Charles F. Kettring prize. Fundamental studies with cisplatin

Rosenberg, Barnett

doi:10.1002/1097-0142(19850515)55:10<2303::aid-cncr2820551002>3.0.co;2-l

Cited by 482 publications

(187 citation statements)

References 34 publications

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“…It reacts with DNA to form DNA adducts, which are DNAintrastrand and DNA-interstrand cross-links. Cisplatin is both a mutagen and carcinogen (18)(19)(20)(21)(22).…”

Section: Discussionmentioning

confidence: 99%

The frequencies of micronuclei induced by cisplatin in newborn rat astrocytes are increased by 50-Hz, 7.5- and 10-mT electromagnetic fields

Miyakoshi

Yoshioka

Toyama

et al. 2005

Environ Health Prev Med

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Objectives: Epidemiological studies have suggested that exposure to environmental and occupational electromagnetic fields (EMFs) contribute to the induction of brain tumors, leukemia, and other neoplasms. The aim of this study was to investigate the genotoxic effects of exposure to 50-Hz EMFs, and of co-exposure to cisplatin, a mutagen and carcinogen, and 50-Hz EMFs, using an in vivo newborn rat astrocyte micronucleus assay.Methods: Three day-old male Sprague-Dawley rats were co-exposed to 50-Hz EMFs and 1.25 or 2.5 mg/kg of cisplatin. Brain cells were dissociated into single cells and cultured for 96 hours, then stained with acridine orange and an antibody against glial fibrillary acidic protein. The frequency of micronucleated astrocytes was counted with a fluorescent microscope.Results: The frequency of micronuclei was not increased in rat astrocytes exposed to EMFs alone. However, the frequencies of micronuclei in co-exposure to 2.5 mg/kg cisplatin and EMFs (7.5-and 10-mT) were significantly increased, compared with those in exposure to 2.5 mg/kg cisplatin alone (shamexposure, 0-mT EMFs) for 72 hours (p<0.01).Conclusion: Exposure to EMFs alone did not have a genotoxic effect but co-exposure to EMFs increased the genotoxic activity induced by cisplatin. Our findings suggest that EMFs enhance the genotoxic effects of cisplatin.

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“…It reacts with DNA to form DNA adducts, which are DNAintrastrand and DNA-interstrand cross-links. Cisplatin is both a mutagen and carcinogen (18)(19)(20)(21)(22).…”

Section: Discussionmentioning

confidence: 99%

The frequencies of micronuclei induced by cisplatin in newborn rat astrocytes are increased by 50-Hz, 7.5- and 10-mT electromagnetic fields

Miyakoshi

Yoshioka

Toyama

et al. 2005

Environ Health Prev Med

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“…The damaged DNA elicits DNA repair mechanism. Cisplatin is a very strong anticancer drug but the full therapeutic exploitation of cisplatin is limited owing to its toxicity in healthy tissues (Rosenberg, 2006;Kumari et al, 2010). The selective delivery of cisplatin to tumor cells would considerably reduce drug toxicity, and improve its therapeutic index.…”

Section: Cisplatinmentioning

confidence: 99%

PLGA-Based Nanoparticles as Cancer Drug Delivery Systems

Mirakabad

Nejati-Koshki²,

Akbarzadeh³

et al. 2014

Asian Pacific Journal of Cancer Prevention

411

154

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“…For our study, we chose the LoVo Dx model because, if compared with the LoVo parental cell line, it presents a higher level of c-myb expression (Melani et al, 1991). Specifically, we investigated whether the inhibition of a growth-promoting gene such as cmyb affected the antineoplastic activity of cisplatin (CDDP), a chemotherapeutic agent widely used in the treatment of several solid human malignancies (Rosenberg, 1985), including colon carcinoma (Scheithauer et al, 1991;Rowinsky et al, 1991).…”

mentioning

confidence: 99%

Effect of cisplatin and c-myb antisense phosphorothioate oligodeoxynucleotides combination on a human colon carcinoma cell line in vitro and in vivo

Bufalo¹,

Cucco²,

Leonetti³

et al. 1996

Br J Cancer

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Summary We investigated the effect of c-myb antisense phosphorothioate oligodeoxynucleotides [(S)ODNs] and cisplatin (CDDP) combination on the human colon carcinoma cell line LoVo Dx both in vitro and in nude mice bearing LoVo Dx solid tumour. We show that antisense (S)ODN treatment decreases c-myb mRNA and protein expression, induces growth arrest in the GI phase of the cell cycle, and inhibits cell proliferation. In vivo treatment with c-myb antisense (S)ODNs results in a reduction in tumour growth. A greater inhibition of cell proliferation in vitro and a higher increase of tumour growth inhibition and growth delay in vivo were obtained with the combination of (S)ODNs and CDDP than when the two agents were administered separately. This comparative study, using the same tumour cell line in vitro and in vivo, suggests that c-myb antisense (S)ODNs might be useful in the therapy of colon cancer in combination with antineoplastic drugs.

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Charles F. Kettring prize. Fundamental studies with cisplatin

Cited by 482 publications

References 34 publications

The frequencies of micronuclei induced by cisplatin in newborn rat astrocytes are increased by 50-Hz, 7.5- and 10-mT electromagnetic fields

The frequencies of micronuclei induced by cisplatin in newborn rat astrocytes are increased by 50-Hz, 7.5- and 10-mT electromagnetic fields

PLGA-Based Nanoparticles as Cancer Drug Delivery Systems

Effect of cisplatin and c-myb antisense phosphorothioate oligodeoxynucleotides combination on a human colon carcinoma cell line in vitro and in vivo

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