A phase II trial of gemcitabine plus carboplatin in advanced transitional cell carcinoma of the urothelium

Xu, Nong; Zhang, Xiao Chen; Xiong, Jian; Fang, Wei; Lan, Yu; Qian, Jun; Zhang, Ling

doi:10.1186/1471-2407-7-98

Cited by 23 publications

(7 citation statements)

References 36 publications

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“…Cells (4x10 5 ) were seeded into 6-well culture plates and allowed to grow to ~90-95% confluence in serum-free medium for 48 h. Similar sized wounds were introduced to monolayer cells using a sterile yellow pipette tip, and remove the medium with floating cells carefully. Pre-warmed medium (2 ml) with low dose of epirubicin (2.5 μg/ml) was added.…”

Section: -(45-dimethyl Thiazol-2-yl)-25-diphenyl Tetrazolium Bromimentioning

confidence: 99%

The role of Id-1 in chemosensitivity and epirubicin-induced apoptosis in bladder cancer cells

Han²,

Wang³

et al. 2009

Oncol Rep

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Abstract. Recurrence and progression are the major problems in the treatment of bladder cancer. Increased expression of Id-1, a basic helix-loop-helix transcription factor, has recently been shown in several types of advanced cancer. Some studies have provided evidence to suggest that Id-1 can be considered a potential therapeutic target. The objective of this study was to investigate the role of Id-1 in the chemosensitivity of bladder cancer cells, and the effect of Id-1 on chemotherapeutic drug-induced apoptosis in bladder cancer cells. We compared the different sensitivity to epirubicin in RT112 and MGH-U1 cell lines with different Id-1 expression. Then, we transfected different vectors into RT112 and MGH-U1 respectively, and generated the stable Id-1 up-regulation and down-regulation transfectants. The results of cell viability assay showed up-regulation of Id-1 in RT112 leading to increased sensitivity in response to epirubicin, and downregulation of Id-1 increased cellular sensitivity to epirubicin. Furthermore, the analysis of apoptosis related protein revealed that up-regulation of Id-1 suppressed epirubicininduced apoptosis and down-regulation of Id-1 leading to increased epirubicin-induced apoptosis. Wound closure assay showed up-regulation of Id-1 leading to improved migration abilities of bladder cancer cells under chemotherapy. Our results suggest that up-regulation of Id-1 in bladder cancer cells lead to increased cell viability in response to epirubicin by its improved anti-apoptotic role, and down-regulation of Id-1 increases cellular sensitivity to epirubicin by increased anticancer drug-induced apoptosis.

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Section: -(45-dimethyl Thiazol-2-yl)-25-diphenyl Tetrazolium Bromimentioning

confidence: 99%

The role of Id-1 in chemosensitivity and epirubicin-induced apoptosis in bladder cancer cells

Han²,

Wang³

et al. 2009

Oncol Rep

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“…There are many reports as to the safety and efficacy of carboplatin-based chemotherapy for metastatic advanced bladder cancer (8,9,17,18). Regrettably, several reports demonstrated that the survival was shorter for CaG than GC.…”

Section: Discussionmentioning

confidence: 99%

“…Carboplatin is an alkylating anti-cancer agent and less nephrotoxic than cisplatin (7). A carboplatincontaining chemotherapy has been reported to play a potential role in advanced bladder cancer patients with renal impairment (8,9). In a neoadjuvant setting, less toxicity is an important matter, and in particular, the decline in renal dysfunction by chemotherapy affects the perioperative management of cystectomy (10) and may affect postoperative life.…”

Section: Introductionmentioning

confidence: 99%

Neoadjuvant Gemcitabine Plus Carboplatin for Locally Advanced Bladder Cancer

Iwasaki

Obara

Kato

et al. 2012

Japanese Journal of Clinical Oncology

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Objective: Although cisplatin-based neoadjuvant chemotherapy followed by cystectomy was demonstrated to improve the survival among patients with locally advanced bladder cancer, its severe adverse events, including nephrotoxicity, are critical issues. We investigated the safety and activity of carboplatin, a mild nephrotoxic agent, combined with gemcitabine as a neoadjuvant chemotherapy compared with methotrexate, vinblastine, doxorubicin and cisplatin for patients with locally advanced bladder cancer. Methods: We retrospectively evaluated 68 patients with locally advanced bladder cancer who received neoadjuvant methotrexate, vinblastine, doxorubicin and cisplatin (n ¼ 34) or gemcitabine and carboplatin (n ¼ 34) followed by cystectomy at our institute. The adverse events, chemotherapy delivery profile, rate of down-stage and recurrence-free survival were assessed for methotrexate, vinblastine, doxorubicin and cisplatin compared with gemcitabine and carboplatin. Results: The mean cycles of methotrexate, vinblastine, doxorubicin and cisplatin, and gemcitabine and carboplatin, were 2.5 and 2.7, respectively. The hematologic adverse events of Grade 3 or 4 neutropenia, anemia and thrombocytopenia for methotrexate, vinblastine, doxorubicin and cisplatin were 15, 18 and 0%, respectively. The occurrences for gemcitabine and carboplatin were 53, 21 and 50%, respectively. Grade 3 or 4 non-hematologic toxicities for methotrexate, vinblastine, doxorubicin and cisplatin were nausea and vomiting in 24%, and were not observed for gemcitabine and carboplatin. The lowest median estimated glomerular filtration rate during methotrexate, vinblastine, doxorubicin, and cisplatin and gemcitabine and carboplatin was 55.8 and 70.6 ml/min/1.73 m 2 , respectively (P ¼ 0.002). The rate of downstage to pT1 or less was 59% for methotrexate, vinblastine, doxorubicin and cisplatin, and 53% for gemcitabine and carboplatin (P ¼ 0.624). The recurrence-free survival of methotrexate, vinblastine, doxorubicin and cisplatin, and gemcitabine and carboplatin, at 36 months from the diagnosis was 79 and 75%, respectively (P ¼ 0.85). Conclusions: Neoadjuvant gemcitabine and carboplatin showed less non-hematologic toxicity than methotrexate, vinblastine, doxorubicin and cisplatin, and especially less nephrotoxicity was demonstrated for gemcitabine and carboplatin. Although observed during the short term, the recurrence-free survival for gemcitabine and carboplatin was comparable to that for methotrexate, vinblastine, doxorubicin and cisplatin.

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“…The combination of gemcitabine and carboplatin was developed for patients with metastatic transitional cell carcinoma (TCC) of the bladder unfit for cisplatin-based therapy and subsequently was adopted by additional investigators for such patients (2)(3)(4)(5)(6)(7)(8)(9)(10)(11)(12)(13).…”

Section: Introductionmentioning

confidence: 99%

Combination of gemcitabine and carboplatin in urothelial cancer patients unfit for cisplatin due to impaired renal or cardiac function

Sella

Kovel

2012

Int. braz j urol.

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A phase II trial of gemcitabine plus carboplatin in advanced transitional cell carcinoma of the urothelium

Cited by 23 publications

References 36 publications

The role of Id-1 in chemosensitivity and epirubicin-induced apoptosis in bladder cancer cells

The role of Id-1 in chemosensitivity and epirubicin-induced apoptosis in bladder cancer cells

Neoadjuvant Gemcitabine Plus Carboplatin for Locally Advanced Bladder Cancer

Combination of gemcitabine and carboplatin in urothelial cancer patients unfit for cisplatin due to impaired renal or cardiac function

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