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The mode of action of taxol: apoptosis at low concentration and necrosis at high concentration.
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The cytotoxicity of Taxol represents both inhibition of cell proliferation and cell death. The drug blocked cells in the G2/M phase of the cell cycle. It has also been reported that Taxol induced cell apoptosis; however, the mode of action of Taxol is far from clear. In this communication, the
Divergent effects of taxol on tumor necrosis factor-alpha-mediated cytolysis of ovarian carcinoma cells.
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OBJECTIVE
Our objective was to study the combined effect of taxol and tumor necrosis factor-alpha on the cytolysis of human ovarian carcinoma cell lines, because taxol has been shown to be active against ovarian carcinoma and has also been shown to increase tumor necrosis factor-alpha release from
Taxol toxicity. Epithelial necrosis in the gastrointestinal tract associated with polymerized microtubule accumulation and mitotic arrest.
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Taxol, an antineoplastic agent with a novel mechanism of action, is currently undergoing Phase I trials at The Johns Hopkins Hospital, Baltimore. The authors recently observed striking mitotic arrest associated with epithelial necrosis and ulceration in an esophageal biopsy specimen. The biopsy
Tumor necrosis factor-related apoptosis inducing ligand overexpression and Taxol treatment suppresses the growth of cervical cancer cells in vitro and in vivo.
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Tumor necrosis factor-related apoptosis inducing ligand (TRAIL) is a member of tumor necrosis factor (TNF) superfamily and functions to promote apoptosis by binding to cell surface death receptor (DR)4 and DR5. Cancer cells are more sensitive than normal cells to TRAIL-induced apoptosis, and
Taxol enhances but does not induce interleukin-1 beta and tumor necrosis factor-alpha production.
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Taxol is a potent, microtubule-stabilizing, antineoplastic drug that induces interleukin-1-beta (IL-1-beta) and tumor necrosis factor-alpha (TNF-alpha) release by thioglycolate-elicited mouse peritoneal macrophages. Because taxol use and subsequent cytokine release in human subjects could be
Relationship between the structure of taxol and other taxanes on induction of tumor necrosis factor-alpha gene expression and cytotoxicity.
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Taxol is an antitumor drug with cytotoxic properties that correlate with its microtubule-stabilizing activities. It has been reported that taxol parallels lipopolysaccharide in its effects on the induction of tumor necrosis factor-alpha (TNF-alpha) gene expression in macrophages (C. Bogdan and A.
Taxol, a microtubule-stabilizing antineoplastic agent, induces expression of tumor necrosis factor alpha and interleukin-1 in macrophages.
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Taxol, a naturally occurring diterpene with antitumor activity, induces tubulin polymerization to generate abnormally stable and nonfunctional microtubules. Previously, we showed that taxol has lipopolysaccharide (LPS)-like effects on macrophages. As LPS is a potent inducer of macrophage cytokine
CD14 is not involved in Rhodobacter sphaeroides diphosphoryl lipid A inhibition of tumor necrosis factor alpha and nitric oxide induction by taxol in murine macrophages.
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Taxol, a microtubule stabilizer with anticancer activity, mimics the actions of lipopolysaccharide (LPS) on murine macrophages in vitro. Recently, it was shown that taxol-induced macrophage activation was inhibited by the LPS antagonist Rhodobacter sphaeroides diphosphoryl lipid A (RsDPLA). To
Micromolar taxol, with or without hyperthermia, induces mitotic catastrophe and cell necrosis in HeLa cells.
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OBJECTIVE
Although the mode of action of taxol, when used in nanomolar or micromolar concentrations during long periods, is extensively studied, there are few data available on taxol-mediated cytotoxicity when the drug is applied for a short time alone or in combination with hyperthermia. We studied
Apoptotic cells subjected to cold/warming exposure disorganize apoptotic microtubule network and undergo secondary necrosis.
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Apoptotic microtubule network (AMN) is organized during apoptosis, forming a cortical structure beneath the plasma membrane which plays a critical role in preserving cell morphology and plasma membrane integrity. The aim of this study was to examine the effect of cold/warming exposure on apoptotic
Cellular resistance to vincristine suppresses NF-kappa B activation and apoptosis but enhances c-Jun-NH2-terminal protein kinase activation by tumor necrosis.
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Tumor necrosis factor (TNF) is a pleiotropic cytokine that potentiates the cytotoxic effects of chemotherapeutic drugs. Although emergence of resistance to chemotherapeutic drugs is a major problem in cancer therapy, its mechanism is incompletely understood. Recently, activation of a nuclear
Taxol induces paraptosis independent of both protein synthesis and MAPK pathway.
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Our recent studies have shown that high concentration of taxol induced a caspase-independent paraptosis-like cell death and cytoplasmic vacuolization derived predominantly from endoplasmic reticulum (ER) swelling in human lung carcinoma cell lines (ASTC-a-1). In this report, we further explored the
RAW264 macrophages stably transfected with an HIV-1 LTR reporter gene provide a sensitive bioassay for analysis of signalling pathways in macrophages stimulated with lipopolysaccharide, TNF-alpha or taxol.
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Bacterial lipopolysaccharide (LPS) modulates expression of a variety of genes in macrophages, and additionally activates viral promoters including the HIV-1 LTR. The HIV-1 LTR driving the luciferase reporter gene was stably transfected into the murine macrophage cell line, RAW264. In stably
The effects of thalidomide and minocycline on taxol-induced hyperalgesia in rats.
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Chemotherapy-induced pain is the most common treatment-limiting complication encountered by cancer patients receiving taxane-, vinca alkaloid- or platin-based chemotherapy. Several lines of evidence indicate that activation of pro-inflammatory cascades involving the release of cytokines including
Taxol, a microtubule stabilizer, improves cardiac functional recovery during postischemic reperfusion in rat in vitro.
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OBJECTIVE
Microtubule disruption contributes to cellular and organic dysfunction, and is implicated in ischemia/reperfusion (I/R) injury. The purpose of this study was to explore the effects of taxol, a microtubule stabilizer, on cardiac functional recovery during reperfusion.
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