Chemotherapy in advanced bladder cancer: current status and future

Ismaili, Nabil; Amzerin, Mounia; Fléchon, Aude

doi:10.1186/1756-8722-4-35

Cited by 67 publications

(50 citation statements)

References 81 publications

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“…Cis-diamminedichloroplatinum II (cisplatin) is one of the most potent antitumor agents and has clinical activity against a wide variety of solid tumors, such as ovary, lung, head and neck, and bladder cancer (1)(2)(3)(4)(5). It is generally accepted that the cytotoxic activity of cisplatin results from its interactions with DNA, inhibition of DNA replication and DNA repair, disturbance of the cell cycle and the beneficial process of apoptosis in cancer therapy (6)(7)(8).…”

Section: Introductionmentioning

confidence: 99%

Factors involved in the cisplatin resistance of KCP-4 human epidermoid carcinoma cells

et al. 2013

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Abstract. KCP-4 is a cisplatin-resistant cell line established from human epidermoid carcinoma KB-3-1 cells. Although our previous study revealed that one of the mechanisms for cisplatin resistance in KCP-4 cells is the activation of NF-κB, its high resistance is considered to be induced by multiple mechanisms. In the present study, we explored other factors involved in the development of cisplatin resistance in KCP-4 cells. Since it has been reported that an unknown efflux pump exports cisplatin from KCP-4 cells in an ATP-dependent manner, we examined 48 types of ATP-binding cassette proteins as candidate cisplatin efflux transporters. The mRNA expression levels of ABCA1, ABCA3, ABCA7 and ABCB10 in KCP-4 cells were higher when compared to those in KB-3-1 cells. These expression levels in cisplatin-sensitive revertant KCP-4 cells (KCP-4R cells), were reduced in parallel with the sensitivity of these cells to cisplatin and their intracellular accumulation of cisplatin. Next, we investigated the occurrence of mutations in p53 in KCP-4 cells. We found a heterozygous missense mutation at codon 72 (p.Pro72Arg) in p53 of both KCP-4 and KB-3-1 cells, but the protein expression level of p53 in KCP-4 cells was higher when compared to that in KB-3-1. These results suggest that ABCA1, ABCA3, ABCA7 and ABCB10 are candidate genes for the cisplatin efflux transporter that is involved in the cisplatin resistance of KCP-4 cells, and that the mutation at codon 72 of p53 may contribute to the development of cisplatin resistance.

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Section: Introductionmentioning

confidence: 99%

Factors involved in the cisplatin resistance of KCP-4 human epidermoid carcinoma cells

et al. 2013

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“…Since 1990, the combination of methotrexatevinblastine-doxorubicin-cisplatin (MVAC) has been considered as standard first-line treatment in metastatic bladder cancer. [1] However, a high toxicity profile of MVAC chemotherapy leads the way to new therapeutic requests in this field. Gemcitabine is an active and safe monotherapy option for the treatment of metastatic bladder cancer and it is more active when combined with platinum-based agents.…”

Section: Introductionmentioning

confidence: 99%

“…[9,10] So, triple chemotherapy regimens were applied, however, they were more toxic and less effective. [1] The combination of cisplatin with taxanes provided promising effectiveness with improved overall response rate (ORRs) of 50-70 percent [11][12][13][14] , but it remained inferior to the MVAC as shown by a phase III randomized study (ORR was 37.4% vs. 54.2% p=0.017, TTP was 6.1 vs. 9.4 months, p=0.003). [15] Moreover, after failure of cisplatin-based first-line therapy, there have been just a few agents such as eribulin, taxanes, vinflunine, and pemetrexed which resulted in a low response rate about 7 to 38%.…”

Section: Introductionmentioning

confidence: 99%

Maintenance treatment with gemcitabine have a promising activity on metastatic bladder cancer survival

