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prostaglandin/sarcoma
L'enllaç es desa al porta-retalls
Pàgina 1 des de 159 resultats
Some effects of the essential fatty acids linoleic acid and alpha-linolenic acid and of their metabolites gamma-linolenic acid, arachidonic acid, eicosapentaenoic acid, docosahexaenoic acid, and of prostaglandins A1 and E1 on the proliferation of human osteogenic sarcoma cells in culture.
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Gamma-linolenic acid has been shown to suppress the rate of proliferation of a number of malignant cell lines in culture. To test the proposal that this was a specific prostaglandin 1- or 2-series effect, 379 batches of MG63 human osteogenic sarcoma cells were seeded in Greiner flasks and cultured
Beta-adrenergic agonist- and prostaglandin-mediated regulation of cAMP levels in Ewing's sarcoma cells in culture.
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This is the first report demonstrating hormonal control of cAMP levels in Ewing's sarcoma cells. Two classes of hormones, beta-adrenergic agonists and prostaglandins stimulate cAMP production in cultured Ewing's sarcoma cells. The efficacy order for beta-adrenergic agonists is (-)-isoprenaline
Rat osteogenic sarcoma cells: modulation of hormone stimulated cyclic AMP production by prostaglandin antagonists and biosynthesis inhibitors.
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1. The effects of several anti-prostaglandin drugs on parathyroid hormone (PTH) and prostaglandin E2 (PGE2) stimulated cyclic AMP production in freshly isolated rat osteogenic sarcoma cells have been studied. 2. PG biosynthesis inhibitors (aspirin and indomethacin) did not inhibit the effect of PTH
Increased prostaglandin E2 and cAMP phosphodiesterase levels in Kaposi's sarcoma--a virus against host defense mechanism.
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In Kaposi's sarcoma tissue, prostaglandin E2 (PgE2) levels and cAMP phosphodiesterase levels were found to be higher than in surrounding normal tissue. We have shown earlier that PgE2 suppresses interferon (IFN) alpha production. High levels of cAMP phosphodiesterases result in low cAMP levels.
Prostaglandin E2 content of regressing and progressing Moloney sarcomas.
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Regressing mouse Moloney sarcomas contain macrophages that are activated for tumor cell killing, while those found in progressively growing sarcomas either cannot kill or do so very poorly. Prostaglandin E2 (PGE2) has been shown to down-regulate macrophage activation in vitro. The study described
Regulation of creatine kinase activity in rat osteogenic sarcoma cell clones by parathyroid hormone, prostaglandin E2, and vitamin D metabolites.
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We have previously shown that both parathyroid hormone (PTH) and prostaglandin E2 (PGE2) stimulate the activity of creatine kinase BB (CKBB) in rat bone cells in culture. Therefore, morphologically distinct rat osteogenic sarcoma cells in culture were tested for stimulation of CKBB activity by
[The relationship between the prostaglandin E level in the tumor and the times of the metastasis of primary osteogenic sarcoma].
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Radioimmunoassay was used in 46 cases of osteogenic sarcoma to assess prostaglandin E (PgE) levels in tumor tissue. Those levels were found to vary with age. A correlation was established between the effect of preoperative chemoradiation treatment, on the one hand, and degree of treatment-induced
[Prostaglandins of series E in morphologic variants of osteogenic sarcoma and evaluation of the degree of therapeutic pathomorphism of the tumor].
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The content of prostaglandins E (PGE) is studied in osteogenic sarcomas from 191 patients. The level of PGE after a neo-adjuvant therapy of osteogenic sarcoma depends upon the individual susceptibility to the drug. Inverse correlation is found between the PGE content in the tumor and the degree of
[The secretion of type-E prostaglandins and the sensitivity to hydrogen peroxide of Syrian hamster clone cells transformed by the Rous sarcoma virus].
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Seven clonal sublines of the strain of syrian hamster embryo cells transformed in vitro by the Rous sarcoma virus were obtained. All clones possessed both high resistance to damage by hydrogen peroxide and a capacity to release E-type prostaglandins in response to contact with NK-cells in vitro. The
Prostaglandin synthesis inhibition: effect on bone changes and sarcoma tumor induction in balb/c mice.
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An increase in prostaglandins (PGs) of the E series has been demonstrated in Moloney sarcoma virus (MSV)-induced leg tumors of 6-week-old BALB/c male mice. The level of the hormone has been shown to increase with the tumor diameter and decrease with tumor regression. At the peak of tumor size the
Piracy of prostaglandin E2/EP receptor-mediated signaling by Kaposi's sarcoma-associated herpes virus (HHV-8) for latency gene expression: strategy of a successful pathogen.
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Kaposi's sarcoma-associated herpes virus (KSHV) is implicated in the pathogenesis of KS, a chronic inflammation-associated malignancy. Cyclooxygenase-2 (COX-2) and its metabolite prostaglandin E2 (PGE2), two pivotal proinflammatory/oncogeneic molecules, are proposed to play roles in the expression
Membranes from a transplantable osteogenic sarcoma responsive to parathyroid hormone and prostaglandins: regulation of adenylate cyclase and of hormone metabolism.
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Adenylate cyclase activity in particulate fractions from a transplantable rat osteogenic sarcoma was stimulated in a dose-dependent manner by prostaglandins E1 and E2 (PGE1 and PGE2) and parathyroid hormone (PTH). Prostaglandin F2alpha was active at a high concentration (3 x 10(-4) mol/l).
Cytotoxic effects of 15-deoxy-Δ12,14-prostaglandin J2 alone and in combination with dasatinib against uterine sarcoma in vitro.
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Effective chemotherapeutic strategies for uterine sarcoma are lacking; existing therapies achieve poor response rates. Previous studies have identified the prostaglandin 15-deoxy-Δ12,14-prostaglandin J2 (15d-PGJ2) as a potential anticancer treatment; however, its effectiveness in uterine sarcoma has
Cyclooxygenase-2-prostaglandin E2-eicosanoid receptor inflammatory axis: a key player in Kaposi's sarcoma-associated herpes virus associated malignancies.
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The role of cyclooxygenase-2 (COX-2), its lipid metabolite prostaglandin E2 (PGE2), and Eicosanoid (EP) receptors (EP; 1-4) underlying the proinflammatory mechanistic aspects of Burkitt's lymphoma, nasopharyngeal carcinoma, cervical cancer, prostate cancer, colon cancer, and Kaposi's sarcoma (KS) is
Rat osteogenic sarcoma cells:effects of some prostaglandins, their metabolites and analogues on cyclic AMP production.
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Cyclic AMP production by freshly isolated cells, from a 32P-induced transplantable rat osteogenic sarcoma, was stimulated by PGE1, PGE2 and to a less extent by PGF2alpha and PGA2. In the case of PGE2, the cyclic AMP content of cells was maximal within 5 min. The 13,14-dihydroderivatives of PGE1,
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