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prostaglandin/kanker
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Expression of prostaglandin G/H synthase-1 and -2 protein in human colon cancer.
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Prostaglandin G/H synthase (PGHS), a key enzyme leading to the formation of prostaglandins, is the target of nonsteroidal antiinflammatory drugs. Two forms of the enzyme have been identified, PGHS-1 and PGHS-2. Epidemiological evidence has suggested that aspirin and other nonsteroidal
The Role of Prostaglandin-Endoperoxide Synthase-2 in Chemoresistance of Non-Small Cell Lung Cancer.
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The prostaglandin-endoperoxide synthase-2 (PTGS2) plays essential roles in diverse pathological process. Although recent studies implied that PTGS2 was closely related with chemoresistance, the precise roles and the underlying mechanisms of PTGS2 in the developing process of chemoresistance in
Cyclooxygenase-2/prostaglandin E2 pathway mediates icariside II induced apoptosis in human PC-3 prostate cancer cells.
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Icariside II (IS) isolated from the roots of Epimedium koreanum Nakai was known to have antioxidant activity and inhibit melanogenesis and hypoxia inducible factor. We report here for the first time that IS induces apoptosis through its anti-inflammatory effects in PC-3 prostate cancer cells. IS
Isolation of saponins with the inhibitory effect on nitric oxide, prostaglandin E2 and tumor necrosis factor-alpha production from Pleurospermum kamtschaticum.
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As an attempt to search for bioactive natural products exerting antiinflammatory activity, we have isolated two saponins were isolated from the aerial portion of Pleurospermum kamtschaticum (Umbelliferae) by nitrite assay activity-directed chromatographic fractionation. They were identified as
Stimulation or endothelin-1 secretion by human breast cancer cells through protein kinase A activation: a possible novel paracrine loop involving breast fibroblast-derived prostaglandin E2.
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Breast cancer cells secrete endothelin-1 (ET-1), which may act as a paracrine mitogen in breast tumours. The paracrine factors and signal transduction pathways responsible for regulating ET-1 production in breast cancer are unknown. In this study we have examined the involvement of the protein
Microsomal prostaglandin E2 synthase-1 in breast cancer: a potential target for therapy.
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The anti-tumour actions of cyclooxygenases (COX) are thought to be mediated by inhibition of prostaglandin E(2) (PGE(2)) synthesis. However, COX-2 inhibition also alters cellular production of other prostaglandins such as prostacyclin (PGI(2)). The latter action is believed to be important for the
Inhibition of microsomal prostaglandin E synthase-1 as targeted therapy in cancer treatment.
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The bioactive lipid prostaglandin E2 (PGE2) is involved in several steps of carcinogenesis in some of the most common cancers, e.g. colon cancer, lung cancer, prostate cancer and breast cancer. Non-steroidal anti-inflammatory drugs (NSAIDs) that target cyclooxygenase (COX) activity, the first step
NF-κB targets miR-16 and miR-21 in gastric cancer: involvement of prostaglandin E receptors.
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Cigarette smoke is one of the risk factors for gastric cancer and nicotine has been reported to promote tumor growth. Deregulation of microRNA (miRNA) and cyclooxygenase-2 (COX-2) expressions are hallmarks of many cancers including gastric cancer. Here, we used an miRNA array platform covering a
Inhibition of cancer cell proliferation and prostaglandin E2 synthesis by Scutellaria baicalensis.
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Scutellaria baicalensis is a widely used Chinese herbal medicine that has been used historically in anti-inflammatory and anticancer therapy. The purpose of this study is to verify its anticancer activity on head and neck squamous cell carcinoma (HNSCC) in vitro and in vivo and to investigate its
Urinary prostaglandin E2 metabolite and gastric cancer risk in the Shanghai women's health study.
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Chronic inflammation has been implicated in the etiology of gastric cancer. Prostaglandin E(2) (PGE(2)) is one of the major end-products of the cyclooxygenase-2 pathway, an enzyme that is an important mediator of inflammation. Using a novel method of quantifying the primary urinary metabolite of
The multi-faceted roles of prostaglandin E2 in cancer-infiltrating mononuclear phagocyte biology.
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Extensive research in the last two decades implemented that the inflammatory cell infiltrate, especially in solid tumors, is a major determinant for patient prognosis. Mononuclear phagocytes, i.e. monocytes/macrophages, dendritic cells and myeloid-derived suppressor cells, constitute the majority of
Oncolytic herpes simplex virus 1 encoding 15-prostaglandin dehydrogenase mitigates immune suppression and reduces ectopic primary and metastatic breast cancer in mice.
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Oncolytic herpes simplex virus 1 (HSV-1) viruses armed with immunomodulatory transgenes have shown potential for enhanced antitumor therapy by overcoming tumor-based immune suppression and promoting antitumor effector cell development. Previously, we reported that the new oncolytic HSV-1 virus,
Prostaglandin and hydroxyeicosatetraenoic acid synthesis by human mesenchymal tumors.
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The metabolism of arachidonic acid was investigated by radioimmunoassay and chromatographic techniques in 5 sarcomas and one embryonal carcinoma of human origin maintained as transplantable tumors in nude mice. The results obtained indicate that: the absolute quantities of arachidonic acid
[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
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