cells by a mechanism not involving either increased cAMP or increased secretion of IGF-I, IGF-II or TGF beta. 131 2


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