Intravenous carboplatin for recurrent malignant glioma: a phase II study.

Yung, W. K. Alfred; Mechtler, Laszlo; Gleason, Mary Jo

doi:10.1200/jco.1991.9.5.860

Cited by 162 publications

(74 citation statements)

References 9 publications

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“…Carboplatin is an alkylating agent widely used in the treatment of human tumours, and the synergistic effect when used together with etoposide has been proved either in vitro and in vivo. Carboplatin has exhibited activity against malignant glioma in vitro (Dodion et al, 1988), and it has been widely used to treat both paediatric (Gaynon et al, 1990;Friedman et al, 1992;Gururangan et al, 2002) and adult (Poisson et al, 1991;Twelves et al, 1991;Yung et al, 1991;Warnick et al, 1994) brain tumour patients.…”

Section: Discussionmentioning

confidence: 99%

Phase II trial of carboplatin and etoposide for patients with recurrent high-grade glioma

et al. 2004

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We present the results of a phase II trial of carboplatin and etoposide (CE) combination as first-line chemotherapy in patients with recurrent glioblastoma multiforme (GBM) and anaplastic astrocytoma (AA) after surgery and radiotherapy. We assess the activity and the tolerability of this combination. 30 patients with GBM (25) and AA (5) were treated with VP-16 (etoposide) 120 mg m À2 and CBCDA (carboplatin) 100 mg m À2 for 3 days every 4 weeks. Moreover, we performed a retrospective analysis of topoisomerase IIa gene status using chromogenic in situ hybridisation. The median age was 54 years (21 -73 years); Eastern Cooperative Oncology Group performance score was 0-1 in 25 patients and 2 in five patients. All patients had been previously treated with surgical resection (21 radical resections) followed by radiation therapy (40 -60 Gy). We observed six (20%) complete responses, three (10%) partial responses and 12 (40%) stable diseases, with a response rate of 30%. The median time to progression was 4 months, while progression-free survival at 6 months was 33.3%. The median survival time was 10 months. Neutropenia occurred in 9 patients: four patients had grade 4, two patients grade 3 and three patients grade 2. In the conclusion of this clinical trial, the CE combination has shown activity in recurrent GBM and AA, with a good toxicity profile. Alterations in the copy number of topoisomerase IIa gene seem to be a rare event and in our series do not influence response to the CE combination.

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Section: Discussionmentioning

confidence: 99%

Phase II trial of carboplatin and etoposide for patients with recurrent high-grade glioma

et al. 2004

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“…24,[42][43][44][45][46][47] Similarly, carboplatin (with or without teniposide) has been used in several trials for recurrent AO with response rates of 9% to 13% and 35% PFS-6, results less robust than the present analysis. 14,15,48,49 The present retrospective analysis was directed at the 1p19q codeleted AO/AOA population who had failed prior alkylator-based chemotherapy (both TMZ and nitrosoureas) and for whom further treatment appeared warranted. Treatment with bevacizumab did not require histological proof of recurrent AO/AOA, and the possibility of radiation necrosis as opposed to recurrent tumor is possible.…”

Section: Discussionmentioning

confidence: 99%

“…13 Those drugs most active are the nitrosoureas, such as carmustine (BCNU) and lomustine (CCNU), in addition to temozolomide (TMZ), procarbazine, cis-retinoic acid, and platinum compounds. 1,2,4,5,[10][11][12]14,17,[23][24][25][26][27] Bevacizumab, with or without irinotecan (CPT-11), has activity in recurrent glioblastoma (GBM), and a small data set exists for activity as well in recurrent anaplastic gliomas. [28][29][30][31][32][33][34] The objective of this single institution retrospective analysis was to observe whether bevacizumab as a single agent, given every 2 weeks, could significantly delay progression in patients with neuroradiographically recurrent 1p19q codeleted AO/AOA as determined by PFS-6.…”

