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epipodophyllotoxin/vinca

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ArticlesClinical trialsPatents
7 results

Antitumor antibiotics, epipodophyllotoxins, and vinca alkaloids.

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This paper reviews manuscripts published from June 1991 to June 1992 that, in the author's opinion, have added to the understanding and clinical use of a group of commonly used antineoplastic agents. New developments highlighted include 1) clarification of the mechanism of action of the

Current developments in antitumor antibiotics, epipodophyllotoxins, and vinca alkaloids.

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The antitumor antibiotics, epipodophyllotoxins, and vinca alkaloids represent a major portion of the therapeutic armamentarium against almost all treatable neoplasms. However, their use has been limited by the acquisition of drug resistance as well as by serious nonhematologic toxicities such as

Comparative effects of vinca alkaloids (VCR, VDS) and epipodophyllotoxin (VP16) on murine myeloblastic leukaemia.

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Antitumor antibiotics, epipodophyllotoxins, and vinca alkaloids: clinical developments.

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Reversal of Vinca alkaloid resistance but not multiple drug resistance in human leukemic cells by verapamil.

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We examined the ability of verapamil, a Ca2+ channel blocker, to overcome Vinca alkaloid and multiple drug resistance in our CEM/VLB100 and CEM/DOX human leukemic lymphoblasts. Compared with the parent CCRF-CEM cells, CEM/VLB100 cells are approximately equal to 200- to 800-fold resistant to

[Characterization of the mechanism of cross-resistance to vinca alkaloids and taxoids in the human J82 bladder tumor cell line].

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A phenotype of resistance to the new vinca alkaloid Navelbine was induced in the J82 human bladder carcinoma cells. The resistance factor of the resistant cell line (J82-NVB) to Navelbine was 17. The resistance phenotype of these cells is not a multidrug-resistance (MDR) phenotype. J82-NVB cells

Cross-resistance patterns and antigen expression in Vinca alkaloid- and other multiple drug-resistant human leukemic cell lines.

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The studies presented in this report demonstrate that Vinca alkaloid-resistant human leukemic lymphoblasts display patterns of cross-resistance to other drugs that differ from those of cell lines selected for primary resistance to anthracyclines or epipodophyllotoxins. These various drug-resistant
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