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Phase II Study of Carboplatin in
Children With Progressive Low-Grade Gliomas
Sridharan Gururangan,
Christina M. Cavazos, David Ashley, James
E. Herndon, II, Carol S. Bruggers, Albert
Moghrabi, Deborah L. Scarcella, Melody
Watral, Sandra Tourt-Uhlig, David Reardon,
Henry S. Friedman
Duke University Medical Center,
Durham, NC; Primary Children’s Medical Center, Salt Lake City, UT;
Hospital Sainte-Justine, Montreal, Canada; and Royal Melbourne
Children’s Hospital, Melbourne, Australia. Address reprint requests
to Sridharan Gururangan, MRCP, The Brain Tumor Center at Duke, Duke
University Medical Center, Box 3624, DUMC, Durham, NC 27710; email:
mailto:gurur002@mc.duke.edu . Submitted December 3, 2001; accepted
March 21, 2002.
Purpose. To assess the
rate of tumor response and activity of carboplatin in
stabilizing the growth of progressive low-grade gliomas.
Patients and Methods.
Eligible patients received carboplatin 560 mg/m2
intravenously every 4 weeks for 1 year after maximum tumor
response or until disease progression or unacceptable toxicity.
Results. Between October
1993 and October 2000, 81 children (median age, 79 months;
range, 6 to 204) were enrolled onto this study.
Patients received a median of 11 cycles of carboplatin (range,
one to 29).
Median follow-up from the time of enrollment was 55 months
(range, 10 to 93).
The overall objective response (complete response [CR] +
partial response [PR] + minor response [MR]) and disease
stabilization (CR + PR + stable disease + MR) rates to
carboplatin treatment were 28% (95% confidence interval
[CI], 18% to 38%) and 85% (95% CI, 74% to 93%), respectively.
Eleven and 14 patients suffered progressive disease on study and
after stopping therapy, respectively.
Toxicity was predominantly myelosuppression and included
grade 3/4 neutropenia in 56 patients and grade 3/4
thrombocytopenia in 40 patients.
The 3-year failure-free survival (FFS) and overall survival
(OS) for all patients were 64% (95% CI, 54% to 76%) and 84%
(95% CI, 76% to 93%), respectively.
Patients with diencephalic tumors had inferior FFS and OS compared
with those with tumor at other sites (38% v 74% for FFS, P
= .011; 54% v 91% for OS, P = .004).
Neurofibromatosis type 1 patients with progressive
low-grade glioma had a significantly better OS (95% v
80%; P = .052).
Conclusion. Carboplatin,
in the schedule used in this study, produced disease
stabilization or improvement in a majority of children with
progressive low-grade glioma, with manageable toxicity.
Improved treatment strategies are particularly required for
patients with diencephalic tumors.
Presented in part at the
Thirty-Seventh Annual Meeting of the American Society of
Clinical Oncology, San Francisco, CA, May 12-15, 2001.
© 2002 American Society for
Clinical Oncology
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