Results 211 to 220 of about 104,183 (265)

Targeting ANXA4 to Overcome Cisplatin Resistance in Ovarian Cancer: A Bioinformatics and in Vitro Study. [PDF]

Onco Targets Ther
Wang Y, Xie Q.
europepmc   +1 more source

HnRPD/AUF1 facilitates human ovarian cancer progression through activating FLI1 and maintaining cisplatin resistance. [PDF]

Mol Cancer
Tang C, Zhu C, An Z, Cao B, Xu Q, Li L, Bao Y, Li J.   +7 more
europepmc   +1 more source

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Mechanisms of resistance to cisplatin

Mutation Research - Fundamental and Molecular Mechanisms of Mutagenesis, 2001
The 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 and Transcription Factors

Current Medicinal Chemistry-Anti-Cancer Agents, 2005
Cisplatin 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, Hiroto, Izumi, Hiroshi, Ishiguchi, Yoichiro, Yoshida, Mizuho, Tanabe, Takeshi, Yoshida, Tomonori, Igarashi, Ichiro, Niina, Tetsuro, Wakasugi, Takuya, Imaizumi, Yasutomo, Momii, Michihiko, Kuwano, Kimitoshi, Kohno   +12 more
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Mechanisms of cellular resistance to cisplatin

Medical Oncology and Tumor Pharmacotherapy, 1988
Treatment 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 in human cancers

Pharmacology & Therapeutics, 1991
Cancer 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, M, Kashani-Sabet, T, Tone, T, Funato   +3 more
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Cisplatin resistance and oncogenes - a review

Anti-Cancer Drugs, 2000
Cisplatin 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, W, Voigt, A, Grothey, B T, Hill, H J, Schmoll   +4 more
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Mechanisms of resistance to cisplatin and carboplatin

Critical Reviews in Oncology/Hematology, 2007
While cisplatin and carboplatin are active versus most common cancers, epithelial malignancies are incurable when metastatic. Even if an initial response occurs, acquired resistance due to mutations and epigenetic events limits efficacy. Resistance may be due to excess of a resistance factor, to saturation of factors required for tumor cell killing, or
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Mechanisms of resistance to cisplatin

1991
A 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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Cisplatin Resistance Associated with PARP Hyperactivation

Cancer Research, 2013
Abstract 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., Vitale, I., Galluzzi, L., Adam, J., Olaussen, K., Kepp, O., Senovilla, L., Talhaoui, I., Guegan, J., Enot, D., Talbot, M., Robin, A., Girard, Pascal, Orear, C., Lissa, D., Sukkurwala, A., Garcia, P., Behnam-Motlagh, P., Kohno, K., Wu, G., Brenner, Catherine, Dessen, P., Saparbaev, M., Soria, J.-C., Castedo, M., Kroemer, G.   +25 more
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