• Title, Summary, Keyword: cisplatin

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Concurrent Weekly Cisplatin Versus Triweekly Cisplatin with Radiotherapy in the Treatment of Cervical Cancer: A Meta-analysis Result

  • Hu, Yan;Cai, Zhi-Qiang;Su, Xiao-Yan
    • Asian Pacific Journal of Cancer Prevention
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    • v.13 no.9
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    • pp.4301-4304
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    • 2012
  • Aims: To evaluate the adverse effect and survival outcome of weekly and triweekly cisplatin with radiotherapy in treatment of cervical cancer. Methods: After an extensive literature search between 1995-2011, we analyzed 7 studies to compare weekly cisplatin and triweekly cisplatin combined radiotherapy. Results: Our analysis established that weekly cisplatin has a lower risk of hematologic toxicity than triweekly cisplatin with concurrent radiotherapy in the treatment of cervical cancer. However, there were no differences in progression free survival and overall survival between weekly cisplatin and triweekly cisplatin (p>0.05). Conclusions: Weekly cisplatin combined with concurrent radiation has lower risk in hematologic toxicity than triweekly cisplatin, but does not improve survival. Triweekly cisplatin treatment has longer intervals and is therefore more convenient. Clinicians and patients can choose either weekly cisplatin or triweekly cisplatin combined radiotherapy for cervical cancer.

Protective Effects of Vitamin C on Cisplatin Naphrotoxicity

  • Choung, Se-Young;Kong, Jae-Myeong
    • Archives of Pharmacal Research
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    • v.17 no.1
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    • pp.11-16
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    • 1994
  • Cis-dichlorodiammineplatinum(II)(cisplatin) is one of the most effective antitumor agents currently available for cancer therapy. However, its clinical use has been limited by its severe side effects, especially nephrotoxicity. To evaluate the effect or radical scavengers on cisplatin nephrotoxicity in rats, cisplatin and Vitamin C were given intraperitoneally. Remarkable protective effects of Vitamin C against nephrotoxicity of cisplatin were observed when Vitamin C was administered to rats 1hr before cisplatin injection. hepatotoxicity induced by combination treament of cisplatin and Vitamin C was evaluated by measuring serum glutamic pyruvate transmainase(sGPT) and serum glutamic oxalate transminase(sGOT). Combination treatment did not affect the levels of sGPT and sGOT, and any combination treatment did not induce metallothionein biosynthesis in kidny, Vitamin C which has radical scavenging effect induce metallothionein biosynthesis in kidney. Vitamin C which has radical scavenging effect directly reduced nephrotoxicity of cisplatin in vivo. Thus, it seems that free radical is the cause of cisplatin nepthrotoxicity. Also, combination treatment did not reduce anticancer activity of cisplatin. The present results indicate that Vitamin C, when it is given with cisplatin, may provide protection against cisplatin nephrotoxicity without reducing anticancer activity.

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Epigenetic modification of α-N-acetylgalactosaminidase enhances cisplatin resistance in ovarian cancer

  • Ha, Ye-Na;Sung, Hye Youn;Yang, San-Duk;Chae, Yun Ju;Ju, Woong;Ahn, Jung-Hyuck
    • The Korean Journal of Physiology and Pharmacology
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    • v.22 no.1
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    • pp.43-51
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    • 2018
  • Although cisplatin is one of the most effective antitumor drugs for ovarian cancer, the emergence of chemoresistance to cisplatin in over 80% of initially responsive patients is a major barrier to successful therapy. The precise mechanisms underlying the development of cisplatin resistance are not fully understood, but alteration of DNA methylation associated with aberrant gene silencing may play a role. To identify epigenetically regulated genes directly associated with ovarian cancer cisplatin resistance, we compared the expression and methylation profiles of cisplatin-sensitive and -resistant human ovarian cancer cell lines. We identified ${\alpha}$-N-acetylgalactosaminidase (NAGA) as one of the key candidate genes for cisplatin drug response. Interestingly, in cisplatin-resistant cell lines, NAGA was significantly down-regulated and hypermethylated at a promoter CpG site at position +251 relative to the transcriptional start site. Low NAGA expression in cisplatin-resistant cell lines was restored by treatment with a DNA demethylation agent, indicating transcriptional silencing by hyper-DNA methylation. Furthermore, overexpression of NAGA in cisplatin-resistant lines induced cytotoxicity in response to cisplatin, whereas depletion of NAGA expression increased cisplatin chemoresistance, suggesting an essential role of NAGA in sensitizing ovarian cells to cisplatin. These findings indicate that NAGA acts as a cisplatin sensitizer and its gene silencing by hypermethylation confers resistance to cisplatin in ovarian cancer. Therefore, we suggest NAGA may be a promising potential therapeutic target for improvement of sensitivity to cisplatin in ovarian cancer.

