teniposide/necrosis

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Carboplatin and teniposide concurrent with radiotherapy in patients with glioblastoma multiforme: a phase II study.

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BACKGROUND The outcome after treatment for glioblastoma remains poor. Therefore, the authors evaluated the long term efficacy and toxicity of treatment with radiotherapy and concurrent carboplatin plus teniposide followed by three cycles of carmustine in patients who underwent resection for

APRIL, a new member of the tumor necrosis factor family, modulates death ligand-induced apoptosis.

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APRIL (a proliferation-inducing ligand) is a newly identified member of the tumor necrosis factor (TNF) family. Tumor growth-promoting as well as apoptosis-inducing effects of APRIL have been described. Here, we report that five of 12 human malignant glioma cell lines express APRIL. APRIL gene

Synergistic enhancement by tumor necrosis factor of in vitro cytotoxicity from chemotherapeutic drugs targeted at DNA topoisomerase II.

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Recombinant human tumor necrosis factor (rHTNF) alone had no effect on L929 tumor cells at 100 units/ml for 20 h of continuous exposure. However, under the same conditions, rHTNF markedly enhanced the cytotoxicity of Adriamycin, actinomycin D, 4'-(9-acridinylamino)-methanesulfon-m-anisidide,

Tumor necrosis factor enhances the in vitro and in vivo efficacy of chemotherapeutic drugs targeted at DNA topoisomerase II in the treatment of murine bladder cancer.

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Recombinant human tumor necrosis factor (rTNF) is a macrophage secretory protein with antitumor activity. The murine bladder tumor cell line MBT-2 was used to evaluate the in vitro and in vivo antitumor effects of rTNF in combination with chemotherapeutic drugs targeted at DNA topoisomerase II.

Potentiation of topoisomerase inhibitor-induced DNA strand breakage and cytotoxicity by tumor necrosis factor: enhancement of topoisomerase activity as a mechanism of potentiation.

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A combination of tumor necrosis factor (TNF) and the topoisomerase I inhibitor, camptothecin, or the topoisomerase II inhibitors, teniposide and amsacrine, produced dose-dependent synergistic cytotoxicity against the murine L929 fibrosarcoma cells. Similar synergy was not observed with a combination

Biochemical modulation of cytotoxic drugs by cytokines: molecular mechanisms in experimental oncology.

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The combination of cytokines and cytotoxic drugs offers a new approach to increase the therapeutic index in the treatment of neoplastic diseases. There is no consensus on optimal strategies for combining these agents so far. The molecular mechanisms underlying the interaction, however, should be

Autologous bone marrow transplantation with monoclonal antibody purged marrow for high risk acute lymphoblastic leukemia.

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Fifty-four patients with acute lymphoblastic leukemia (ALL: 1 relapse, 21 high risk first complete remission (CR 1), 29 second CR (CR 2), and 3 third CR (CR 3) were treated by autologous bone marrow transplantation at three centers. Before storage, the marrows were purged ex vivo with appropriate

Cytostatic and cytotoxic effects of fostriecin on human promyelocytic HL-60 and lymphocytic MOLT-4 leukemic cells.

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Exposure of exponentially growing human promyelocytic of lymphocytic leukemic cells to the putative DNA topoisomerase II inhibitor fostriecin (FST), at a concentration of 1 microM, results in the suppression of their rate of progression through the S and G2 phases of the cell cycle. At

[Anti-cancer drug sensitivity test against human testicular cancer xenograft--comparison with clinical results of chemotherapy].

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The antitumor effect of vinblastine (VBL), vincristine (VCR), etoposide (VP-16), teniposide (VM-26), cisplatin (CDDP), CBDCA (JM-8, Carboplatin), CHIP (JM-9), DWA2114R and recombinant human tumor necrosis factor (TNF) on four human testicular cancers heterotransplanted in nude mice were studied. The

Synergistic antitumor effects of topoisomerase inhibitors and natural cell-mediated cytotoxicity.

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The mechanism of augmentation of tumor cell killing by immune effector cells and chemotherapeutic drugs was studied. The effect of treating tumor cells with various antineoplastic drugs on their sensitivity to murine natural cell-mediated cytotoxicity in vitro was investigated. Pretreatment with

Modulation of growth and radiochemosensitivity of human malignant glioma cells by acidosis.

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BACKGROUND Glioblastoma commonly is characterized by hypoxia and acidosis and the histologic features of tissue necrosis and neovascularization. Current approaches of adjuvant radiochemotherapy for patients with glioblastoma have only a modest impact on the natural course of this

Immunochemotherapy of malignant glioma: synergistic activity of CD95 ligand and chemotherapeutics.

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Malignant glioma cells are susceptible to CD95(Fas/APO-)-mediated apoptosis triggered by agonistic antibody. Here we examined the proapoptotic effects of the natural CD95 ligand, a cytotoxic cytokine homologous to tumor necrosis factor, on malignant glioma cell lines LN-229, LN-308 and T98G. We

Inhibition of tumor angiogenesis and tumor growth by the DSL domain of human Delta-like 1 targeted to vascular endothelial cells.

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The growth of solid tumors depends on neovascularization. Several therapies targeting tumor angiogenesis have been developed. However, poor response in some tumors and emerging resistance necessitate further investigations of new drug targets. Notch signal pathway plays a pivotal role in vascular

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