Combined continuous infusion etoposide with high-dose cyclophosphamide for refractory neuroblastoma: a phase II study from the Société Française d'Oncologie Pédiatrique.

Méresse, Valérie; Vassal, Gilles; Michon, Jean; Cervens, C De; Courbon, B; Rubie, H; Pérel, Yves; Landman, Judith; Chastagnier, P; Valck, C. De

doi:10.1200/jco.1993.11.4.630

Cited by 29 publications

(16 citation statements)

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“…The two xenografts were clearly sensitive to alkylating agents (cyclophosphamide, thiotepa) and cisplatin, with SK-N-MC being more sensitive than IGR-N835. This is in good agreement with the established sensitivity of pPNETs and neuroblastomas (Hayes et al, 1989;Meresse et al, 1993;Kushner et al, 1994). Conversely, the two xenografts were refractory to taxol and etoposide.…”

Section: Discussionsupporting

confidence: 90%

“…Cyclophosphamide and etoposide are currently used in conventional chemotherapy protocols to treat patients with neuroblastoma and Ewing's sarcoma (Hayes et al, 1989;Meresse et al, 1993;Kushner et al, 1994). Cisplatin is a major drug used to treat neuroblastoma (Philip et al, 1987;Kushner et al, 1994).…”

Section: Discussionmentioning

confidence: 99%

“…A recent up-front phase II study on taxol has shown an 18% response rate in neuroblastoma patients (Kretschmar et al, 1995). Etoposide is widely used in paediatric oncology in combination with other drugs such as cyclophosphamide and platinum compounds (cisplatin or carboplatin) (Philip et al, 1987;Meresse et al, 1993). However, phase II studies of singleagent etoposide showed very low response rates (<10%) in neuroblastoma and Ewing's sarcoma patients (Kung et al, 1988).…”

Section: Discussionmentioning

confidence: 99%

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Therapeutic activity of CPT-11, a DNA-topoisomerase I inhibitor, against peripheral primitive neuroectodermal tumour and neuroblastoma xenografts

Vassal

Mj²,

Mc³

et al. 1996

Br J Cancer

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Summary The anti-tumour activity of CPT-l 1, a topoisomerase I inhibitor, was evaluated in four human neural-crest-derived paediatric tumour xenografts: one peripheral primitive neuroectodermal tumour (pPNET) (SK-N-MC) and three neuroblastomas. Two models, SK-N-MC and IGR-N835, were established in athymic mice from a previously established in vitro cell line. Two new neuroblastoma xenograft models, IGR-NB3 and IGR-NB8, were derived from previously untreated non-metastatic neuroblastomas. They exhibited the classic histological features of immature neuroblastoma along with N-myc amplification, paradiploidy, chromosome lp deletions and overexpression of the human mdrl gene. These tumour markers have been shown to be poor prognostic factors in children treated for neuroblastoma. CPT-11 was tested against advanced stage subcutaneous tumours. CPT-11 was administered i.v. using an intermittent (q4d x 3) and a daily x 5 schedule. The optimal dosage and schedule was 40 mg kg-' daily for 5 days. At this highest non-toxic dose, CPT-11 induced 100% tumour-free survivors on day 121 in mice bearing the pPNET SK-N-MC xenograft. For the three neuroblastoma xenografts, 38-100% complete tumour regressions were observed with a tumour growth delay from 38 to 42 days, and anti-tumour activity was clearly sustained at a lower dosage (27 mg kg-' day-'). The efficacy of five anti-cancer drugs commonly used in paediatric oncology or in clinical development was evaluated against SK-N-MC and IGR-N835. The sensitivity of these two xenografts to cyclophosphamide, thiotepa and cisplatin was of the same order of magnitude as that of CPT-11, but they were refractory to etoposide and taxol. In conclusion, CPT-11 demonstrated significant activity against pPNET and neuroblastoma xenografts. Further clinical development of CPT-11 in paediatric oncology is warranted.

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Section: Discussionsupporting

confidence: 90%

Section: Discussionmentioning

confidence: 99%

Section: Discussionmentioning

confidence: 99%

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Therapeutic activity of CPT-11, a DNA-topoisomerase I inhibitor, against peripheral primitive neuroectodermal tumour and neuroblastoma xenografts

Vassal

Mj²,

Mc³

et al. 1996

Br J Cancer

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“…Combinations of 2 components of ICE (carboplatin plus etoposide 12 and ifosfamide plus etoposide 13 ) have well established anti-NB activity. The same holds for 2-drug combinations of related agents, namely, cyclophosphamide plus carboplatin, 32 cyclophosphamide plus etoposide, 33 and cisplatin plus etoposide. 34 Indeed, a literature review (Table 3) amply documents the activity of ICE against newly diagnosed as well as resistant NB and provides a broader context for this synergistically interacting 3-drug combination than our single-institution experience with HD-ICE.…”

