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)

Monoclonal antibody 791T/36 directed against surface antigen on the human osteosarcoma cell line and cross-reacting with surface antigen p72 presenting on human PHA-stimulated T-lymphoblasts was used in analysis of p72 antigen expression on human mononuclear peripheral blood cells, between 2-4 days of culture. Using FACS-IV system and fluorescence microscope, it was shown that expression of p72-antigen is dependent on PHA-stimulation and the ability of lymphocytes proliferation. The expression of p72 preceding the entry of the cells into the cell cycle. This is not significantly dependent of cell size, stage of the cycle, and RNA-transcription activity. In PHA-stimulated cultures, between 2-4 days, the number of lymphoblasts expressing enough receptors for 791T/36 monoclonal antibody is sufficient to exhibit a distinct effect of Ricin A-chain conjugated with 791T/36 over 50% inhibition of 3H-Thymidine incorporation into the cells. These observations emphasises the importance of cross-reactions in cases using immunotoxins.
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PMID:[Study of expression of surface antigen p72 using monoclonal antibody 79IT/36 and the effect of ricin A chain-bound 79IT/36 on phytohemagglutinin-stimulated human lymphocytes]. 261 66

The study of bone cancer has been difficult in part due to a lack of appropriate in vitro osteosarcoma model systems. The development of such systems is essential if a clearer understanding of the biology of and mechanisms behind the formation and progression of bone cancers is to be obtained. We report here the development of an in vitro model system which demonstrates important characteristics generally associated with osteosarcoma. The chick periosteal osteogenesis model was infected with the Fujinami Sarcoma Virus (FSV) containing the v-fps oncogene which encodes for a P140gag-fps protein-tyrosine kinase. Under the appropriate conditions FSV infected cultures developed bone and cartilaginous tissues which showed histopathological findings consistent with osteosarcoma. Biochemical data indicating massive increases in alkaline phosphatase activity, protein content, 3H-Thymidine incorporation as well as expression of active P140gag-fps confirm that transformation has occurred in FSV infected cultures. This novel in vitro model system should prove most useful in the study of bone cancer.
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PMID:In vitro transformation of osteoblasts: putative formation of osteosarcoma in vitro. 282 12

Monoclonal antibody 791T/36, directed against surface antigen on the human osteosarcoma cell line (791T), and cross-reacting with surface antigen p72 expressed on activated (PHA, MLR) human peripheral blood mononuclear cells (PBM), was used in analysis of p72 antigen in vitro. Using FACS-IV system and fluorescence microscope, it was shown that expression of p72 antigen on PBM cells is dependent on phytohaemagglutinin (PHA) stimulation, and alloantigens in mixed lymphocyte reaction (MLR). The increase of p72 expression is always connected with lymphocytes proliferation activity (FACS-IV analysis and 3H-Thymidine incorporation assay). The expression of p72 is not significantly dependent on cell size, and stage of the cell in the cell cycle. A suggestion, that p72 is a one of so-called "proliferation antigens" is discussed. Present study emphasizes a problem of cross-reactivity in the context of possible errors in diagnosis and therapy, when a monoclonal antibody cross-reacts with cells other than intendent target cells.
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PMID:Cross-reaction of 791T/36 monoclonal antibody with immunological activated human peripheral blood mononuclear cells. 326 80

[3H]Thymidine (TdR) incorporation by human osteosarcoma cell line MG-63 was significantly stimulated at as early as 3 h after the addition of either TIMP-1 or TIMP-2 alone. Maximum stimulation was attained at a concentration of either 20 ng/ml (0.71 nM) TIMP-1 or 1.0 ng/ml (46 pM) TIMP-2. Tyrosine kinase inhibitors such as genistein, erbstatin, and herbimycin A almost completely inhibited the [3H]TdR incorporation stimulated by either of the TIMPs. However, essentially no effect was observed with H-89, H-7, bisindolylmaleimide and K-252a. These inhibition studies suggest a crucial role for tyrosine kinase in the signal transduction of TIMPs. Phosphotyrosine-containing proteins were significantly elevated by the treatment with both TIMPs. We also found that either TIMP stimulated an increase in mitogen-activated protein (MAP) kinase activity, suggesting that MAP kinase plays a role in TIMP-dependent growth signaling.
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PMID:Tyrosine phosphorylation is crucial for growth signaling by tissue inhibitors of metalloproteinases (TIMP-1 and TIMP-2). 890 76

