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Selective Akt inactivation and tumor necrosis actor-related apoptosis-inducing ligand sensitization of renal cancer cells by low concentrations of paclitaxel.

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Recent studies demonstrated that the resistance of cancer cells to tumor necrosis factor-related apoptosis-inducing ligand (TRAIL) could be reversed by various chemotherapeutic agents. In the present study, we investigated the role of Akt in the apoptosis resistance to TRAIL and chemotherapeutic

Role of tumor necrosis factor alpha-induced protein 1 in paclitaxel resistance.

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Paclitaxel has been extensively used as an antitumor drug to treat a broad range of epithelial cancers, including breast and cervical cancers. However, the efficacy of this drug is greatly limited by the development of acquired resistance. Identification of the underlying resistance mechanisms may

An effective in vitro antitumor response against human pancreatic carcinoma with paclitaxel and daunorubicin by induction of both necrosis and apoptosis.

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The highly metastatic human pancreatic cell line L3.6 was used to study mechanisms for antitumor activity with various chemotherapeutic drug combinations. The most effective drugs were daunorubicin (IC50 0.4 microM), doxorubicin (IC50 22 microM), paclitaxel (IC50 5.3 microM) and 5-fluorouracil (IC50

Cell cycle specific induction of apoptosis and necrosis by paclitaxel in the leukemic U937 cells.

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Induction of cell apoptosis and necrosis by paclitaxel was investigated in human leukemic U937 cells. To explore whether paclitaxel induces both apoptosis and necrosis in different cell cycle stages, we synchronized the cells in G1, S and G2/M stages by counterflow centrifugal elutriation (CCE). The

Induction of tumor necrosis factor by bryostatin 1 is involved in synergistic interactions with paclitaxel in human myeloid leukemia cells.

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Interactions between the protein kinase C (PKC) activator/down-regulator bryostatin 1 and paclitaxel have been examined in human myeloid leukemia cells (U937) and in highly paclitaxel-resistant cells ectopically expressing a Bcl-2 phosphorylation loop-deleted protein (Delta Bcl-2). Treatment (24

Skin necrosis in the presence of paclitaxel and fluorometholone.

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Paclitaxel (Taxol) can induce full-thickness skin necrosis at sites distant from those of injection. This side effect may be potentiated in the presence of fluorometholone (FML).

[A Case of Axillary Arterial Bleeding after Axillary Metastatic Lymph Node Necrosis during Treatment with Paclitaxel and Bevacizumabfor Breast Cancer].

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A 44-year-old woman was diagnosed cT4bcN3cM1(LYM), Stage IV triple-negative breast cancer.Enhanced computed tomography revealed ipsilateral axillary lymph node metastasis, 10 cm in diameter.The supraclavicular and cervical lymph nodes also had metastases.She received paclitaxel(90mg/m2, on days 1,

A Rare Case of Paclitaxel and/or Trastuzumab Induced Acute Hepatic Necrosis.

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Paclitaxel induced mild derangement of liver functions including bilirubin, alkaline phosphatase, and AST has been infrequently noticed in clinical trials. Contrary to Paclitaxel, hepatocellular injury, hepatitis, and liver tenderness are common laboratory and clinical findings with Trastuzumab.

A retrospective review of paclitaxel-associated gastrointestinal necrosis in patients with epithelial ovarian cancer.

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Seven patients with gastrointestinal necrosis following paclitaxel chemotherapy are reported. Four of seven patients had platinum refractory disease, while 3/7 patients received primary paclitaxel therapy. Complications occurred 5 to 16 days following paclitaxel therapy. The most common clinical

Rapid tumor necrosis and massive hemorrhage induced by bevacizumab and paclitaxel combination therapy in a case of advanced breast cancer.

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Bevacizumab when combined with chemotherapy exerts significant activity against many solid tumors through tumor angiogenesis inhibition; however, it can induce severe side effects. We report the rare case of a 27-year-old premenopausal woman with locally advanced breast cancer that was marked by

Inhibition of tumor necrosis factor alpha-stimulated aromatase activity by microtubule-stabilizing agents, paclitaxel and 2-methoxyestradiol.

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The aromatase enzyme, which converts androstenedione to oestrone, regulates the availability of oestrogen to support the growth of hormone-dependent breast tumours. Cytokines, such as interleukin 6 (IL-6) and tumour necrosis factor alpha (TNFalpha) or prostaglandin E(2) (PGE(2)), can stimulate

Synergistic antitumor activity of cisplatin, paclitaxel, and gemcitabine with tumor vasculature-targeted tumor necrosis factor-alpha.

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OBJECTIVE Subnanogram doses of NGR-tumor necrosis factor (TNF), a TNF-alpha derivative able to target tumor neovessels, can enhance the antitumor activity of doxorubicin and melphalan in murine models. We have examined the antitumor activity of NGR-TNF in combination with various chemotherapeutic

Potentiation of antitumor efficacy of paclitaxel by recombinant tumor necrosis factor-alpha.

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We studied the combination of tumor necrosis factor (TNF) and paclitaxel. Our aim was to determine whether TNF increases the antitumor efficacy of paclitaxel and if so whether the increase is mediated through the enhancement of apoptosis induction by paclitaxel. Mice bearing 6 mm MCa-K or MCa-4

Severe necrosis due to paclitaxel extravasation.

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Paclitaxel is an antineoplastic agent derived from the bark of the Pacific yew tree that has activity against many tumors including breast and ovarian carcinomas. In the past, its extravasation quality has been considered to be a local irritant; however, recent reports suggest that the agent may be

Structural significance of the benzoyl group at the C-3'-N position of paclitaxel for nitric oxide and tumor necrosis factor production by murine macrophages.

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The antitumor agent paclitaxel (Taxol) mimics the actions of lipopolysaccharide (LPS) on murine macrophages (M phi). Recently, we have shown that the benzoyl group at the C-3' position of paclitaxel is the most important site to induce nitric oxide (NO) and tumor necrosis factor (TNF) production by

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