Dose escalation study of docetaxel and nedaplatin in patients with relapsed or refractory squamous cell carcinoma of the esophagus pretreated using cisplatin, 5-fluorouracil, and radiation

Yoshioka, Takashi; Sakayori, Masato; Kato, Shunsuke; Chiba, Natsuko; Miyazaki, Shukichi; Nemoto, Kenji; Shibata, Hiroyuki; Shimodaira, Hideki; Ohtsuka, Kazunori; Kakudo, Yuichi; Sakata, Yuh; Ishioka, Chikashi

doi:10.1007/s10147-006-0610-5

Cited by 24 publications

(18 citation statements)

References 26 publications

(38 reference statements)

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“…Clinically, an association has been observed between NDP and an improved response in DDP-resistant cancer (13,30,31). Therefore, in the present study, the effect of NDP on A549DDP cells was analyzed by in vitro experimentation, which has not yet been verified in any previous findings.…”

mentioning

confidence: 73%

Nedaplatin sensitization of cisplatin-resistant human non-small cell lung cancer cells

et al. 2016

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Abstract. Cisplatin (DDP) has been one of the most widely used chemotherapy drugs for advanced non-small cell lung cancer. However, the increase in the number of DDP-resistant cancer cells has become a major impediment in the clinical management of cancer. In the present study, for the first time, the 3-(4,5-dimethylthiazol-2yl)-2,5-diphenyltetrazolium bromide assay was used to demonstrate that nedaplatin (NDP) could have a stronger inhibitory effect than DDP alone in DDP-resistant A549 (A549DDP) cells and that it could attenuate the resistance of these cells. Additionally, flow cytometry analysis showed that the apoptosis rate of these resistant cells when exposed to NDP was markedly increased and the number of cells in the G2 stage of the cell cycle was significantly increased. Furthermore, western blot analysis indicated that NDP decreased the protein expression of P-glycoprotein, tumor protein p53 and B-cell lymphoma 2, and increased the expression of Bcl-2-associated X protein, all of which could possibly improve the NDP intracellular drug concentration and promote cell apoptosis. These observations suggested that NDP could have higher efficacy in DDP-resistant lung cancer cells, and further studies applying more detailed analyses are warranted to elucidate the mechanism(s) behind this effect.

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confidence: 73%

Nedaplatin sensitization of cisplatin-resistant human non-small cell lung cancer cells

et al. 2016

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“…The reasons why we adopted this protocol were as follows: (1) Yoshioka et al [23] reported the optimum dosing of docetaxel and nedaplatin was 30 mg/m 2 and 80 mg/m 2 , respectively, in the phase I study.…”

Section: Treatment Schedulementioning

confidence: 99%

“…In a phase II clinical study of single-agent nedaplatin for esophageal cancer, the overall response rate was 51.7% (15/29) [22]. Yoshioka et al [23] evaluated the feasibility of combination chemotherapy using docetaxel and nedaplatin for recurrent ESCC, and achieved complete and partial responses in 3.6 and 35.7% of patients, respectively. Combination chemotherapy using docetaxel and nedaplatin was recently suggested as a treatment for recurrent ESCC in outpatient settings [24].…”

Section: Introductionmentioning

confidence: 99%

Second-line combination chemotherapy with docetaxel and nedaplatin for metastatic or recurrent squamous cell carcinoma of the esophagus refractory to chemotherapy with 5-fluorouracil plus cisplatin

et al. 2011

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Background There is no standard second-line chemotherapy regimen after failure of the standard 5-fluorouracil and cisplatin in the treatment of esophageal cancer. We retrospectively investigated the efficacy and toxicity of combination chemotherapy using docetaxel and nedaplatin for patients with metastatic or recurrent squamous cell carcinoma of the esophagus refractory to prior chemotherapy with 5-fluorouracil and cisplatin, and evaluated the prognostic significance of clinical factors in these patients. Methods Patients received docetaxel (30 mg/m 2 intravenously) on day 1 and subsequently nedaplatin (40 mg/m 2 intravenously) on day 1 of each 2-week period thereafter. We analyzed the response rate, progression-free survival time, overall survival and toxicity in 30 patients treated with combination therapy using docetaxel and nedaplatin. Background characteristics at the time of initiating the combination chemotherapy were analyzed as prognostic factors. Results A median of four cycles (range 1-20) were administered to 30 patients. The median follow-up was 6.7 months (range 0.8-39.4). Of 27 patients with measurable lesions, 5 had a partial response, 10 had stable disease and 12 had progressive disease. The median progressionfree survival and overall survival was 2.5 and 7.5 months, respectively. Grade 3-4 toxicities were leukocytopenia (13.3%), neutropenia (23.3%), anemia (23.3%), thrombocytopenia (3.3%), anorexia (6.6%) and fatigue (3.3%). Multivariate analysis revealed that the inflammation-based Glasgow prognostic score was an independent negative prognostic factor for overall survival. Conclusions The combination chemotherapy with docetaxel and nedaplatin is a feasible and promising regimen as a second-line therapy in metastatic or recurrent esophageal cancer refractory to chemotherapy with 5-fluorouracil and cisplatin.

