Phase II study of paclitaxel in patients with relapsed or cisplatin-refractory testicular cancer

Bokemeyer, Carsten; Beyer, Jörg; Metzner, Bernd; Rüther, U.; Harstrick, A.; Weißbach, L.; Kohrmann, U; Verbeek, Wieke H.M.; Schmoll, H.-J.

doi:10.1093/oxfordjournals.annonc.a010473

Cited by 134 publications

(61 citation statements)

References 7 publications

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“…20 The remaining seven patients, as well as patients with recurrence of disease after salvage high-dose chemotherapy, received further palliative treatment for refractory disease with various agents such as orally administered etoposide, oxaliplatin, bendamustine, or gemcitabine within trials of the GTCSG. [21][22][23][24] The tissue samples from patients with resistant disease were derived from tumors resected at initial diagnosis (n ϭ 14), from secondary resection of residual masses containing viable tumor cells (n ϭ 4), or from metastatic tumors (n ϭ 4). The specimens of the responsive cases were derived from orchiectomy (n ϭ 10) or from retroperitoneal biopsies (n ϭ 2).…”

Section: Patients and Tissue Samplesmentioning

confidence: 99%

Absence of c‐KIT and members of the epidermal growth factor receptor family in refractory germ cell cancer

Kollmannsberger

Mayer

Preßler

et al. 2002

Cancer

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BACKGROUNDGerm cell tumors (GCTs) in adolescent and young males are very sensitive to cisplatin‐based chemotherapy. However, 10–20% of the patients cannot be cured by currently available therapeutic options. Once a tumor does not respond to cisplatin, current therapeutic modalities offer only a chance for short palliation. Recently, new treatment options that interfere with various receptor tyrosine kinases, including c‐KIT and members of the epidermal growth factor receptor (EGFR) family, have been used successfully in chemotherapy‐resistant tumors overexpressing c‐KIT, ERB‐B2, or EGFR.METHODSWe studied the presence of c‐KIT and the four members of the EGFR family by immunohistochemistry, as well as by ERB‐B2 gene amplification using fluorescent in situ hybridization, in a series of 22 patients with cisplatin‐resistant GCTs in search of new treatment targets. The results in these refractory tumors were compared with those of 12 patients with chemosensitive GCTs diagnosed in an advanced metastatic stage.RESULTSThe data obtained in both groups did not differ in any of the investigated biologic markers. c‐KIT was detected in the one case of pure seminoma studied and in the seminomatous components of combined tumors. The presence of EGFR was restricted to trophoblastic giant cells and the syncytiotrophoblastic elements of four nonseminomas including one pure choriocarcinoma and to a secondary non–germ cell malignancy, which had developed most likely from a mature teratoma. ERB‐B2 was moderately positive in the secondary non–germ cell malignancy, in one mature teratoma component of a mixed nonseminoma, and together with EGFR in the syncytiotrophoblastic cells of a pure choriocarcinoma. Of all samples investigated, this latter case was the only one showing an amplification of the ERB‐B2 gene in the syncytiotrophoblasts. ERB‐B3 and ERB‐B4 were detected rarely.CONCLUSIONThe majority of refractory GCTs do not qualify for treatment with new biologic agents targeting the receptor tyrosine kinases EGFR, ERB‐B2, or c‐KIT. The lack of differences between the tumors of refractory and the responsive patients indicates that overexpression of any of these receptor tyrosine kinases does not contribute to a resistant phenotype in GCTs. Cancer 2002;95:301–8. © 2002 American Cancer Society.DOI 10.1002/cncr.10671

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Section: Patients and Tissue Samplesmentioning

confidence: 99%

Absence of c‐KIT and members of the epidermal growth factor receptor family in refractory germ cell cancer

Kollmannsberger

Mayer

Preßler

et al. 2002

Cancer

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“…In another phase II German trial, 24 patients with relapsed, mostly cisplatin-refractory, metastatic GCTs were treated with 3-hour paclitaxel infusions of 225 mg/m 2 every 3 weeks [15]. The patients had received a median of seven platinum-containing treatment cycles prior to paclitaxel, and 12 patients had previously received high-dose carboplatin/etoposide-based salvage therapy with autologous stem cell support.…”

Section: Paclitaxelmentioning

confidence: 99%

Management of Recurrent Testicular Germ Cell Tumors

2007

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LEARNING OBJECTIVESAfter completing this course, the reader will be able to:1. Discuss the different salvage conventional and high-dose chemotherapy regimens for germ cell tumors.2. List the prognostic factors for recurrent germ cell tumors.3. Explain the role of surgical salvage therapy for recurrent germ cell tumors.Access and take the CME test online and receive 1 AMA PRA Category 1 Credit ™ at CME.TheOncologist.com CME CME ABSTRACTAlthough front-line chemotherapy cures most men with testicular germ cell tumors, salvage therapy is still important in a small but significant minority. Second-line conventional-dose or high-dose chemotherapy with stem cell rescue may cure 25%-50% of patients. New chemotherapeutic agents, including the taxanes gemcitabine and oxaliplatin, have added to the therapeutic armamentarium. Salvage surgical resection has an important role in selected patients. Cisplatin-refractory patients have a poor prognosis with current therapy, and novel chemotherapeutic and biologic agents need to be discovered for such patients. The Oncologist 2007;12:51-61

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“…[56][57][58][59][60][61][62][63][64][65][66][67][68][69] Paclitaxel was shown to Chemo., chemotherapy; CR, complete response; NED, no evidence of disease; VeIP, vinblastine, ifosfamide, cisplatin; VIP, etoposide (VP-16), ifosfamide, cisplatin. be effective for previously treated testicular cancer because of its unique mechanism of antitumor activity and the premature stabilization of the microtubules assembly, which is different from that of DNAdamaging agents such as cisplatin and ifosfamide.…”

Section: Poor-prognosis Diseasementioning

confidence: 99%

“…The first trial of paclitaxel in pretreated germ cell tumors was undertaken by Motzer et al 56 The effective rate of paclitaxel in the salvage treatment of refractory testicular cancer ranged from 11 to 26% (Table 5). [56][57][58][59][60][61][62][63][64][65][66][67][68][69] More recently, high effective rates (68% and 80%) of a combination chemotherapy with paclitaxel, ifosfamide and cisplatin (TIP) in the treatment of refractory disease were reported by Beyer et al and Motzer et al 60,61 The results reported by Motzer et al showed a high response rate to the TIP regimen in patients with relapsed testicular cancer after conventional dose first-line chemotherapy. 61 Motzer and associates also reported the result of dose-intensive salvage therapy with paclitaxel, ifosfamide, carboplatin and etoposide (PICP) for cisplatin-resistant germ cell tumor patients with unfavorable prognostic features, achieving a 57% CR rate.…”

Section: Poor-prognosis Diseasementioning

confidence: 99%

Current status and future perspectives in the treatment of advanced testicular cancer

Miki

Nakao

2002

Int J of Urology

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Phase II study of paclitaxel in patients with relapsed or cisplatin-refractory testicular cancer

Abstract: Paclitaxel demonstrates significant antitumor activity in 25% of patients with relapsed or cisplatin-refractory testicular cancer. Combination regimens including paclitaxel may be warranted.

Cited by 134 publications

References 7 publications

Absence of c‐KIT and members of the epidermal growth factor receptor family in refractory germ cell cancer

Absence of c‐KIT and members of the epidermal growth factor receptor family in refractory germ cell cancer

Management of Recurrent Testicular Germ Cell Tumors

Current status and future perspectives in the treatment of advanced testicular cancer

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