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confidence: 99%

Bevacizumab for recurrent alkylator‐refractory anaplastic oligodendroglioma

Chamberlain

Johnston

2009

Cancer

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BACKGROUND:A retrospective evaluation of single agent bevacizumab was carried out in adults with recurrent alkylator‐refractory 1p19q codeleted anaplastic oligodendrogliomas (AO) with an objective of determining progression‐free survival (PFS). There is no standard therapy for alkylator‐resistant AO, and hence a need exists for new therapies.METHODS:Twenty‐two patients aged 24 to 60 years with recurrent AO were treated. All patients had previously been treated with surgery, radiotherapy, adjuvant chemotherapy (temozolomide, 17; carmustine wafers, 4; carmustine, 1), and 1 salvage regimen (procarbazine, lomustine, and vincristine, 15; temozolomide, 6; carmustine wafers, 1). Eleven patients underwent repeat surgery. Patients were treated at second recurrence with bevacizumab, once every 2 weeks, defined as a single cycle. Neurological evaluation was performed every 2 weeks, and neuroradiographic assessment was made after the initial 2 cycles of bevacizumab and subsequently after every 4 cycles of bevacizumab.RESULTS:A total of 391 cycles of bevacizumab (median, 14.5 cycles; range, 2‐39 cycles) were administered. Bevacizumab‐related toxicity included fatigue (14 patients; 4 grade 3), leukopenia (9; 1 grade 3), anemia (5; 0 grade 3), hypertension (5; 1 grade 3), deep vein thrombosis (4; 1 grade 3), and wound dehiscence (2; 1 grade 3). Fifteen (68%) patients demonstrated a partial radiographic response, 1 (5.0%) demonstrated stable disease, and 6 (27%) demonstrated progressive disease after 2 cycles of bevacizumab. Time to tumor progression ranged from 1 to 18 months (median, 6.75 months). Survival ranged from 3 to 19 months (median, 8.5 months). Six‐month and 12‐month PFS were 68% and 23%, respectively.CONCLUSIONS:Bevacizumab demonstrated efficacy and acceptable toxicity in this cohort of adults with recurrent 1p19q codeleted alkylator‐refractory AO. Cancer 2009. © 2009 American Cancer Society.

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“…[14][15][16][17] Similarly, the objective response rate of cyclophosphamide was 22.5%, with 40% stable disease in temozolomide-refractory AG. PFS-6 was 30%.…”

Section: Discussionmentioning

confidence: 97%

Combination of Cyclophosphamide and Carboplatin in Recurrent Malignant Gliomas.

Demırcı¹

2013

UHOD

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Eventually, all patients with malignant gliomas recur or progress. Unfortunately, the optimal regimen in the salvage setting has not yet been defined. We retrospectively evaluated 52 patients with malignant gliomas who failed temozolomide therapy and were treated with a combination of intravenous carboplatin and oral cyclophosphamide. The median age of all patients, including those with glioblastoma multiforme (GBM) (n= 40) and anaplastic glioma (AG) (n= 12), was 45.5 years (range 23-68). All patients were treated with consolidation temozolomide after chemoradiotherapy. After temozolomide failure, second surgery was performed on 15, reirradiation on four and radiosurgery on three patients. The median number of chemotherapy cycles was 4 (range 1-8), the clinical benefit was 67.3%, a partial response was achieved in 26.9% and stable disease in 40.4%. In the GBM group, median progressionfree survival (PFS) and overall survival (OS) were 3 (95% CI, 2.31-3.69) and 8 (95% CI, 4.76-11.24) months, respectively. In the AG group, median PFS and OS were 5 (95% CI, 3.51-6.49) and 11 (95% CI, 6.38-15.62) months, respectively. The six-month PFS rate was 25%. Only one patient survived 18 months after treatment. Serious toxicity was mainly hematological.The combination of carboplatin and oral cyclophosphamide is a valuable option in temozolomide refractory patients with malignant glioma.

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Intravenous carboplatin for recurrent malignant glioma: a phase II study.

Cited by 162 publications

References 9 publications

Phase II trial of carboplatin and etoposide for patients with recurrent high-grade glioma

Phase II trial of carboplatin and etoposide for patients with recurrent high-grade glioma

Bevacizumab for recurrent alkylator‐refractory anaplastic oligodendroglioma

Combination of Cyclophosphamide and Carboplatin in Recurrent Malignant Gliomas.

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