Cisplatin Generates Superoxide Anion by Interaction with DNA in a Cell-Free System

Masuda, Hiroto; Tanaka, Toshiko; Takahama, Umeo

doi:10.1006/bbrc.1994.2306

Cited by 241 publications

(134 citation statements)

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“…Yokomizo et al (18) showed that several human bladder and prostatic cancer cell lines with high thioredoxin levels were associated with the resistance to cisplatin, mitomycin C, doxorubicin, and etoposide. Cisplatin produces superoxide anions when it reacts with its target DNA in a cell-free system (34). Mitomycin C, doxorubicin, and etoposide are also thought to induce oxidative stress (18).…”

Section: Discussionmentioning

confidence: 99%

High Thioredoxin Expression Is Associated with Resistance to Docetaxel in Primary Breast Cancer

Kim

Miyoshi

Taguchi

et al. 2005

Clinical Cancer Research

161

115

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Purpose: Thioredoxin overexpression is suggested to be associated with resistance to several chemotherapeutic agents in vitro. In the present study, it has been studied whether or not high thioredoxin expression is associated with resistance to docetaxel therapy in breast cancer patients. Patients and Methods: Sixty-three primary breast cancer patients were treated with docetaxel (60 mg/m 2 , q3w) for four cycles in the neoadjuvant setting. Expression of thioredoxin, estrogen receptor (ER), p53, BRCA-1, and Bcl-2 in tumor tissues obtained before docetaxel therapy was studied by immunohistochemistry (thioredoxin, p53, BRCA-1, and Bcl-2) and enzyme immunoassay (ER), and relationship of expression of these biomarkers with a pathologic response was investigated.Results: There was no significant correlation between the expression of p53, BRCA-1, or Bcl-2 and a response to docetaxel. However, tumors with high thioredoxin expression showed a significantly lower response rate (0%) than those with low thioredoxin expression (30.6%; P = 0.018) and ER-negative tumors showed a significantly higher response rate (32.4%) than ER-positive tumors (10.7%; P = 0.043).Thioredoxin expression significantly increased after docetaxel therapy (mean, 56.1%) as compared with that before docetaxel therapy (mean, 28.6%; P < 0.0001) but there was no significant association between the extent of increase in thioredoxin expression and response. Conclusion: High thioredoxin expression in prechemotherapy tumor samples, but not the increase in thioredoxin expression induced by docetaxel, is associated with resistance to docetaxel in breast cancer.Thioredoxin and ER might be clinically useful in the prediction of a response to docetaxel. Docetaxel, which belongs to taxanes, is one of the most powerful anticancer drugs for breast cancer, and an increasing number of breast cancer patients have been treated with docetaxel not only in the metastatic setting but also in the adjuvant setting, and more recently, in the neoadjuvant setting. The response rate of docetaxel, however, is f50% even in the first-line chemotherapy and it decreases to 20% to 30% in the second-or third-line chemotherapy (1 -3). Therefore, it is of vital importance to select the patients who are very likely to respond to docetaxel to eliminate the unnecessary treatment.

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Section: Discussionmentioning

confidence: 99%

High Thioredoxin Expression Is Associated with Resistance to Docetaxel in Primary Breast Cancer

Kim

Miyoshi

Taguchi

et al. 2005

Clinical Cancer Research

161

115

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“…Finally, the cisplatin-induced cytotoxicity seems to be closely associated with the increased production of reactive oxygen species (ROS) [15] and ROS contribute to cell death partly through effects on various cellular signalling pathways, including the mitogen-activated protein kinase (MAPK) pathway [16].…”

Section: Muscella Et Al -Role Of Egfr In Cisplatin-treated Cells -4mentioning

confidence: 99%

Functions of epidermal growth factor receptor in cisplatin response of thyroid cells

Muscella

Urso

Calabriso

et al. 2009

Biochemical Pharmacology

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“…DDP is highty mutagenic, causing sister-chromatid exchange and chromosomal aberrations in cultured mammalian cells, mouse bone marrow cells, and peripheral blood lymphocytes of patients (Kliesch and Adler, 1987;Adler and El-Tarras, 1989;Ohe et al, 1990;Osanto et al, 1991;Krishnaswamy and Dewey, 1993). The generation of free radicals is believed to be an important mechanism in the development of DDP toxicity (Masuda et al, 1994;Baliga et al, 1998).…”

Section: Introductionmentioning

confidence: 99%

Anticlastogenic effect of vitamin C on cisplatin in vivo

1999

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The ability of vitamin C (VC) to protect against the clastogenic action of the chemotherapeutic agent cisplatin (DDP, cis-diamminedichloroplatinun II) in rat bone marrow cells was evaluated. DDP was administered to Wistar rats either alone or after treatment with VC. The rats were treated with VC (50, 100 or 200 mg/kg body weight) by gavage 10 min before the administration of DDP (5 mg/kg body weight, ip) and then sacrificed 24 h after treatment. VC significantly reduced (by about 70%) the clastogenicity of DDP in rat bone marrow cells. The antioxidant action of VC presumably modulates the clastogenic action of DDP.
Neste estudo foi avaliado o efeito protetor da vitamina C (VC) sobre a ação clastogênica da cisplatina (DDP) em células da medula óssea de ratos. A DDP, um agente quimioterápico, foi injetada em ratos Wistar sozinha ou após o tratamento com a VC. Os animais foram tratados com VC (50, 100 or 200 mg/kg de peso corporal) por gavagem 10 min antes da administração intraperitoneal de DDP (5 mg/kg de peso corporal). Os resultados obtidos mostraram que a VC foi efetiva na redução estatisticamente significativa da clastogenicidade da DDP em ratos Wistar (aproximadamente 70%). O efeito antioxidante da VC foi proposto para explicar a modulação da ação clastogênica da DDP

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Cisplatin Generates Superoxide Anion by Interaction with DNA in a Cell-Free System

Cited by 241 publications

References 0 publications

High Thioredoxin Expression Is Associated with Resistance to Docetaxel in Primary Breast Cancer

High Thioredoxin Expression Is Associated with Resistance to Docetaxel in Primary Breast Cancer

Functions of epidermal growth factor receptor in cisplatin response of thyroid cells

Anticlastogenic effect of vitamin C on cisplatin in vivo

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