Section: Discussionmentioning

confidence: 83%

Ifosfamide, carboplatin, and etoposide for neuroblastoma

Kushner

Modak

Krämer

et al. 2012

Cancer

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BACKGROUND:The authors report a retrospective analysis of high-dose ifosfamide, carboplatin, and etoposide (HD-ICE) for patients with refractory or relapsed neuroblastoma (NB). A major reason for using this regimen was the long time since patients received previous treatment with a platinum compound. The authors also summarized the published experience on ICE in patients with NB. METHODS: Treatment comprised ifosfamide (2000 mg/m 2 daily for 5 days), carboplatin (500 mg/m 2 daily for 2 days), and etoposide (100 mg/m 2 daily for 5 days). Patients who had poor hematologic reserve (platelet count <100,000/lL) from previous therapy received peripheral blood stem cells (PBSCs) after HD-ICE. Disease status before and after HD-ICE was defined according to International Neuroblastoma Response Criteria (expanded to include 123 I-metaiodobenzylguanidine findings). Publications that were informative about ICE for NB were reviewed. RESULTS: Seventy-four patients received 92 cycles of ICE, including 37 patients who received PBSC rescue. Grade 3 toxicities were rare: 1-3 patients had encephalopathy, mucositis, or gastroenteritis. Bacteremia was documented in 24 of 92 cycles (26%). The absolute neutrophil count reached 500/lL on day 17-30 (median, day 22) in patients who had satisfactory hematologic reserve. Disease regressions (major and minor responses) were achieved by 14 of 17 patients (82%) with a new relapse, 13 of 26 patients (50%) with refractory NB, and 12 of 34 patients (35%) who were treated for progressive disease during chemotherapy (P ¼ .005). In the literature, patients received ICE at lower dosages and achieved major response rates >36% in phase 1 and 2 studies (in which less comprehensive staging evaluations were used) that involved resistant NB and >70% in induction for newly diagnosed NB. CONCLUSIONS: HD-ICE is appealing as salvage treatment or consolidative therapy because of its anti-NB activity and the low risk of major nonhematologic toxicity. PBSC support is unnecessary for patients who had intact hematologic reserve.

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“…The LMCE5 induction gave similar total dose of cisplatinum though with lower dose intensity. The main objective Clinical LMCE5 strategy in NB D Frappaz et al of this induction was to test a dose effect relationship of etoposide and cyclophosphamide (Meresse et al, 1993). The total dose of etoposide and cyclophosphamide was increased 2 -4-fold (Table 1).…”

Section: Discussionmentioning

confidence: 99%

The LMCE5 unselected cohort of 25 children consecutively diagnosed with untreated stage 4 neuroblastoma over 1 year at diagnosis

et al. 2002

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The Lyon-Marseille-Curie-Est (LMCE) of France cooperative group has previously reported successive series of unselected stage four children older than 1 year at diagnosis with metastatic neuroblastoma (LMCE 1 and 3). The goal of LMCE 5 study was to increase progression free survival rate as compared to LMCE 1 and 3. Based on improvements reported with post induction chemotherapy, the LMCE 5 used post induction for all children, but omitted total body irradiation and immunomagnetic purging in megatherapy regimen for all children. Twenty-five sequentially diagnosed children received an induction regimen which compared with previous induction included an increased dose of etoposide and cyclophosphamide, delivered similar dose of cisplatinum, and deleted doxorubicin and vincristin. After surgery treatment was stratified based on response and eligible children received etoposide carboplatin (LMCE 5A : n=10)+doxorubicin (LMCE 5B -C n=13) followed by megatherapy (melphalan without total body irradiation and unpurged peripheral blood stem cell rescue). The increase in drug doses during induction did not improve remission rate. The progression free survival at 6 years is 8%. It is significantly worse than LMCE 3, and equivalent to LMCE 1 study though toxic death rate has decreased with increasing experience. Failure to improve the response rate during induction and reducing the megatherapy regimen may be the main factors in this disappointing result. Modified strategies for induction, non toxic alternative to total body irradiation, and post megatherapy regimen should be developed.

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Combined continuous infusion etoposide with high-dose cyclophosphamide for refractory neuroblastoma: a phase II study from the Société Française d'Oncologie Pédiatrique.

Abstract: This new drug combination appears to be effective in advanced neuroblastoma. Its toxicity remains manageable, with no life-threatening complications. Further evaluation in patients with less-advanced disease is warranted.

Cited by 29 publications

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Therapeutic activity of CPT-11, a DNA-topoisomerase I inhibitor, against peripheral primitive neuroectodermal tumour and neuroblastoma xenografts

Therapeutic activity of CPT-11, a DNA-topoisomerase I inhibitor, against peripheral primitive neuroectodermal tumour and neuroblastoma xenografts

Ifosfamide, carboplatin, and etoposide for neuroblastoma

The LMCE5 unselected cohort of 25 children consecutively diagnosed with untreated stage 4 neuroblastoma over 1 year at diagnosis

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