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)

Uptake of 86Rb was used to follow the activity of Na-K-2Cl cotransport in the osteosarcoma cell line UMR-106-01. The ouabain-resistant fraction of 86Rb uptake was sensitive to bumetanide and furosemide. Furosemide-sensitive 86Rb uptake required the presence of Na+, K+, and Cl- in the incubation medium. These observations indicate the presence of a Na-K-2Cl cotransport system in osteoblasts. Cotransporter activity was stimulated by agonists which increase adenosine 3',5'-cyclic monophosphate (cAMP), cytosolic free Ca2+ ([Ca2+]i), and protein kinase C (PKC) activity such as parathyroid hormone (PTH) and prostaglandin E2 (PGE2). However, endothelin, which increases [Ca2+]i and PKC activity without affecting cellular levels of cAMP, was ineffective in stimulating the cotransporter. Accordingly, increasing cellular cAMP with forskolin was as effective as PTH and PGE2 in stimulating the cotransporter. Stimulation of PKC with TPA inhibited the cotransporter in a time- and concentration-dependent manner. No stimulation of cotransport could be demonstrated at any 12-O-tetradecanoyl-phorbol-13-acetate (TPA) concentration or incubation time. The Na-K-2Cl cotransporter was stimulated by cell shrinkage. Maximal stimulation was observed after swelling the cells in hypotonic medium and subsequent shrinkage in isotonic medium. Stimulation by cell shrinkage can be demonstrated in control, agonist-, cAMP-, and TPA-treated cells. These observations suggest that 1) the osteoblastic Na-K-2Cl cotransporter is activated by calciotropic hormones predominantly through an increase in cellular cAMP, and 2) in osteoblasts, the cotransporter is independently regulated by different biochemical pathways.
Am J Physiol 1991 Sep
PMID:Regulation of Na-K-2Cl cotransport in osteoblasts. 171 50

Determination of cell volume by an electronic cell-sizing technique was used to study the role of ion transporters in cell volume regulation by the osteosarcoma cell line UMR-106-01. Swelling the cells in hypotonic medium was followed by regulatory volume decrease (RVD). The rate of RVD was strongly dependent on the subpassage used and increased with increasing subpassages. Swelling-evoked changes in cytosolic free Ca2+ ([Ca2+]i) did not account for this behavior, since it was similar in cells from all subpassages. Increasing plasma membrane K+ permeability with valinomycin resulted in a similar rate of RVD in cells from different subpassages, suggesting increased K+ channel activity or other electrogenic transporter with increased subpassages. In contrast, the mechanisms responsible for regulatory volume increase (RVI) were fully active in cells from all subpassages. Increasing medium osmolarity of cells bathed in isotonic medium induced slow and incomplete RVI. In addition, shrinking cells exposed to hypotonic medium before completion of RVD resulted in impaired RVI. Effective RVI could be observed only after completion of RVD of cells exposed to hypotonic medium. Removal of extracellular Na+ or K+ completely blocked RVI, whereas removal of external Cl- partially blocked RVI. The effect of K+ removal probably reflects in part inhibition of Na-K-2Cl cotransport and in part inhibition of the Na+ pump.(ABSTRACT TRUNCATED AT 250 WORDS)
Am J Physiol 1991 Sep
PMID:Regulation of cell volume by the osteosarcoma cell line UMR-106-01. 171 51

