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)

Pentavalent 99Tcm-dimercaptosuccinic acid (99Tcm-(V)DMSA) has established uses in the detection and diagnosis of medullary thyroid carcinoma, osteosarcoma, amyloidosis and many soft tissue tumours, but is not readily available as a commercial kit. We have evaluated published methods for preparation of 99Tcm-(V)DMSA that are based on the modification of 99Tcm-(III)DMSA commercial kits. The criteria for assessment were achievement of satisfactory radiochemical purity and practical considerations regarding the ease of synthesis. Quantification of the desired product's activity was achieved via thin-layer chromatography (silica gel) with an n-butanol:acetic acid:water solvent system. The developed plates were imaged on a gamma camera and analysed using standard software. The methods investigated were designated as Birmingham, Cambridge and Canterbury: the latter two were very similar. With experience, the methods eventually produced similar radiochemical purities of > 90%. However, the Birmingham method was found to be more satisfactory in terms of its reliability and simplicity of synthesis.
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PMID:A critical evaluation of methods for preparing pentavalent 99Tcm-DMSA. 1045 86

Although quantitative measurement of skeletal alkaline phosphatase (sALP) activity in serum can provide an index of the rate of bone formation, the metabolic process that determines the release of sALP - from the surface of osteoblasts, into circulation-is unknown. The current studies were intended to examine the hypothesis that the release of sALP from human osteoblasts is a consequence of apoptotic cell death. We measured the release of sALP activity from human osteosarcoma (SaOS-2) cells and normal human bone cells, under basal conditions and in response to agents that increased apoptosis (TNF-a, okadiac acid) and agents that inhibit apoptosis (IGF-I, calpain, and caspase inhibitors). Apoptosis was determined by the presence of nucleosomes (histone-associated DNA) in the cytoplasm of the cells by using a commercial kit. The results of these studies showed that TNF-a and okadiac acid caused dose- and time-dependent increases in apoptosis in the SaOS-2 cells (r = 0.78 for doses of TNF-a and r = 0.93 for doses of okadiac acid, P <0.005 for each), with associated decreases in cell layer protein (P <0.05 for each) and concomitant increases in the release of sALP activity (e.g., r = 0.89 for TNF-a and r = 0.75 for okadiac acid, P <0.001 for each). In contrast, caspase and calpain inhibitors reduced apoptosis, increased cell layer protein, and decreased the release of sALP activity (P <0.05 for each). Exposure to IGF-I also decreased apoptosis, in a time- and dose-dependent manner (e.g., r = 0.93, P <0.001 for IGF-I doses), with associated proportional effects to increase cell layer protein (P <0.001) and decrease the release of sALP activity (P <0.001). IGF-I also inhibited the actions of TNF-a and okadiac acid to increase apoptosis and sALP release. The associations between apoptosis and sALP release were not unique to osteosarcoma (i.e., SaOS-2) cells, but also seen with osteoblast-line cells derived from normal human bone. Together, these data demonstrate that the release of sALP activity from human osteoblast-line cells in vitro is associated with, and may be a consequence of, apoptotic cell death. These findings are consistent with the general hypothesis that the appearance of sALP activity in serum may reflect the turnover of osteoblast-line cells.
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PMID:Apoptosis may determine the release of skeletal alkaline phosphatase activity from human osteoblast-line cells. 1203 23

Oxytocin receptors have recently been demonstrated in human osteoblast-like (hOB) cells. In this study, oxytocin 100-1000 pmol/l increased cell proliferation of primary cultures of hOB cells, measured by [3H]thymidine incorporation, (P<0.01). In human osteosarcoma cell-line (SaOS-2), oxytocin 100 pmol/l increased cell proliferation (measured by [3H]thymidine incorporation and a commercially available kit) and protein synthesis ([3H]proline incorporation) (P<0.05). The increase in cell proliferation was abolished when SaOS-2 cells were incubated with an oxytocin antagonist and oxytocin. Oxytocin 100 pmol/l decreased interleukin-6 (IL-6) production of the hOB cells (23.4+/-1.96 versus 33.4+/-2.65 pg/well; P<0.001). These findings indicate that oxytocin may affect bone metabolism in humans.
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PMID:Oxytocin stimulates proliferation of human osteoblast-like cells. 1212 40

