Ototoxicity of the New Platinum AnticancerAgent TRK-710 in Comparison with Cisplatin

Saito, Takehisa; Manabe, Yasuhiro; Saitô, Hitoshi

doi:10.1159/000276752

Cited by 7 publications

(4 citation statements)

References 13 publications

(16 reference statements)

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“…16,128 A Phase I trial showed that TRK-710 displayed lower nephrotoxicity and myelosuppression compared with cisplatin. 129 No other Phase I or II results have been reported.…”

Section: Miboplatinmentioning

confidence: 99%

The status of platinum anticancer drugs in the clinic and in clinical trials

et al. 2010

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Since its approval in 1979 cisplatin has become an important component in chemotherapy regimes for\ud the treatment of ovarian, testicular, lung and bladder cancers, as well as lymphomas, myelomas and\ud melanoma. Unfortunately its continued use is greatly limited by severe dose limiting side effects and\ud intrinsic or acquired drug resistance. Over the last 30 years, 23 other platinum-based drugs have entered\ud clinical trials with only two (carboplatin and oxaliplatin) of these gaining international marketing\ud approval, and another three (nedaplatin, lobaplatin and heptaplatin) gaining approval in individual\ud nations. During this time there have been more failures than successes with the development of 14 drugs\ud being halted during clinical trials. Currently there are four drugs in the various phases of clinical trial\ud (satraplatin, picoplatin, LipoplatinTM and ProLindacTM). No new small molecule platinum drug has\ud entered clinical trials since 1999 which is representative of a shift in focus away from drug design and\ud towards drug delivery in the last decade. In this perspective article we update the status of platinum\ud anticancer drugs currently approved for use, those undergoing clinical trials and those discontinued\ud during clinical trials, and discuss the results in the context of where we believe the field will develop over\ud the next decade

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“…16,128 A Phase I trial showed that TRK-710 displayed lower nephrotoxicity and myelosuppression compared with cisplatin. 129 No other Phase I or II results have been reported.…”

Section: Miboplatinmentioning

confidence: 99%

The status of platinum anticancer drugs in the clinic and in clinical trials

et al. 2010

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“…Typically, it is initiated in the outer hair cells (OHCs), followed by the inner hair cells (IHCs). Hair cell damage begins at the basal turn of the cochlea and spreads gradually to the apex in vivo with an increasing drug dose [7]. In addition to damaging the hair cells, cisplatin also damages spiral ganglion neurons in the modiolus and the marginal epithelium on the stria vascularis [8,9,10].…”

Section: Introductionmentioning

confidence: 99%

Low, but Not High, Doses of Cisplatin Damage Cochlear Hair Cells in C57 Mouse Organotypic Cultures

Zeng

Xianlin²,

Chen³

et al. 2016

ORL

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Aims: The purpose of this study was to investigate the characteristics of cisplatin-induced C57 mouse cochlear hair cell damage in vitro. Methods: Forty-seven cochleae harvested from 2- to 4-day-old C57 mice were used. Forty specimens were treated with different concentrations of cisplatin (10, 25, 50, 100, 400, and 1,000 μmol/l) for 48 h. The remaining seven specimens were used as a control group. Results: The rate of hair cell loss increased from 14.5 to 78.4% over cisplatin concentrations of 10 to 100 μmol/l, whereas hair cell loss decreased to 48.8 and 8.77% at concentrations of 400 and 1,000 μmol/l, respectively. Apoptosis was detected by DAPI staining in the areas of hair cell damage. Hair cell loss rates differed significantly among the cisplatin-treated groups. Linear regression analysis of cisplatin dose versus hair cell number showed a significant negative correlation for cisplatin doses up to 100 μmol/l and a positive correlation with further increases up to 1,000 μmol/l. Conclusions: We conclude that cisplatin-induced hair cell damage was concentration dependent only up to a certain dose and that injury resistance may occur in cochlear cells treated with higher doses of cisplatin.

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“…[27][28][29] Moreover, a phase I trial in Japan showed that the new platinum analogue, TRK-710, has a lesser degree of nephrotoxicity and myelosuppression. 30) Both cisplatin and carboplatin cause hematopoietic disorders as side effects, [26][27][28][29] and they are administered intravenously.…”

mentioning

confidence: 99%

Release of Cytokines from Human Umbilical Vein Endothelial Cells Treated with Platinum Compounds in vitro

Shi¹,

Inoue²,

Shinozaki³

et al. 1998

Japanese Journal of Cancer Research

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Endothelial cells (EC) produce cytokines, such as interleukin (IL)-1, IL-6, IL-8 and granulocytemacrophage colony-stimulating factor (GM-CSF). These cytokines have an important role in the proliferation and differentiation of hematopoietic progenitor cells. On the other hand, anticancer agents generally cause hematopoietic disorders. However, little is known about the effects of chemotherapeutic agents on the secretion of cytokines from EC. Therefore, we investigated if treatment with platinum compounds may stimulate EC to secrete cytokines. EC newly isolated from a human umbilical vein were exposed to cisplatin, carboplatin, or TRK-710 for 80 min, then the cells were washed and placed in fresh medium. The levels of cytokines in the fresh medium were measured by the ELISA method, the levels of intracellular hydrogen peroxide (H 2 O 2 ) were measured by flow cytometry, and the rhodamine 123-stained live mitochondria of the EC were observed under a confocal laser microscope. Platinum compounds induced cytokine production in human EC: cisplatin most prominently induced the release of IL-1 and IL-6, and TRK-710 had the greatest ability to induce the release of GM-CSF. Intracellular H 2 O 2 production and IL-8 release were transiently induced immediately after treatment with platinum compounds, leading to IL-1 release when H 2 O 2 production was eliminated. These results may provide new insights into the hematological toxicity induced by anticancer agents and the role of IL-1 and IL-6 secreted from EC in this toxicity.

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Ototoxicity of the New Platinum AnticancerAgent TRK-710 in Comparison with Cisplatin

Cited by 7 publications

References 13 publications

The status of platinum anticancer drugs in the clinic and in clinical trials

The status of platinum anticancer drugs in the clinic and in clinical trials

Low, but Not High, Doses of Cisplatin Damage Cochlear Hair Cells in C57 Mouse Organotypic Cultures

Release of Cytokines from Human Umbilical Vein Endothelial Cells Treated with Platinum Compounds in vitro

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