Kuş

Aktaş

2017

Turkish Journal of Urology

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Objective: To investigate the effects of gemcitabine maintenance treatment on survival in patients with metastatic bladder cancer. Material and methods:Gemcitabine maintenance monotherapy was administered following the standard platinum-gemcitabine therapy in patients with metastatic bladder cancer. Patients who had responded to standard treatment received maintenance gemcitabine therapy as 1000 mg/m 2 on days 1 and 8 every three weeks until progression or development of unacceptable toxicity. The following clinical factors were noted: performance status, age, sex, stage, site of metastasis, choice of cisplatin-gemcitabine or carboplatin-gemcitabine, response rates to the initial chemotherapy. Progression-free survival (PFS) and overall survival (OS) for standard treatment, and following gemcitabine monotreatment and for maintenance gemcitabine therapy were calculated using Kaplan-Meier method.Results: A total of 88 patients with metastatic bladder cancer treated between February 2009 to October 2015 were evaluated retrospectively and 23 patients (26.1%) who had responded to six cycles of platinumgemcitabine treatment were included in this study. Maintenance gamcitabine was administered for a median of 7 times (range 3-14 times). Grade 3 hematotoxicity according to the criteria of the Common Terminology Criteria of Adverse Events was observed in 7 (30.4%) patients. Median PFS of patients was 46 (range: 30-82) weeks for platinum-based treatment plus maintenance gemcitabine therapy. A higher median PFS was obtained in patients who were <65 year-olds, without organ metastasis with objective response rate, however, it was statistically insignificant. Conclusion:Gemcitabine maintenance therapy in metastatic bladder cancer patients who did not shown progression after the standard platinum-gemcitabine treatment contributes to survival and presents low toxicity profile, when compared to historical controls.

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“…In addition, despite adequate local therapy for patients with muscle-invasive disease by radical surgery, more than one-third of these patients ultimately develop metastatic disease [2]. Urothelial carcinoma has been regarded as a disease comparatively sensitive to chemotherapeutic agents; therefore, systemic chemotherapy remains the standard of care for patients with metastatic urothelial carcinoma [3]. …”

Section: Introductionmentioning

confidence: 99%

“…Recently, several combination chemotherapies with novel active agents have been applied to advanced urothelial carcinoma resistant to the cisplatin-based regimen [3,6,7,8,9,10]. Vinflunine in combination with best supportive care has demonstrated a 2-month survival advantage as second-line chemotherapy after failure of cisplatin-based regimens compared to best supportive care alone in a phase 3 trial [6].…”

Section: Introductionmentioning

confidence: 99%

Clinical Outcome of Paclitaxel and Carboplatin as Second-Line Chemotherapy for Advanced Urothelial Carcinoma Resistant to First-Line Therapy with Gemcitabine and Cisplatin

Taguchi

Yokoyama²,

Miyazaki³

et al. 2013

Urol Int

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Objective: The objective was to investigate the efficacy and tolerability of combined therapy with paclitaxel and carboplatin (TC) in patients with advanced urothelial carcinoma after the failure of first-line chemotherapy with gemcitabine and cisplatin (GC). Patients and Methods: This was a retrospective study including a total of 16 patients with advanced urothelial carcinoma who showed evidence of progressive and/or recurrent disease after first-line therapy with GC and subsequently received second-line chemotherapy consisting of paclitaxel (175 mg/m²) and carboplatin (area under the curve 5). TC therapy was repeated every 3 weeks and was continued until disease progression or intolerable toxicity was observed. Results: The baseline patient characteristics were rather favorable; only 3 of 16 patients had liver metastases and 7 patients had an Eastern Cooperative Oncology Group performance status of 0. Of these, response to TC therapy was achieved in 5 (31.3%), including 2 with complete and 3 with partial response. The median progression-free and overall survival times in the 16 patients were 7.9 and 17.3 months, respectively. Conclusions: TC therapy appeared to show modest activity with acceptable tolerability in patients refractory to GC therapy; therefore, TC chemotherapy might be considered as an alternative option as a second-line regimen for advanced urothelial carcinoma following GC therapy.

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Chemotherapy in advanced bladder cancer: current status and future

Cited by 67 publications

References 81 publications

Factors involved in the cisplatin resistance of KCP-4 human epidermoid carcinoma cells

Factors involved in the cisplatin resistance of KCP-4 human epidermoid carcinoma cells

Maintenance treatment with gemcitabine have a promising activity on metastatic bladder cancer survival

Clinical Outcome of Paclitaxel and Carboplatin as Second-Line Chemotherapy for Advanced Urothelial Carcinoma Resistant to First-Line Therapy with Gemcitabine and Cisplatin

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