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Cisplatin Resistance and Transcription Factors
Current Medicinal Chemistry-Anti-Cancer Agents, 2005Cisplatin is one of the most potent and widely used anti-cancer agents in the treatment of various solid tumors. However, the development of resistance to cisplatin is a major obstacle in clinical treatment. Several mechanisms are thought to be involved in cisplatin resistance, including decreased intracellular drug accumulation, increased levels of ...
Takayuki, Torigoe +12 more
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Mechanisms of resistance to cisplatin
Mutation Research/Fundamental and Molecular Mechanisms of Mutagenesis, 2001The use of cisplatin in cancer chemotherapy is limited by acquired or intrinsic resistance of cells to the drug. Cisplatin enters the cells and its chloride ligands are replaced by water, forming aquated species that react with nucleophilic sites in cellular macromolecules.
M, Kartalou, J M, Essigmann
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Cisplatin resistance in human cancers
Pharmacology & Therapeutics, 1991Cancer chemotherapeutic agents primarily act by damaging cellular DNA directly or indirectly. Tumor cells, in contrast to normal cells, respond to cisplatin with transient gene expression to protect and/or repair their chromosomes. Repeated cisplatin treatments results in a stable resistant cell line with enhanced gene expression but lacking gene ...
K J, Scanlon +3 more
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Acquired Radiation Resistance Induces Thiol-dependent Cisplatin Cross-resistance
Radiation Research, 2023Resistance to radiation remains a significant clinical challenge in non-small cell lung carcinoma (NSCLC). It is therefore important to identify the underlying molecular and cellular features that drive acquired resistance. We generated genetically matched NSCLC cell lines to investigate characteristics of acquired resistance.
Samir V, Jenkins +9 more
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Cisplatin Resistance Associated with PARP Hyperactivation
Cancer Research, 2013Abstract Non–small cell lung carcinoma patients are frequently treated with cisplatin (CDDP), most often yielding temporary clinical responses. Here, we show that PARP1 is highly expressed and constitutively hyperactivated in a majority of human CDDP-resistant cancer cells of distinct histologic origin.
Michels, J. +25 more
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Mechanisms of cellular resistance to cisplatin
Medical Oncology and Tumor Pharmacotherapy, 1988Treatment of cancer patients often fails because of the resistance in the tumor to chemotherapeutic drugs. A better understanding of mechanisms which are active in resistant cells might lead to measures to circumvent the resistance. This review deals with the mechanisms of action of cisplatin (CDDP) and the various causes for CDDP resistance in the ...
G A, Hospers, N H, Mulder, E G, De Vries
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Cisplatin resistance and oncogenes - a review
Anti-Cancer Drugs, 2000Cisplatin is among the most widely used broadly active cytotoxic anticancer drugs; however, its clinical efficacy is often limited by primary or the development of secondary resistance. Several mechanisms have been implicated in cisplatin resistance, including reduced drug uptake, increased cellular thiol/folate levels and increased DNA repair.
W, Dempke +4 more
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Anti-cancer drug design, 1999
Resistance to cis-diamminedichloroplatinum(II) (cisplatin), a DNA damaging agent, is a major obstacle for its clinical effectiveness. Multiple mechanisms may be involved in cisplatin resistance. Frequently cited mechanisms include reduced accumulation, elevated levels of glutathione (GSH) and metallothionein, and enhanced DNA repair.
S, Akiyama +3 more
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Resistance to cis-diamminedichloroplatinum(II) (cisplatin), a DNA damaging agent, is a major obstacle for its clinical effectiveness. Multiple mechanisms may be involved in cisplatin resistance. Frequently cited mechanisms include reduced accumulation, elevated levels of glutathione (GSH) and metallothionein, and enhanced DNA repair.
S, Akiyama +3 more
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Mechanisms of resistance to cisplatin
1991A number of changes have been detected in cisplatin-resistant cells, some of which are likely to be directly involved in the mechanism of resistance. The four most cited mechanisms are reduced accumulation, increased glutathione, increased metallothionein, and enhanced DNA repair.
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