We compared the separate effects of 1alpha,25-dihydroxyvitamin D3 (1alpha,25(OH)2D3) and its analog, 1alpha,25-dihydroxy-16ene,23yne-vitamin D3 (1alpha25(OH)2-16ene,23yne-D3), as well as their interactions with 17-beta estradiol (E2) in our human osteosarcoma SaOS-2 cell models representing two stages of differentiation, the SaOS+DEX and SaOS-DEX cells. SaOS+DEX cells have been previously shown to express higher PTH-stimulated adenylate cyclase (PTH-AC) and basal alkaline phosphatase (ALP) activities compared with SaOS-DEX cells. ALP: In SaOS+DEX cells, 0.1 nmol/L analog, but not 1alpha,25(OH)2D3, increased ALP activity 1.7-fold (p < 0.05). Instead, 1 nmol/L 1alpha,25(OH)2D3 increased ALP 1.4-fold (p < 0.05). In these cells, E2 enhanced 1alpha,25(OH)2D3-stimulated ALP activity (ANOVA, F = 51.22, p <0.0001), while inhibiting the effect of the analog. [3H]-Thymidine uptake: In SaOS+DEX cells, 1alpha,25(OH)2D3 had biphasic effects (ANOVA, F = 13.08, p < 0.0001), which were not altered by E2. In contrast, the analog was stimulatory only with E2 (ANOVA, F = 3.59, p < 0.025). Osteocalcin (OC): 1alpha,25(OH)2D3 and its analog stimulated OC production in SaOS-DEX cells with smaller effects in SaOS+DEX cells. In SaOS-DEX cells, E2 enhanced the effect of 1alpha,25(OH)2D3, but not that of the analog. PTH-AC: In SaOS-DEX cells, 100 nmol/L analog inhibited PTH-AC activities by 50% (p < 0.01), whereas 1alpha,25(OH)2D3 had little effect. In SaOS+DEX cells, both compounds inhibited PTH-AC approximately 35%. E2 inhibited the effect of the analog in SaOS-DEX cells, but enhanced the effects of both compounds in SaOS+DEX cells. These results show that the analog 1alpha,25(OH)2-16ene,23yne-D3 was effective in regulating osteoblastic function; its effects were modulated by E2 and dependent upon the stage of osteoblast differentiation.
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PMID:Effects of 1alpha,25-dihydroxy-16ene, 23yne-vitamin D3 on osteoblastic function in human osteosarcoma SaOS-2 cells: differentiation-stage dependence and modulation by 17-beta estradiol. 896 29

We have studied the effects of low-energy, low-frequency pulsed electromagnetic fields (PEMF) on cell proliferation, in both human osteoblast-like cells obtained from bone specimens and in human MG-63 osteosarcoma cell line. Assessment of osteoblastic phenotype was performed both by immunolabeling with antiosteonectin antibody and by verifying the presence of parathyroid hormone receptors. The cells were placed in multiwell plates and set in a tissue culture incubator between a pair of Helmholtz coils powered by a pulse generator (1.3 ms, 75 Hz) for different periods of time. [3H]Thymidine incorporation was used to evaluate cell proliferation. Since it had previously been observed that the osteoblast proliferative response to PEMF exposure may also be conditioned by the presence of serum in the medium, experiments were carried out at different serum concentrations. [3H]Thymidine incorporation increases in osteoblast-like cells, when they are exposed to PEMF in the presence of 10% fetal calf serum (FCS). The greatest effect is observed after 24 hours of PEMF exposure. No effects on cell proliferation are observed when osteoblast-like cells are exposed to PEMF in the presence of 0.5% FCS or in a serum-free medium. On the other hand, PEMF-exposed MG-63 cells show increased cell proliferation either at 10% FCS, 0.5% FCS and in serum-free medium. Nevertheless, the maximum effect of PEMF exposure on MG-63 cell proliferation depends on the percentage of FCS in the medium. The higher the FCS concentration, the faster the proliferative response to PEMF exposure. Our results show that, although MG-63 cells display some similarity with human bone cells, their responses to PEMF's exposure are quite different from that observed in normal human bone cells.
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PMID:Responses of human MG-63 osteosarcoma cell line and human osteoblast-like cells to pulsed electromagnetic fields. 938 42