The present study was conducted to determine the effect of the inflammatory mediator interleukin 1alpha (IL-1alpha) on osteogenesis using rat osteoblasts. We examined the effect of IL-1alpha on cell proliferation, alkaline phosphatase (ALPase) activity, mineralized nodule formation, and the expression of extracellular matrix proteins in rat osteosarcoma cell lines. The cells were cultured with alpha-minimum essential medium containing 10% fetal bovine serum with and without 0, 1, 10, and 100 units/ml of IL-1alpha for up to 14 days. The mineralized nodule formation was examined by alizarin red staining, and the calcium content in mineralized nodules was determined using a Calcium C-Test kit. The expression of extracellular matrix proteins was estimated by determining levels of mRNAs using the semiquantitative reverse transcription-polymerase chain reaction. The mineralized nodule formation and the calcium content in mineralized nodules were remarkably suppressed by IL-1alpha after 5 days of culture. The ALPase activity decreased in a dose-dependent manner in the presence of IL-1alpha after 7 days of culture. The expression of type I collagen was decreased after 3 days of culture with IL-1alpha. The expression of bone sialoprotein was slightly decreased at days 3 and 5, and the expression of osteopontin was increased at days 3, 5, and 7 of culture with IL-1alpha. These results suggest that IL-1alpha suppresses osteogenesis through a decrease in ALPase and type I collagen production by osteoblasts.
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PMID:IL-1alpha affects mineralized nodule formation by rat osteoblasts. 1535 Aug 29

Several in vitro and in vivo studies have indicated that tobacco smoking may be an important risk factor for the development and severity of inflammatory periodontal disease. In the present study, we examined the effect of nicotine on cell proliferation, alkaline phosphatase (ALPase) activity, mineralized nodule formation, and the expression of extracellular matrix proteins in the human osteosarcoma cell line Saos-2. The cells were cultured with Dulbecco's modified Eagle medium containing 10% fetal bovine serum with 0, 10(-4) M, and 10(-3) M nicotine for up to 14 days. Mineralized nodule formation was examined by alizarin red staining, and the calcium content in mineralized nodules was determined using a calcium E-test kit. The expression of extracellular matrix proteins was estimated by determining the levels of their mRNAs using the real-time polymerase chain reaction. Mineralized nodule formation and calcium content in mineralized nodules were remarkably suppressed by nicotine on days 10 and 14 of culture, respectively. ALPase activity as well as type I collagen and osteopontin expression also decreased in the presence of nicotine after 5, 10, and 14 days of culture, respectively. By contrast, the amount of bone sialoprotein increased during 14 days of culture with nicotine. These results suggest that nicotine suppresses osteogenesis through a decrease in ALPase and type I collagen production by osteoblasts.
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PMID:Nicotine affects mineralized nodule formation by the human osteosarcoma cell line Saos-2. 1594 96

Cyclooxygenase (COX) inhibitors, already widely used to reduce fever, inflammation and pain, are under increasing consideration as potential agents for the prevention and treatment of neoplasia. As COX-2 was detected in human and canine osteosarcomas, we have evaluated the effect of the preferential COX-2 inhibitor meloxicam on an established D-17 canine osteosarcoma cell line, which expressed, as well as COX-1 and COX-2 also COX-3 (as demonstrated by Western blot). An XTT proliferation kit was used to assess surviving cells after drug treatment. At low concentrations (1, 2, 4 and 10 microm) meloxicam caused an increase in cell numbers while a marked anti-proliferative effect was observed at higher concentrations (100, 200 microm) after 3 days and also 3 weeks of incubation. The chemotherapeutic drug doxorubicin showed a cytotoxic effect at all concentrations (60-1920 nm). Exposure of tumour cells to combinations of meloxicam and doxorubicin revealed synergistic effects (with 240 nm doxorubicin), as well as sub-additive and antagonistic results, especially if combined with concentrations of meloxicam typically found in serum. Care should be taken in concluding, on the basis of one in vitro study, that meloxicam does not have a role in the treatment of canine osteosarcomas given that the results from in vivo studies may differ.
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PMID:In vitro effects of meloxicam with or without doxorubicin on canine osteosarcoma cells. 1642 Feb 97