Our previous studies have shown that insulin-like growth factor-II (IGF-II) is an important autocrine/paracrine regulator of human bone cell proliferation. In this study, we sought to look at the regulation of IGF-II production by human bone cells since IGF-II synthesis is a key variable that regulates the actions of IGF-II at a local site of bone. For studies of IGF-II regulation, we used TE85 human osteosarcoma cells as a model system since these cells exhibited several characteristics which are similar to that of untransformed normal human bone cells. In this study, we investigated the effects of agents which increase intracellular cAMP (forskolin, isobutylmethyl xanthine and prostaglandin E2) and N6,O2' dibutyryl adenosine 3',5'-cyclic monophosphate (DBcAMP) on the IGF-II regulatory system. It was found that these agents caused an increase in the production of an IGFBP in TE85 cells. Subsequent studies on the purification and characterization of IGFBP from DBcAMP treated TE85 cell conditioned medium revealed that the IGFBP produced by TE85 cells in response to DBcAMP treatment was identical to that of 25 kDa inhibitory IGFBP (now designated as IGFBP-4) purified from TE89 human bone cells based on: 1) N-terminal amino acid sequence, 2) amino acid composition, 3) molecular weight and 4) inhibitory actions on basal and IGF-II induced bone cell proliferation. In addition, forskolin and DBcAMP also caused a dose dependent decrease in the production of IGF-II. Consistent with these results, DBcAMP and agents which increase intracellular cAMP inhibited TE85 cell proliferation in a dose dependent manner.(ABSTRACT TRUNCATED AT 250 WORDS)
Growth Regul 1991 Sep
PMID:Evidence that the inhibition of TE85 human bone cell proliferation by agents which stimulate cAMP production may in part be mediated by changes in the IGF-II regulatory system. 172 35

Trains of long-duration "action potentials" were induced by Ba2+ in osteoblast-like rat osteosarcoma cells (ROS 17/2.8), under current clamp and voltage clamp. Large depolarizing pulses were seen in microelectrode measurements at 37 degrees C following the addition of 10 or 20 mM Ba2+ to physiological bathing medium. Application of BAY K 8644 resulted in the onset of the pulses at earlier times and at more negative potentials. The pulses were blocked by nifedipine and Cd2+, but not by Ni2+. Large inward current pulses were seen in whole-cell patch technique voltage-clamp measurements at 37 degrees C in the presence of from 10 to 110 mM Ba2+ in the bathing medium. The current pulses were not seen at 22 degrees C in the presence of 110 mM Ba2+, but could be induced by BAY K 8644. These pulses were not blocked by TTX, but were blocked by nifedipine, Cd2+, Zn2+, Co2+, and by an increase in bathing [Ca2+]. The shape and frequency of the current pulses were the same as for voltage pulses under current clamp. A model that can explain these observations involves opening of L-type Ca2+ channels in a voltage-independent manner by cytosolic Ba2+ via a screening of Ca2+ from sites that produce either inactivation or a lower probability of opening in the activated state. There would be a closing of these channels at higher [Ba2+] as Ba2+ is forced onto these sites. A refractory period is also required to give repeated pulses of openings.
J Membr Biol 1991 Sep
PMID:Ba(2+)-induced action potentials in osteoblastic cells. 174 4

The new concept of retinoma, or retinocytoma, brings up the rare 'spontaneous regressions' long-reported in the literature. Systematic investigation of all relatives of children suffering from retinoblastoma is showing up more and more retinoma cases undetected until now. From 1975 to 1990 the authors have identified 11 retinoma cases amongst 103 retinoblastoma patients and their families. The average age of the retinoma patients is 23 years with a mean follow-up of four years. There are four bilateral cases, one of which with phthisis bulbi, three unilateral retinomas associated with retinoblastoma of the fellow-enucleated eye, and four unilateral cases. Of the 11 retinomas, seven patients have a family history of retinoblastoma. Of the seven patients of procreating age, 16 offspring, three abortions and two miscarriages are noted. Of the 16 offspring, 12 developed retinoblastoma, 11 of which bilaterally. One 21-year-old patient presented in the process of malignant transformation. A child, enucleated for retinoblastoma of one eye and showing lesions conforming to retinoma in the fellow eye at two years of age, suffered an osteosarcoma when nine years old. The authors' data show that retinoblastoma and retinoma follow the same genetic changes and consequently require the same investigation and follow-up. This study indicates a frequency of retinoma of 10% amongst retinoblastoma patients and their families which is higher than that usually quoted.
Ophthalmic Paediatr Genet 1991 Sep
PMID:Retinoma. Case studies. 175 60