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“…Nedaplatin exerts anti-tumor effects following uptake into tumor cells by binding to DNA bases and inhibiting DNA replication, similar to cisplatin and carboplatin (5). However, the ability of cancer cells to become resistant to nedaplatin remains a notable obstacle to successful chemotherapy; resistance of numerous species of cancer cells to nedaplatin can be reversed by combining with chemotherapeutic agents, including 5-fluorouracil, docetaxel and vindesine (6)(7)(8). The identification of new chemotherapy regimens incorporating nedaplatin with other chemotherapeutic agents can enhance the knowledge of nedaplatin resistance and support the development of nedaplatin-based approaches to cancer therapy.…”

Section: Introductionmentioning

confidence: 99%

Nedaplatin enhanced apoptotic effects of ABT-737 in human cancer cells via Mcl-1 inhibition

Zhang

Weng

et al. 2016

Oncology Letters

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Abstract. Platinum compounds, such as cisplatin, carboplatin, oxaliplatin and nedaplatin, are widely used to treat a number of solid malignancies. Nedaplatin is a second-generation platinum complex, based on its pronounced anti-cancer activities against several solid tumors being equivalent to that of cisplatin, but with lower nephrotoxicity. In this context, the present study aimed to investigate the potential anti-cancer effect by combining nedaplatin with ABT-737. It was found that nedaplatin greatly increased ABT-737-mediated apoptosis in A549 and 95-D cells, accompanied by enhanced cleavage of poly(ADP-ribose) polymerase and caspase-3. In addition, this enhancement was also paralleled by cytochrome c release and dissipation of mitochondrial membrane potential. Additional mechanistic investigations revealed that nedaplatin plus ABT-737 exerted a synergistic effect on cancer cells through their ability to accelerate the degradation of Mcl-1. The present study has revealed nedaplatin as a pertinent sensitizer to ABT-737, which opens up new avenues for this promising BH3-mimetic molecule in the clinic. IntroductionNedaplatin, a platinum derivative synthesized to overcome problems of cisplatin resistance, was developed by Shionogi Pharmaceutical Company in 1983 with the aim to provide a treatment with effectiveness similar to cisplatin, but with less nephrotoxicity and gastrointestinal toxicities (1). Nedaplatin produces promising response rates in clinical trials as a monotherapy for the treatment of squamous cell carcinoma of the uterus, cervix, head and neck, ovary, lung and esophagus (2-4). Nedaplatin exerts anti-tumor effects following uptake into tumor cells by binding to DNA bases and inhibiting DNA replication, similar to cisplatin and carboplatin (5). However, the ability of cancer cells to become resistant to nedaplatin remains a notable obstacle to successful chemotherapy; resistance of numerous species of cancer cells to nedaplatin can be reversed by combining with chemotherapeutic agents, including 5-fluorouracil, docetaxel and vindesine (6-8). The identification of new chemotherapy regimens incorporating nedaplatin with other chemotherapeutic agents can enhance the knowledge of nedaplatin resistance and support the development of nedaplatin-based approaches to cancer therapy.The B-cell lymphoma 2 (Bcl-2) family members serve as primary regulators of apoptosis and include both pro-and anti-apoptotic molecules (9). Overexpression of anti-apoptotic Bcl-2 family proteins has been associated with chemotherapy resistance in multiple human cancers (10). Myeloid cell leukemia 1 (Mcl-1), an anti-apoptotic protein in the Bcl-2 family, is frequently observed in numerous tumor types and contributes to chemotherapeutic resistance (11).ABT-737 is a small molecule inhibitor of Bcl-2 family proteins. It can bind Bcl-2 and B-cell lymphoma-extra large (Bcl-xL) with high affinity. ABT-737 has shown single agent and combination therapy efficacy against multiple myeloma, acute myeloid leukemia, lymphoma and solid tumor...

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Dose escalation study of docetaxel and nedaplatin in patients with relapsed or refractory squamous cell carcinoma of the esophagus pretreated using cisplatin, 5-fluorouracil, and radiation

Abstract: The recommended doses of docetaxel and nedaplatin were 30 and 80 mg/m(2), respectively. This combination could be a potential second-line treatment for this target population.

Cited by 24 publications

References 26 publications

Nedaplatin sensitization of cisplatin-resistant human non-small cell lung cancer cells

Nedaplatin sensitization of cisplatin-resistant human non-small cell lung cancer cells

Second-line combination chemotherapy with docetaxel and nedaplatin for metastatic or recurrent squamous cell carcinoma of the esophagus refractory to chemotherapy with 5-fluorouracil plus cisplatin

Nedaplatin enhanced apoptotic effects of ABT-737 in human cancer cells via Mcl-1 inhibition

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