Particular aspects of platinum compounds used at present in cancer treatment

Desoize, B; Madoulet, Claudie

doi:10.1016/s1040-8428(01)00219-0

Cited by 341 publications

(224 citation statements)

References 40 publications

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“…The PK of carboplatin is linear and often described by a polyexponential decline [27]. Compared to carboplatin, which is relatively short, the platinum-DNA adducts, a reactive form of carboplatin, are stable on the time scale of days to weeks [28,29].…”

Section: Discussionmentioning

confidence: 99%

Pharmacodynamic model for chemotherapy-induced anemia in rats

Woo

Krzyzanski

Jusko

2007

Cancer Chemother Pharmacol

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Anticancer agents often cause bone marrow toxicity resulting in progressive anemia which may influence the therapeutic effects of erythropoietic-stimulating agents. The objective of this study was to develop a pharmacodynamic (PD) model to describe chemotherapy-induced anemia in rats. Anemia was induced in male Wistar rats with a single intravenous (i.v.) injection of 60 mg/kg carboplatin. Hematological responses including reticulocytes, red blood cells (RBC), hemoglobin, and endogenous rat erythropoietin (EPO) were measured for up to 4 weeks. A catenary, lifespanbased, indirect response model served as a basic PD model to represent erythroid cellular populations in the bone marrow and blood involved in erythropoiesis. The model assumed that actively proliferating progenitor cells in the bone marrow are sensitive to anti-cancer agents and subject to an irreversible removal process. The removal rate of the target cells is proportional to drug activity concentrations and the cell numbers. An additional RBC loss from the circulation resulting from thrombocytopenia was described by a first-order process. The turnover process of rat EPO and EPOmediated feedback inhibition mechanism regulated by hemoglobin changes were incorporated. Reticulocyte counts decreased rapidly and reached a nadir by day 3 after administration of carboplatin and returned to the baseline by day 13. This was followed by a gradual increase and the rebound peak occurred at about day 15. The hemoglobin nadir was approximately 9 g/dl observed at about 11-13 days compared to its normal value of 13 g/dl and hemoglobin returned to the baseline by day 30. The increase in endogenous rat EPO mirrored inversely hemoglobin changes and the maximum increase was observed soon after the hemoglobin nadir. The carboplatin-treated rats exhibited progressive anemia. The proposed model adequately described the time course of hematological changes after carboplatin in rats and can be a useful tool to explore potential strategies for the management of anemia caused by chemotherapy.

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Section: Discussionmentioning

confidence: 99%

Pharmacodynamic model for chemotherapy-induced anemia in rats

Woo

Krzyzanski

Jusko

2007

Cancer Chemother Pharmacol

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“…Numerous reports have gradually clarified the major pathways involved in CDDP resistance. Cells can become resistant to CDDP through reduced drug uptake, enhanced drug detoxification, augmented DNA repair, and increased tolerance for DNA damage (Desoize and Madoulet, 2002). The mechanisms of oxaliplatin resistance are less well established and should never be considered identical to those underlying CDDP resistance because CDDP chemistry is not necessarily applicable for oxaliplatin.…”

mentioning

confidence: 99%

Combined modalities of resistance in an oxaliplatin-resistant human gastric cancer cell line with enhanced sensitivity to 5-fluorouracil

Chen

Tsou

et al. 2007

Br J Cancer

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To identify mechanisms underlying oxaliplatin resistance, a subline of the human gastric adenocarcinoma TSGH cell line, S3, was made resistant to oxaliplatin by continuous selection against increasing drug concentrations. Compared with the parental TSGH cells, the S3 subline showed 58-fold resistance to oxaliplatin; it also displayed 11-, 2-, and 4.7-fold resistance to cis-diammine-dichloroplatinum (II) (CDDP), copper sulphate, and arsenic trioxide, respectively. Interestingly, S3 cells were fourfold more susceptible to 5-fluorouracilinduced cytotoxicity due to downregulation of thymidylate synthase. Despite elevated glutathione levels in S3 cells, there was no alteration of resistant phenotype to oxaliplatin or CDDP when cells were co-treated with glutathione-depleting agent, l-buthionine-(S,R)-sulphoximine. Cellular CDDP and oxaliplatin accumulation was decreased in S3 cells. In addition, amounts of oxaliplatin-and CDDP -DNA adducts in S3 cells were about 15 and 40% of those seen with TSGH cells, respectively. Western blot analysis showed increased the expression level of copper transporter ATP7A in S3 cells compared with TSGH cells. Partial reversal of the resistance of S3 cells to oxaliplatin and CDDP was observed by treating cell with ATP7A-targeted siRNA oligonucleotides or P-type ATPaseinhibitor sodium orthovanadate. Besides, host reactivation assay revealed enhanced repair of oxaliplatin-or CDDP-damaged DNA in S3 cells compared with TSGH cells. Together, our results show that the mechanism responsible for oxaliplatin and CDDP resistance in S3 cells is the combination of increased DNA repair and overexpression of ATP7A. Downregulation of thymidylate synthase in S3 cells renders them more susceptible to 5-fluorouracil-induced cytotoxicity. These findings could pave ways for future efforts to overcome oxaliplatin resistance.

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“…After an intravenous infusion, metal-based anticancer compounds form a variety of hydrolyzed intermediates in the blood (Desoize & Madoulet, 2002;Alessio et al, 2004). These reactive species become rapidly partitioned into plasma protein-bound metal, free plasma metal, tissue metal, white blood cell metal, and erythrocyte-sequestered metal.…”

Section: Metal-based Anticancer Agents In Biological Fluids/cellsmentioning

confidence: 99%

The application of inductively coupled plasma mass spectrometry in clinical pharmacological oncology research

Brouwers

Tibben

Rosing

et al. 2008

Mass Spectrometry Reviews

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Metal-based anticancer agents are frequently used in the treatment of a wide variety of cancer types. The monitoring of these anticancer agents in biological samples is important to understand their pharmacokinetics, pharmacodynamics, and metabolism. In addition, determination of metals originating from anticancer agents is relevant to assess occupational exposure of health care personnel working with these drugs. The high sensitivity of inductively coupled plasma mass spectrometry (ICP-MS) has resulted in an increased popularity of this technique for the analysis of metal-based anticancer drugs. In addition to the quantitative analysis of the metal of interest in a sample, ICP-MS can be used as an ultrasensitive metal selective detector in combination with speciation techniques such as liquid chromatography. In the current review we provide a systematic survey of publications describing the analysis of platinum-and ruthenium-containing anticancer agents using ICP-MS, focused on the determination of total metal concentrations and on the speciation of metal compounds in biological fluids, DNA-and protein-adducts, and environmental samples. We conclude that ICP-MS is a powerful tool for the quantitative analysis of metal-based anticancer agents from multiple sample sources.

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Particular aspects of platinum compounds used at present in cancer treatment

Cited by 341 publications

References 40 publications

Pharmacodynamic model for chemotherapy-induced anemia in rats

Pharmacodynamic model for chemotherapy-induced anemia in rats

Combined modalities of resistance in an oxaliplatin-resistant human gastric cancer cell line with enhanced sensitivity to 5-fluorouracil

The application of inductively coupled plasma mass spectrometry in clinical pharmacological oncology research

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