Adenovirus-Mediated Antisense Telomerase with Cisplatin Increased the Susceptibility of Cisplatin Resistant Ovarian Cancer Cell Line

  • Kim, Dae-Shick;Song, Joon-Seok;Lee, Kyu-Wan;Kim, Mee-Hye;Kim, Kyung-Tai;Kim, Hysook;Kim, Young-Tae
    • Journal of Microbiology and Biotechnology
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    • v.12 no.5
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    • pp.711-715
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    • 2002
  • Telomerase adds telomeric repeats to chromosomal ends and is known to play an important role in carcinogenesis through cellular immortalization. Since telomerase is an essential pathogenomic factor in malignant tumors, inhibiting telomerase activity is thought to be possible to make telomerase positive tumors more sensitive to cisplatin treatment, which is effective in ovarian cancers, but clinical success Is limited by chemo-resistance. In the present study, cisplatin-sensitive ovarian cancer cell line A2780 and cisplatin-resistant A2780/cp70 cell line were infected with antisense telomerase adenovirus Ad-OA. It was found that the Ad-OA suppressed ovarian cancer cell growth and this effect was mainly due to the induction of caspase-dependent apoptosis. Next, we infected the cisplatin resistant ovarian cancer cell line A2780/ cp70 with Ad-OA and cisplatin concurrently. Interestingly, cisplatin treatment with Ad-Oh was more effective to cisplatin-induced cell death in A2780/cp70 cells compared to cisplatin or the vector group only. These data suggest that cisplatin treatment with Ad-OA may be a new chemo-sensitizer for cisplatin resistant ovarian cancer.

Protective Effect of Brazilin on Cisplatin Nephrotoxicity

  • Kong, Jae-Myeong;Seo, Kyung-Won;Choung, Se-Young
    • Biomolecules & Therapeutics
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    • v.2 no.2
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    • pp.103-107
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    • 1994
  • Cisplatin is one of the most effective antitumor agents currently available for cancer therapy. However, its clinical use has been limited by its severe side effects, especially nephrotoxicity. Therefore, brazilin, which has a radical scavenging effect, was given intraperitoneally to evaluate the effect on cisplatin nephrotoxicity in rats. Remarkable protective effects against nephrotoxicity of cisplatin were observed when brazilin was administered to rats simultaneously with cisplatin. Hepatotoxicity induced by combination treatment of cisplatin and brazilin was evaluated by measuring serum glutamic pyruvate transaminase and serum glutamic oxalate transaminase. Combination treatment did not affect the levels of sGPT and SGOT, and any combination treatment did not induce metallothionein in kidney. Brazilin which has radical scavenging effect directly reduced nephrotoxicity of wisplatin in vivo. Thus, it seems that nephrotoxicity of cisplatin was caused by free radicals. The present results Indicate that brazilin, when it is given with cisplatin, may provide protection against cisplatin nephrotoxicity in rats.

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Studies on the Cisplatin Nephrotoxicity (Cisplatin의 신장독성에 관한 연구)

  • 성하정;이창업;이문한;이영재;류판동;김곤섭
    • Journal of Food Hygiene and Safety
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    • v.8 no.4
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    • pp.189-193
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    • 1993
  • Cisplatin is useful for various cancers including advanced testicular and ovarian cancers. However, clinical use of cisplatin has been limited due to its dose-related neplrotoxicity. Transport studies across the membrane vesicles were performed to study the cisplatin nephrotoxicity. In these experiments, after cisplatin was administered to adult male New Zealand White rabbits, basolateral membrane (BLM) vesicles were prepared from the renal cortex. Para-aminohippurate (PAH) uptakes through BLM vesicles were measured to examine the interactioln of cisplatin on the transports of the substrates. As results of the uptake experiments using the vesicle systems, cisplatin had little effects on PAH transport through BLM vesicle. In conclusion, cisplatin did not cause the damage of basolateral membranes.

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Platinum Transporters and Drug Resistance

  • Choi, Min-Koo;Kim, Dae-Duk
    • Archives of Pharmacal Research
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    • v.29 no.12
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    • pp.1067-1073
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    • 2006
  • Cisplatin, a platinum coordinated complex, is a widely used antineoplastic agent for the treatment of metastatic tumors of the testis, metastatic ovarian tumors, lung cancer, advanced bladder cancer and many other solid tumors. The cytotoxic action of the drug is often thought to be associated with its ability to bind DNA to form cisplatin-DNA adducts. The development of resistance to cisplatin during treatment is common and constitutes a major obstacle to the cure of sensitive tumors. Although to understand the clinically relevant mechanisms of resistance, many studies have been aimed at clarifying the biochemical/molecular alterations of cisplatin-resistance cells, these studies did not conclusively identify the basis of cellular resistance to cisplatin. In this review, cisplatin resistance was discussed in terms of the relevant transporters, such as copper transporters (CTRs), organic cation transporters (OCTs) and multi-drug resistance related transporters (MDRs). These transporters seem to be contributed to cisplatin resistance through the reduction of drug accumulation in the cell. Better understanding the mechanism of cisplatin resistance associated with transporters will provide the useful informations for overcoming the cisplatin resistance.