Oxytocin stimulates proliferation of human osteoblast-like (hOB) cells and human osteosarcoma cells (SaOS-2). In contrast, oxytocin has also been shown to inhibit proliferation of other cell lines such as breast cancer cells. The aim of the present study was to investigate the effects of different concentrations of oxytocin on cell proliferation in osteosarcoma cell lines of different stages of differentiation: SaOS-2, TE-85, and UMR-106. For this purpose cells were incubated with oxytocin (1-1000 pmol/l). Cell proliferation was measured by [(3)H]thymidine incorporation and a commercially available kit (EZ4U). Incubation with oxytocin during 24 h increased proliferation of SaOS-2 cells significantly (100 pmol/l: p<0.01). In contrast, 24 h of incubation with oxytocin decreased proliferation of TE-85 (100 pmol/l: p<0.01) and UMR-106 cells significantly (100 pmol/l: p<0.01). The effects of oxytocin in SaOS-2 and TE-85, but not in UMR-106 cells, were abolished when the cells were incubated with both oxytocin and an oxytocin antagonist (1-deamino-2-D-Tyr-(Oet)-4-Thr-8-Orn-oxytocin). Instead incubation with the oxytocin antagonist alone decreased proliferation of UMR-106 cells significantly (p<0.001). Thus oxytocin has the capacity to both stimulate and inhibit cell proliferation of osteosarcoma cells. This effect might be dependent on the stage of differentiation of the cancer cells.
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PMID:Opposite effects of oxytocin on proliferation of osteosarcoma cell lines. 1838 94

Canine osteosarcoma, an aggressive cancer with early distant metastasis, shows still despite good chemotherapy protocols poor long term survival. The aim of our study was to determine whether sorafenib, a novel multikinase inhibitor, has any effect on D-17 canine osteosarcoma cells. A cell proliferation kit was used for detecting surviving cells after treatment for 72 h with sorafenib or carboplatin or their combination. A significant decrease of neoplastic cells was observed after incubation with 0.5-16 microM sorafenib or with 80-640 microM carboplatin. Using immunocytochemistry for activated caspase 3 to evaluate apoptosis, we found significantly more positive cells in the sorafenib treated groups. Paradoxically, expression of the nuclear proliferation marker Ki-67 was also significantly higher in sorafenib treated cells. The drug sorafenib showed potent antitumour activity against D-17 canine osteosarcoma cells in vitro, suggesting a potential as a therapeutic tool in the treatment of bone cancer in dogs.
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PMID:The tyrosine kinase inhibitor sorafenib decreases cell number and induces apoptosis in a canine osteosarcoma cell line. 1966 56

Three different cell lines (murine macrophages, HeLa and osteosarcoma cells) were assayed in order to check for the manifestation of the cytopathic effects of three strains of Acanthamoeba recently isolated in our laboratory from contact lens cases: CLC-16, CLC-41.r and CLC-51-l. Adhesion and cytotoxicity assays were carried out with these strains and the type strain Acanthamoeba castellanii Neff as a control. Briefly, the ability of these amoebae to bind to the three cell lines was calculated and supernatants were examined for cytotoxicity by measuring lactate dehydrogenase released as an estimate of cytotoxicity using a commercial detection kit. The three strains showed high adhesion and cytotoxicity levels when tested in the three cell lines. This study demonstrates the ability of these amoebae to degrade any of the tested cell lines. To the best of our knowledge, this is the first report of the in vitro effects of acanthamoebae on osteosarcoma cells.
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PMID:Acanthamoeba spp.: in vitro effects of clinical isolates on murine macrophages, osteosarcoma and HeLa cells. 1985 90

This study is aimed at investigating the effect of arsenic trioxide (ATO) on p53 null human osteosarcoma MG63 cells and the mechanisms underlying the effect. Apoptotic cells were detected by flow cytometry with Annexin-V-FITC/PI dual staining. Intracellular ROS was measured by flow cytometry using a cell-based ROS assay kit. Catalase activity and mRNAs were analyzed by ELISA and real-time qRT-PCR, respectively. Apoptosis and intracellular ROS of MG63 cells increased in a dose-dependent manner following arsenic treatments. Both were prevented by the presence of the anti-oxidative reagent N-acetyl-L: -cysteine (NAC) or catalase (CAT). Furthermore, the activity and mRNA of catalase were decreased strikingly following arsenic exposure. The present study indicates that p53 null osteosarcoma MG63 cells are susceptible to the ATO; the inhibition of catalase and the resulted intracellular ROS accumulation are an important molecular mechanism under which ATO induces apoptosis of p53-deficient osteosarcoma cells.
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PMID:Arsenic trioxide induces apoptosis of p53 null osteosarcoma MG63 cells through the inhibition of catalase. 2130 89


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