teniposide/borstkanker

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Teniposide in advanced breast cancer. A phase II trial in patients with no prior chemotherapy.

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The objective response rates were determined using teniposide as first-line chemotherapy for patients with recurrent breast cancer. Twenty-seven evaluable patients with advanced disease received teniposide 70 mg/m2 i.v. days 1-5 every 3 weeks. A total of 211 courses were given. Responses included

Phase II study of teniposide in advanced breast cancer.

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In a phase II study, 19 patients with previously treated, advanced breast cancer received 50 mg/m2 teniposide (VM-26) i.v. on days 1-5 every 3 weeks. One partial response (PR) (5%) was observed. Toxicity consisting of leukopenia and thrombocytopenia was frequent and severe. VM-26 has minimal

Preparation and evaluation of teniposide-loaded polymeric micelles for breast cancer therapy.

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Self-assembled polymeric micelles have been widely applied in anticancer drug delivery systems. Teniposide is a broad spectrum and effective anticancer drug, but its poor water-solubility and adverse effects of commercial formulation (VM-26) restrict its clinical application. In this work,

Ionizing radiation and teniposide increase p21(waf1/cip1) and promote Rb dephosphorylation but fail to suppress E2F activity in MCF-7 breast tumor cells.

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Ionizing radiation and the topoisomerase II inhibitor, teniposide (VM-26) both increase levels of the cyclin dependent kinase inhibitor, p21(waf1/cip1) and promote dephosphorylation of the retinoblastoma tumor suppressor protein, Rb, in MCF-7 breast tumor cells, perturbations associated with

Dissociation between bulk damage to DNA and the antiproliferative activity of teniposide (VM-26) in the MCF-7 breast tumor cell line: evidence for induction of gene-specific damage and alterations in gene expression.

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In the MCF-7 breast tumor cell line, induction of bulk damage to DNA (measured either as total strand breaks or as double-strand breaks) fails to correspond with the antiproliferative activity of the demethylepipodo-phyllotoxin derivative, VM-26. In contrast, VM-26 produces an early (within 2-3 h)

Topoisomerase II trapping agent teniposide induces apoptosis and G2/M or S phase arrest of oral squamous cell carcinoma.

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BACKGROUND Teniposide (VM-26) has been widely used in the treatment of small cell lung cancer, malignant lymphoma, breast cancer, etc. However, there are few reports on VM-26 against oral cancers. The present study was designed to identify the effect of VM-26 against oral squamous cell carcinoma in

Bcnu plus teniposide (vm26) as a 1st line chemotherapy for brain metastases regardless of the origin.

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Twenty-nine patients with brain metastases regardless of the origin were treated with the combination of 1-3-bis-(2-chloroethyl)-1-nitrosourea (BCNU), 120 mg/m2 i.v. every six weeks, and teniposide (VM26), 100 mg/m2 i.v. on the days 1 and 2 of every three-week period. Five objective responses were

Phase II evaluation of teniposide (VM-26) in metastatic breast carcinoma. A Southeastern Cancer Study Group trial.

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The Southeastern Cancer Study Group performed a Phase II study of teniposide in previously treated patients with metastatic breast cancer. No responses were observed in 11 evaluable patients who received teniposide 60 mg/m2 by IV infusion for five consecutive days every three weeks. Toxicity was

Mouse breast cancer resistance protein (Bcrp1/Abcg2) mediates etoposide resistance and transport, but etoposide oral availability is limited primarily by P-glycoprotein.

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The breast cancer resistance protein [BCRP (BCRP/ABCG2)] has not previously been directly identified as a source of resistance to epipodophyllotoxins.However, when P-glycoprotein (P-gp)- and Mrp1-deficient mouse fibroblast and kidney cell lines were selected for resistance to etoposide,

Suppression of c-myc expression and c-Myc function in response to sustained DNA damage in MCF-7 breast tumor cells.

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The topoisomerase II inhibitors teniposide (VM-26), doxorubicin, and amsacrine (m-AMSA), as well as ionizing radiation, induce a transient suppression of c-myc mRNA, which correlates with growth inhibition of MCF-7 breast tumor cells. To further assess the involvement of c-mvc in the DNA

Therapy-related myeloid neoplasms.

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OBJECTIVE The purpose of this review is to update knowledge on therapy-related myeloid neoplasms (t-MN), taking into account the new 2008 WHO classification, new genome-wide approaches for the definition of susceptibility towards t-MN and the introduction of new more aggressive treatments in cancer

Controversies in the management of brain metastases: the role of chemotherapy.

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The role of chemotherapy (CT) for brain metastases (BrM) is still controversial. Limited life expectancy and presence of the blood-brain barrier (BBB) have been considered as contraindications for relatively aggressive therapies, such as CT. Nevertheless, more recent studies emphasise the

Reversal of multidrug resistance by mitochondrial targeted self-assembled nanocarrier based on stearylamine.

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Multidrug resistance (MDR) remains one of the major challenges for successful chemotherapy. Herein, we tried to develope a mitochondria targeted teniposide loaded self-assembled nanocarrier based on stearylamine (SA-TSN) to reverse MDR of breast cancer. SA-TSN was nanometer-sized spherical particles

Lignans and Neolignans: Plant secondary metabolites as a reservoir of biologically active substances.

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Lignans and neolignans are plant secondary metabolites derived from the oxidative coupling of phenylpropanoids. Biological activity of these phenolic compounds ranges from antioxidant, antitumor (terminaloside P, IC₅₀ = 10 nM), anti-inflammatory, anti-neurodegenerative (schibitubin B,

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