Preventive Effect of Crude Drug Preparation (E-kong-san) on Cisplatin induced Nephrotoxicity (생약제제인 이공산(異功散)의 Cisplatin 유도 신장독성 보호 효과)

  • Rho, Young-Soo;Ahn, Kyoo-Seok;Chang, Sung-Goo;Jung, Jee-Chang;Lee, Kyung-Tae
    • Korean Journal of Pharmacognosy
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    • v.29 no.3
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    • pp.258-264
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    • 1998
  • Nephroprotective effects of a crude drug-preparation (Ekongsan) were determined from cisplatin induced renal injury in vivo and in vitro. Ekongsan decreased cisplatin induced the cytotoxicity on rabbit kidney proximal tubule and human renal cortical cells by MTT assays and sustained glucose consumption on cisplatin-induced human renal cortical tissue. Levels of creatinine and blood urea nitrogen (BUN) in serum after administration of cisplatin (0.75 mg/kg, i.p.) to Ekongsan (0.75 g/kg/d, p.o.) pretreated rats were markedly lower compared to those of cisplatin-treated rats. Moreover, the administration of Ekongsan significantly inhibited the loss of body weight of cisplatin-injected rats. These findings suggest that Ekongsan is an active prescription in protection against nephrotoxicity of cisplatin.

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Anticancer Effects and Mechanisms of Co-Treatment of Cisplatin with Taurine in MCF-7 Cells (MCF-7에서 Cisplatin과 타우린의 병용처리로 인한 항암효과 및 관련 기전)

  • Kim, Taehee;Kim, An Keun
    • YAKHAK HOEJI
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    • v.57 no.1
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    • pp.18-23
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    • 2013
  • The objective of this study is to evaluate the synergic effects of combined treatment with taurine and cisplatin in human breast cancer, MCF-7 cells. For this study, MCF-7 cells were treated with taurine (5, 10, and 20 mM) and cisplatin (0.5 ${\mu}M$) for 48 and 72 hrs. Co-treatment of cisplatin with taurine decreased cell proliferation more compared with cisplatin alone. Reduced cell proliferation was caused by apoptosis. Therefore we investigated the apoptotic cells. After treatment of cisplatin and taurine, apoptotic cells were slightly increased. Apoptosis-related proteins, cleaved caspases and cytochrome c were increased. The present study suggests that combination treatment of cisplatin with taurine enhance anticancer activity of cisplatin in MCF-7 cells.

ACTIVATION OF NF-$\kappa$B IN THE CISPLATIN-INDUCED APOPTOSIS OF ORAL SQUAMOUS CELL CARCINOMA (구강편평세포암종에서의 Cisplatin 유도 아폽토시스에서의 NF-$\kappa$B의 활성화)

  • Seo, Jong-Chun;Sung, Iel-Yong;Kim, Jong-Roul
    • Journal of the Korean Association of Oral and Maxillofacial Surgeons
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    • v.32 no.2
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    • pp.94-100
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    • 2006
  • Purpose: This study was done to confirm the role of NF-$\kappa$B in cisplatin-induced apoptosis of oral squamous cell carcinoma. Materials and Methods: Five cell lines originated from different oral cancer patients were tested for the apoptosis by the treatment of cisplatin. These cells showed different degree of cisplatin-resistance and the order is OSCC-2>OSCC-3>OSCC-5> OSCC-1>OSCC-4. OSCC-2 and OSCC-4 cells were assayed for the apoptosis by measuring DNA fragmentation and TUNEL staining after cisplatin treatment. While OSCC-4 cells showed apoptosis, OSCC-2 cells showed no or very slight apoptosis by cisplatin treatment. Next, It was determined whether NF-$\kappa$B activation is required in mediating cisplatin-induced apoptosis of OSCC-4. Result: The result was that elevated NF-$\kappa$B activity mediated cisplatin-induced apoptosis. Conclusion: In conclusion, these findings suggest that NF-$\kappa$B activation is essential to cisplatin-induced apoptosis and it may be involved in cisplatin resistance in OSCC cells.