Recent clinical trials using cisplatin, carboplatin and their combination chemotherapy drugs (Review)

Boulikas, Teni; Vougiouka, Maria

doi:10.3892/or.11.3.559

Cited by 162 publications

(162 citation statements)

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“…However, its clinical use is limited by the onset of severe side effects, such as nephrotoxicity, ototoxicity, bone marrow toxicity, gastrointestinal toxicity, and peripheral neuropathy (Boulikas, 2004;Boulikas and Vougiouka, 2004;Hartmann and Lipp, 2003).…”

Section: Introductionmentioning

confidence: 99%

Epicatechin protects the auditory organ by attenuating cisplatin-induced ototoxicity through inhibition of ERK

et al. 2010

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Section: Introductionmentioning

confidence: 99%

Epicatechin protects the auditory organ by attenuating cisplatin-induced ototoxicity through inhibition of ERK

et al. 2010

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“…1 Cisplatin forms covalent bonds to the N7 positions of DNA purines to form intra-or interstrand crosslinks, and DNA is generally acknowledged as the primary target of cisplatin. 2,3 Cisplatin is a commonly used model agent for induction of DNA damage-dependent apoptosis in vitro.…”

mentioning

confidence: 99%

Acute apoptosis by cisplatin requires induction of reactive oxygen species but is not associated with damage to nuclear DNA

Berndtsson

Hägg

Panaretakis

et al. 2006

Intl Journal of Cancer

196

162

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Cisplatin is a broad-spectrum anticancer drug that is also widely used in experimental studies on DNA damage-induced apoptosis. Induction of apoptosis within 24-48 hr requires cisplatin concentrations that are at least one order of magnitude higher than the IC 50 . Here, we show that such high, apoptosis-inducing cisplatin concentrations induce cellular superoxide formation and that apoptosis is inhibited by superoxide scavengers. The same concentration limit and the requirement for superoxide are also true for induction of caspase activation in enucleated cells (cytoplasts), showing that cisplatin-induced apoptosis occurs independently of nuclear DNA damage. In contrast, lower cisplatin concentrations, which do not induce acute apoptosis, are sufficient for induction of DNA damage signaling. We propose that the antiproliferative effects of cisplatin at IC 50 doses involve premature senescence and secondary, nonstress-induced apoptosis. The higher doses currently used in in vitro studies lead to acute, stress-induced apoptosis that involves induction of superoxide but is largely DNA damage-independent. ' 2006 Wiley-Liss, Inc.Key words: cisplatin; DNA damage; apoptosis; senescence Cis-diamminedichloroplatinum (II) (cisplatin) is a commonly used anticancer agent, especially effective in the treatment of testicular carcinoma and also used to treat other malignancies such as ovarian, cervix, head-and-neck and small-cell lung cancer. 1 Cisplatin forms covalent bonds to the N7 positions of DNA purines to form intra-or interstrand crosslinks, and DNA is generally acknowledged as the primary target of cisplatin. 2,3 Cisplatin is a commonly used model agent for induction of DNA damage-dependent apoptosis in vitro. Acute apoptosis is induced within 24-36 hr, and major efforts have been performed to elucidate apoptotic signaling pathways induced by cisplatin within this time frame. These various studies have highlighted the roles of c-ABL, stressactivated protein kinases and p53 as downstream mediators of cisplatin-induced DNA damage and as mediators of apoptotic signaling (recently reviewed in 3 ). In addition to induction of apoptosis, cisplatin also induces premature senescence. 4 Premature senescence is currently thought to be related to replicative senescence, which has been demonstrated to be a DNA damage response. 5 During replicative senescence, signaling pathways involving ATM (Ataxia telangiectasia mutated) and p53 are activated by telomere uncapping. 5,6 The same signaling mechanisms are believed to be involved in premature senescence induced by DNA damaging drugs. 6,7 Apoptosis and senescence are obviously mutually exclusive cellular outcomes. The factors that decide whether cisplatin will trigger apoptosis or senescence are not clearly understood. In one scenario, senescence and apoptosis represent graded responses to increasing DNA damage. In more complex scenarios, cisplatin induces senescence and apoptosis by different (or partially different) mechanisms.As inducer of apoptosis, cisplatin is used at very d...

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“…Predetermined amounts of ɛ-caprolactone and 1,5-pentanediol (co-initiator) and 0.02 mol % of Sn(Oct) 2 were introduced into a preheated (150°C) 50-mL three-neck round-bottomed flask. The reaction was carried out at 150°C for 5 h under argon atmosphere.…”

Section: Synthesis Of Poly(citric Acid)-block-polycaprolactone-block-mentioning

confidence: 99%

“…PCA-PCL-PCA was synthesized by a previously reported procedure [28] as follows: firstly, poly(ɛ-caprolactone) was synthesized by ring-opening polymerization catalyzed by Sn(Oct) 2 . Predetermined amounts of ɛ-caprolactone and 1,5-pentanediol (co-initiator) and 0.02 mol % of Sn(Oct) 2 were introduced into a preheated (150°C) 50-mL three-neck round-bottomed flask.…”

Section: Synthesis Of Poly(citric Acid)-block-polycaprolactone-block-mentioning

confidence: 99%

“…Cisplatin is one of the most potent anticancer agents available today and is widely used in the treatment of many malignancies, including testicular, ovarian, bladder, head and neck, small cell and nonsmall cell lung cancers [1,2] because of its potent activity to cross-link DNA upon entering the cells. It preferentially binds to the N7 atoms of guanine bases in DNA double-helix strands, thereby preventing the strands from uncoiling and separating.…”

Section: Introductionmentioning

confidence: 99%

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Polymer–metal complex nanoparticles-containing cisplatin and amphiphilic block copolymer for anticancer drug delivery

Gheybi

Niknejad

Entezami

2013

Designed Monomers and Polymers

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Polymer-metal complex nanoparticles-containing cisplatin (cis-dichlorodiammineplatinum(II)), an anticancer drug, was prepared by a ligand-exchange reaction of cisplatin with core-shell-type poly(citric acid)-b-poly(caprolactone)-b-poly(citric acid) (PCA-PCL-PCA). The resulting polymer-platinum complex nanoparticles showed a high loading capacity (up to 44.2% w/w). The TEM observation confirmed that the nanoparticles with spherical shape were formed by the mixing of PCA-PCL-PCA copolymer and cisplatin. According to TEM and DLS, polymer-cisplatin complex nanoparticles showed larger diameters compared with empty block copolymer attributed to some intermolecular crosslinkings through polymer-platinum (II) complex formation. The release profile of the platinum (II) complexes in phosphate-buffered saline medium at 37°C indicated sustained manner of drug release. In vitro cytotoxicity evaluated by MTT assay, demonstrated that the PCA-PCL-PCA block copolymer does not exhibit apparent cytotoxicity. PCA-PCL-PCA-cisplatin complex nanoparticles showed greater cytotoxicity to HeLa cell line contrasted with free cisplatin, attributed to existence of poly (citric acid) moiety.

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Recent clinical trials using cisplatin, carboplatin and their combination chemotherapy drugs (Review)

Cited by 162 publications

References 0 publications

Epicatechin protects the auditory organ by attenuating cisplatin-induced ototoxicity through inhibition of ERK

Epicatechin protects the auditory organ by attenuating cisplatin-induced ototoxicity through inhibition of ERK

Acute apoptosis by cisplatin requires induction of reactive oxygen species but is not associated with damage to nuclear DNA

Polymer–metal complex nanoparticles-containing cisplatin and amphiphilic block copolymer for anticancer drug delivery

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