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lysophosphatidylcholine/krebs
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Seite 1 von 108 Ergebnisse
Lysophosphatidylcholine as a predictor of postoperative complications after colorectal cancer surgery.
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OBJECTIVE
Lysophosphatidylcholine (LPC), which is generated from phosphatidylcholine (PC) and metabolized by autotaxin (ATX), modulates immune responses via its anti-inflammatory property. We investigated the association between LPC and postoperative complications (POCs) after colorectal cancer
A Novel Strategy for Targeted Lipidomics Based on LC-Tandem-MS Parameters Prediction, Quantification, and Multiple Statistical Data Mining: Evaluation of Lysophosphatidylcholines as Potential Cancer Biomarkers.
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Lipid quantification is the ultimate goal in lipidomics studies challenged by the availability of standard compounds. A novel strategy for targeted lipidomics based on LC-MS/MS parameters prediction and multivariate statistical analysis was developed for the quantitation of lysophosphatidylcholines
Cell Death in the Tumor Microenvironment: Implications for Cancer Immunotherapy
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The physiological fate of cells that die by apoptosis is their prompt and efficient removal by efferocytosis. During these processes, apoptotic cells release intracellular constituents that include purine nucleotides, lysophosphatidylcholine (LPC), and Sphingosine-1-phosphate (S1P) that induce
Lysophosphatidate induces chemo-resistance by releasing breast cancer cells from taxol-induced mitotic arrest.
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BACKGROUND
Taxol is a microtubule stabilizing agent that arrests cells in mitosis leading to cell death. Taxol is widely used to treat breast cancer, but resistance occurs in 25-69% of patients and it is vital to understand how Taxol resistance develops to improve chemotherapy. The effects of
Disturbance of phospholipid metabolism during the selective destruction of tumor cells induced by alkyl-lysophospholipids.
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Alkyl-lysophospholipids inhibit the growth of Meth A sarcoma cells in vitro. In contrast, murine bone marrow macrophages are not sensitive to the destructive effect of these substances. Since alkyl-lysophospholipids are antimetabolites in the synthesis of 3-sn-phosphatidylcholine, tumor cell
Potential Nutritional and Metabolomic Advantages of High Fat Oral Supplementation in Pancreatectomized Pancreaticobiliary Cancer Patients.
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We examined the effect of high fat oral nutritional supplement (HFS) on the nutritional status, oral intake, and serum metabolites of postoperative pancreaticobiliary cancer patients. Pancreaticobiliary cancer patients were voluntarily recruited. The HFS group received postoperative oral high fat
Metabolomic analysis uncovered an association of serum phospholipid levels with estrogen-induced mammary tumors in female ACI/Seg rats.
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Estrogen is reported to be involved in mammary tumorigenesis. To unveil metabolic signatures for estrogen-induced mammary tumorigenesis, we carried out serum metabolomic analysis in an estrogen-induced mammary tumor model, female August Copenhagen-Irish/Segaloff (ACI/Seg) rats, using liquid
Lysophospholipid profile in serum and liver by high-fat diet and tumor induction in obesity-resistant BALB/c mice.
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OBJECTIVE
Our previous study revealed that chronic consumption of a high-fat diet (HFD) stimulates colon cancer progression in obesity-resistant BALB/c mice. The aim of the present study was to investigate the significant alteration of metabolites caused by tumor progression and an HFD in the serum
The riminophenazine agents clofazimine and B669 inhibit the proliferation of cancer cell lines in vitro by phospholipase A2-mediated oxidative and nonoxidative mechanisms.
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Clofazimine, a riminophenazine antimicrobial agent, and its analogue B669 were investigated for their effects on FaDu cells, a human squamous carcinoma cell line. These agents, at concentrations within the therapeutic range (0.25-2 micrograms/ml), caused a dose-dependent tumor cell cytotoxicosis
[Study of phospholipid profile of ovarian tumor by high performance liquid chromatography-mass spectrometry].
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Ovarian tumor has been paid more and more attention since its influence on women's health and life quality is increasing. Ovarian cancer is one of the three gynecologic cancers, and its mortality is the highest one of them. Phospholipid metabolic profiling method based on high performance liquid
Lipidomic approach to identify patterns in phospholipid profiles and define class differences in mammary epithelial and breast cancer cells.
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Breast cancer is the leading cause of cancer-related deaths in women. Altered cellular functions of cancer cells lead to uncontrolled cellular growth and morphological changes. Cellular biomembranes are intimately involved in the regulation of cell signaling; however, they remain largely
Tumor necrosis factor-alpha alters phospholipid content in the bronchoalveolar lavage-accessible space of isolated perfused rat lungs.
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OBJECTIVE
To examine the effect of tumor necrosis factor-alpha (TNF-alpha) on pulmonary artery pressure and on total protein, phospholipid, lysophosphatidylcholine, phosphatidylcholine, phosphatidylinositol, and phosphatidylglycerol content in the bronchoalveolar lavage-accessible space of the
Lysophosphatidylcholines and Chlorophyll-Derived Molecules from the Diatom Cylindrotheca closterium with Anti-Inflammatory Activity.
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Microalgae have been shown to be excellent producers of lipids, pigments, carbohydrates, and a plethora of secondary metabolites with possible applications in the pharmacological, nutraceutical, and cosmeceutical sectors. Recently, various microalgal raw extracts have been found to have
ONO-8430506: A Novel Autotaxin Inhibitor That Enhances the Antitumor Effect of Paclitaxel in a Breast Cancer Model
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Lysophosphatidic acid (LPA) is a bioactive lipid mediator that elicits a number of biological functions, including smooth muscle contraction, cell motility, proliferation, and morphological change. LPA is endogenously produced by autotaxin (ATX) from extracellular lysophosphatidylcholine (LPC) in
Role of the autotaxin-lysophosphatidate axis in the development of resistance to cancer therapy.
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Autotaxin (ATX) is a secreted enzyme that hydrolyzes lysophosphatidylcholine to produce lysophosphatidate (LPA), which signals through six G-protein coupled receptors (GPCRs). Signaling through LPA is terminated by its degradation by a family of three lipid phosphate phosphatases (LPPs). LPP1 also
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