We have exposed cultured bone cells to a pulsed electromagnetic field (PEMF) for different times to find the minimal exposure time necessary to stimulate an increase of DNA synthesis. We used two different human osteosarcoma cell lines, TE-85 and MG-63, and human normal osteoblast cell (NHOC) obtained from surgical bone specimens. The cells were placed in multiwell plates and set in a tissue culture incubator between a pair of Helmoltz coils powered by a pulse generator (1.3-ms pulse, repeated at 75 Hz) for different periods of time. [3H]Thymidine incorporation was used to evaluate cell proliferation. The two osteosarcoma cell lines increase their thymidine incorporation when exposed to a PEMF for at least 30 min, both in a medium containing 10% fetal calf serum and in a serum-free medium. NHOC are known to increase their cell proliferation when exposed to PEMF but only if cultured in the presence of 10% fetal calf serum. In this experimental condition, three of the four cell lineages studied required at least 9 h of PEMF exposure to increase their DNA synthesis, whereas one cell lineage increased its cell proliferation after 6 h of PEMF exposure. Our observations confirm the hypothesis that the proliferative responses of NHOC and human osteosarcoma cell lines to PEMF exposure are quite different. Moreover, NHOC required minimal exposure times to PEMF to increase their cell proliferation, similar to that needed to stimulate bone formation in vivo.
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PMID:Correlation between pulsed electromagnetic fields exposure time and cell proliferation increase in human osteosarcoma cell lines and human normal osteoblast cells in vitro. 1019 60

Expression of Fas (CD95, APO-1), a cell surface receptor capable of inducing ligand-mediated apoptosis, is involved in tissue homeostasis and elimination of targeted cells by natural killer and T cells. Corruption of this pathway, such as reduced Fas expression, can allow tumor cells to escape elimination and promote metastatic potential. In this study, the status of Fas expression has been examined in the parental SAOS human osteosarcoma cells that do not metastasize and in selected variants that cause lung metastases in 16 weeks (LM2) or 8 weeks (LM6) after i.v. injection into nude mice. Fas expression correlated with the metastatic potentials of the three cell lines. Northern and fluorescence-activated cell-sorting analyses indicated that LM6 cells expressed Fas at a lower level than seen in the parental cells. Infection of the LM6 cells with an adenoviral vector containing the murine interleukin (IL)-12 gene (AD:mIL-12) or treatment with recombinant murine IL-12 resulted in a dose-dependent up-regulation of FAS: The up-regulation of Fas by IL-12 was also demonstrated in human etoposide-resistant MDA-MB-231 breast cancer cells. [(3)H]Thymidine growth inhibition studies indicated that the cell surface Fas induced after IL-12 exposure was functional and able to mediate cell death on cross-linking with anti-FAS: We also demonstrate that this effect is independent of IFN-gamma. Whereas these cell lines are sensitive to IFN-gamma, incubation with IFN-gamma does not increase susceptibility to Fas-mediated cell death, nor do these cells produce IFN-gamma with or without IL-12 treatment. We hypothesize that expression of Fas may play a role in the elimination of metastatic tumor cells in the lung, an organ in which Fas ligand is expressed. The antitumor activity of IL-12 may be secondary in part to its ability to up-regulate Fas expression on tumor cells, which subsequently increases immune-mediated destruction of osteosarcoma cells.
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PMID:Interleukin (IL)-12 and IL-12 gene transfer up-regulate Fas expression in human osteosarcoma and breast cancer cells. 1135 27