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)

Differences in antigenicity between the human osteosarcoma cell line TE 85/B and its feline sarcoma virus-infected subline NIH E1041 were detected by competitive inhibition of natural cell-mediated cytotoxicity (NCMC). Whether the differences could be attributed to the viral infection was investigated by absorption and elution studies of antibodies that determine the specificity of NCMC against the cell lines. Antibodies from the serum of healthy individuals were first absorbed onto target cells against which they were to be tested and then eluted to provide antibodies putatively specific for the target cells. Trypsin-treated effector cells were restored with the absorbed serum or eluted antibodies and tested against TE 85/B and its intentionally infected sublines. The differences observed previously between TE 85/B and NIH E1041 were extended to the detection of small differences in antigenicity among all sublines. Separately maintained sublines from the same culture became antigenically different with continuous passage. The causes for these specific changes were unknown, but a role for the control of these antigens by NCMC was suggested. Differences in antigenicity between virus-infected sublines cultured separately need not be related to the virus infection.
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PMID:Search for specificity in natural cell-mediated cytotoxicity. 9 84

The tumor line CAC-8, is a serially transplantable adenocarcinoma maintained in nude mice which originated from a hypercalcemic dog. Nude mice with CAC-8 developed a syndrome of humoral hypercalcemia of malignancy. CAC-8 contained a protein factor which stimulated adenylate cyclase of bone and kidney cells in vitro. The adenylate cyclase (AC) of rat osteosarcoma cell lines, ROS 17/2.8 (ROS) and UMR-106, was stimulated by the tumor extract and potentiated by forskolin (0.1 microM). The ROS cells responded to the lowest concentration of CAC-8 extract, but UMR cells responded with a greater increase in AC activity compared to controls following exposure to CAC-8 extract. Pretreatment of ROS 17/2.8 cells with dexamethasone enhanced the response to CAC-8 extract. The opossum kidney cell line (OK) was less sensitive to the AC-stimulating activity of CAC-8 extract, but AC stimulation was increased in the presence of forskolin. Bovine (1-34) parathyroid hormone (BPTH) (10 nM) stimulated AC equally in ROS, UMR, and OK cells. Isoproterenol (1.0 microM) stimulated AC activity in ROS and UMR cells but not in OK cells. The AC-stimulating activity of CAC-8 appeared to bind to the parathyroid hormone receptor of ROS, UMR, and OK cells since addition of the parathyroid hormone receptor antagonist, [8,18norleucine, 34tyrosine]BPTH (3-34) amide, inhibited CAC-8-mediated cyclic adenosine 5'-monophosphate production and alone did not stimulate AC activity. The AC-stimulating activity of CAC-8 was acid and heat stable. Trypsin digestion reduced BPTH and CAC-8 stimulation of AC to near basal levels and treatment of CAC-8 extract with dithiothreitol reduced AC stimulation in UMR cells by approximately 50%. Extracts of the hypercalcemic tumor line (CAC-8) contained bone and kidney AC-stimulating activity which was enhanced by forskolin and dexamethasone, inhibited by [8,18Nle, 34Tyr]BPTH (3-34) amide, heat stable, trypsin sensitive, inactivated by reduction, and had a relative molecular weight of 34,000 by gel exclusion chromatography. Isolation and characterization of the factor(s) produced by CAC-8 that stimulate AC activity will be useful in further understanding the pathogenesis of humoral hypercalemia of malignancy in animal and human patients.
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PMID:Bone and kidney adenylate cyclase-stimulating activity produced by a hypercalcemic canine adenocarcinoma line (CAC-8) maintained in nude mice. 346 38