taxol/neoplasms

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Global functional analysis of nucleophosmin in Taxol response, cancer, chromatin regulation, and ribosomal DNA transcription.

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Analysis of lung cancer response to chemotherapeutic agents showed the accumulation of a Taxol-induced protein that reacted with an anti-phospho-MEK1/2 antibody. Mass spectroscopy identified the protein as nucleophosmin/B23 (NPM), a multifunctional protein with diverse roles: ribosome biosynthesis,

Resistance to Taxol in lung cancer cells associated with increased microtubule dynamics.

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Microtubule dynamics are crucial for mitotic spindle assembly and chromosome movement. Suppression of dynamics by Taxol appears responsible for the drug's potent ability to inhibit mitosis and cell proliferation. Although Taxol is an important chemotherapeutic agent, development of resistance limits

Inhibition of heat shock protein 90 function down-regulates Akt kinase and sensitizes tumors to Taxol.

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The phosphatidylinositol 3'-kinase/Akt pathway is activated frequently in human cancer, and has been implicated in tumor proliferation, cell survival, and resistance to apoptotic stimuli. Akt forms a complex with heat shock protein (Hsp) 90 and Cdc37, and inhibitors of Hsp90 cause Akt degradation.

Role of DDX53 in taxol-resistance of cervix cancer cells in vitro.

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Cancer/Testis antigen DDX53 shows high expression level in various tumors and is involved in anti-cancer drug resistance. However, the functional study of DDX53 in cervix cancer remains unknown. In this study, the role of DDX53 in taxol-resistance of cervix cancer cells was investigated. In

Identification of tumor-specific paclitaxel (Taxol)-responsive regulatory elements in the interleukin-8 promoter.

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Paclitaxel (Taxol) is a novel chemotherapeutic drug that is effective against breast and ovarian cancers. Although the primary target of paclitaxel is microtubules, its efficacy exceeds that of conventional microtubule-disrupting agents, suggesting that it may have additional cellular effects.

Short term culture of breast cancer tissues to study the activity of the anticancer drug taxol in an intact tumor environment.

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BACKGROUND Sensitivity of breast tumors to anticancer drugs depends upon dynamic interactions between epithelial tumor cells and their microenvironment including stromal cells and extracellular matrix. To study drug-sensitivity within different compartments of an individual tumor ex vivo, culture

Taxol as second-line treatment in patients with advanced ovarian cancer after platinum-based first-line chemotherapy.

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Salvage chemotherapy in platin-resistant patients typically results in low response rates and short survival, therefore new active cytotoxic agents must be found. One of these agents is paclitaxel (Taxol), isolated from the bark of the western yew which acts as an antimicrotubule agent. In our study

A polymer additive boosts the anti-cancer efficacy of supramolecular nanofibers of taxol

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A polymer additive of hyaluronic acid (HA) could boost the anti-cancer efficacy of supramolecular nanofibers of a prodrug of taxol (succinated taxol).

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

Therapeutic efficacy of anti-Lewis(y) humanized 3S193 radioimmunotherapy in a breast cancer model: enhanced activity when combined with taxol chemotherapy.

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Monoclonal antibody therapy may provide new treatment options in the management of metastatic breast cancer by selectively targeting tumors and producing a therapeutic effect, by delivering radiation or other toxins directly to tumor cells, or by producing an intrinsic immune inflammatory response.

Low Dose Decitabine Combined with Taxol and Platinum Chemotherapy to Treat Refractory/Recurrent Ovarian Cancer: An Open-Label, Single-Arm, Phase I/II Study.

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OBJECTIVE Previous research has proposed that the hypomethylating agent decitabine can sensitize ovarian cancer cells to chemical agents. In this open-label, phase I/II clinical study, we analyzed the toxicity and efficacy of low dose decitabine combined with taxol and platinum chemotherapy in

A comparative analysis on the efficacy and safety of intaxel® and taxol® in advanced metastatic breast cancer.

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BACKGROUND Among the presently available cytotoxic drugs, paclitaxel, in combination with doxorubicin and carboplatin, come under the highly active therapy for metastatic breast cancer. Between the two brands of paclitaxel (Intaxel, which is marketed by Fresenius Kabi and Taxol, the original

Molecular effects of taxol and caffeine on pancreatic cancer cells.

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Pancreatic cancer is the fifth leading cause of cancer related deaths in the United States. Despite many recent advances in the treatment modalities, the mortality rate still remains very high. Paclitaxel (Taxol) and Caffeine have been used for the treatment of this disease, however the molecular

Paclitaxel (Taxol)/carboplatin combination chemotherapy in the treatment of advanced ovarian cancer.

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The activity of paclitaxel (Taxol; Bristol-Myers Squibb Company, Princeton, NJ) in advanced ovarian cancer, both as a single agent and in combination chemotherapy, has been demonstrated in numerous phase I/II trials. Paclitaxel/platinum combinations have produced encouraging results in phase III

Synthetic paclitaxel-octreotide conjugate reverses the resistance of paclitaxel in A2780/Taxol ovarian cancer cell line.

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The high mortality of ovarian cancer is partly due to the frequent resistance of ovarian cancer to current chemotherapy agents such as paclitaxel and platinum. Somatostatin analogue (SSTA) has been shown to inhibit the proliferation of some tumors through binding to somatostatin receptor (SSTR) and

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