Gene/Protein Disease Symptom Drug Enzyme Compound
Pivot Concepts:   Target Concepts:
Query: EC:5.99.1.2 (topoisomerase)
 9,166 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

The first section of this article reviews recent studies that have clarified both the cellular role of topoisomerase I and the mechanisms of cytotoxicity of the topoisomerase inhibitors, the camptothecins. Different analogs of this new class of antitumor drug have been studied using various dose schedules in the treatment of refractory or recurrent gynecologic cancer. Response rates are between 13% and 25%. The main toxic effects are hematologic and gastrointestinal, the latter remains problematic. Radiotherapy, alkylate, platinum analogues, and topoisomerase II inhibitors are currently being studied in combination with camptothecins.
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PMID:Topoisomerase-I inhibitors in gynecologic tumors. 1008 69

The purpose of the study was to determine whether paclitaxel inhibits the expression of heat shock protein 27 (HSP27) in two gynecologic cancer cell lines compared with other antineoplastic agents having different cytotoxic mechanisms. BG-1 ovarian cancer cells and HeLa uterine cancer cells were treated with a tubulin depolymerization inhibitor (paclitaxel), a topoisomerase-II inhibitor (etoposide), and two tubulin polymerization inhibitors (colcemid and vincristine). Cell kills were evaluated by counting the number of cells. Propidium iodide staining and flow cytometric analysis were applied for the determination of cell-cycle perturbation. HSP27 was stained by the indirect immunofluorescence technique and analyzed with a flow cytometer. In both BG-1 and HeLa cells, growth arrest and G2 / M accumulation were dependent on the dose of each cytotoxic agent. There were positive correlations between HSP27 overexpression and growth arrest and G2 / M accumulation when the cell lines were treated with etoposide, colcemid, or vincristine, but not with paclitaxel. Paclitaxel completely inhibited the expression of HSP27. The results of this study indicated that paclitaxel may possess unique mechanisms able to overcome drug resistance by inhibiting HSP27 expression.
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PMID:Paclitaxel inhibits expression of heat shock protein 27 in ovarian and uterine cancer cells. 1530 55