Intraarterial plus systemic chemotherapy of cis-diamine dichloroplatinum-II and anthracycline together with preoperative radiation and "limb salvage" treatment have increased the chance of local control and facilitated the previous surgically nonresectable to be resectable. Among 30 cases of osteosarcoma from 1986-1989, aged 9-43 years old, 10 of the 17 cases (58.8%) are still alive with the mean disease free survival of 27.8 months. Late pulmonary metastases cause the need for future protocol for prophylactic lung therapy.
J Med Assoc Thai 1991 Sep
PMID:Multidisciplinary "limb salvage" treatment of osteosarcoma. 179 95

The monoclonal antibody against bone morphogenetic protein (BMP-McAb) was first used for demonstration of bone morphogenetic protein (BMP) in 13 patients with osteosarcoma. Using avidin-biotin complex method (ABC), we demonstrated that BMP mainly existed in the tumor cell cytoplasm and tumorous osteoblast with positive staining in 10 out of 13 osteosarcoma patients. Using this staining method, we can not only differentiate osteosarcoma from fibrosarcoma (all are negative) and other non-osteogenic tumors, but also further classify osteosarcoma according to the BMP content and distribution by means of quantitative histological analysis. The BMP quantity of osteosarcoma with the patients' clinical situation will be useful in clinical diagnosis, treatment and prognosis. The relationship between BMP and the formation of the tumorous bone, and the relation between BMP and the process of osteosarcoma are discussed.
Zhonghua Kou Qiang Yi Xue Za Zhi 1991 Sep
PMID:[A quantitative immunohistochemical analysis of bone morphogenetic protein (BMP) in osteosarcoma of jaw]. 181 58

We have generated three murine monoclonal antibodies to the new human osteosarcoma cell line 4444T. Analysis of their binding patterns to tumor cell lines, normal human tissues, and surgical tumor specimens indicates that the antibodies recognize a subset of human sarcomas and stromal tissues but fail to react with carcinomas or normal human epithelial tissue. These mesenchyme-specific monoclonal antibodies bind to antigens in the extracellular matrix. One antibody is specific in its binding to the muscularis arteriosus. We expect these antibodies to aid in the identification of sarcomas and to extend our knowledge of the components of the extracellular matrix and its interaction with tumors.
Clin Immunol Immunopathol 1991 Sep
PMID:Mesenchymal specificity of three new monoclonal antibodies generated to the osteosarcoma cell line 4444T. 186 19

There is considerable interest in the development of anti-idiotypic antibodies as vaccines in a number of diseases, including cancer. We have developed a human anti-idiotypic monoclonal antibody (105AD7) which binds at or very near to the binding site of mouse antitumor monoclonal antibody 791T/36. The 791T/36 antibody binds to a tumor-associated antigen (gp72) expressed on a number of human tumors, including colorectal and ovarian carcinomas and osteogenic sarcoma. This study shows that, in rats and mice, 105AD7 induces delayed-type hypersensitivity to human tumor cells bearing the gp72 antigen. Local transfer of delayed hypersensitivity was also demonstrated using lymphocytes from mice primed with 105AD7. These findings show that the human monoclonal anti-idiotypic antibody 105AD7 is likely to induce cellular immune responses to tumors in cancer patients.
J Natl Cancer Inst 1991 Sep 04
PMID:Induction of delayed hypersensitivity to human tumor cells with a human monoclonal anti-idiotypic antibody. 187 Jan 51

Plain radiography and magnetic resonance (MR) imaging were used to assess the extent of transphyseal involvement in 15 consecutive patients with long bone osteosarcoma and nonfused epiphyses. The findings were correlated with those from surgical and microscopic pathologic examinations. There were no cases of false-positive findings with either MR imaging or plain radiography. Conventional radiography accurately helped predict transphyseal spread in only nine of 15 cases (60%). Spread to the epiphysis was present in 12 of the 15 cases (80%) and was accurately predicted with MR imaging in all 12 cases. This finding contradicts the common misconception that the physis acts as a "barrier" to tumor spread.
Radiology 1991 Sep
PMID:Epiphyseal involvement in osteosarcoma. 187 Dec 99


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