PURPOSE: Glioblastoma multiforme is the prototype of an angiogenic tumour. Under experimental conditions, anti-angiogenic therapy strategies lead to an increased invasion. Here we report on the pattern of tumour recurrence in glioblastoma patients treated with an anti-angiogenic chemotherapy. PATIENTS AND METHODS: A total of 32 patients with glioblastoma multiforme and a residual tumour mass after operation were treated with a continuous low-dose chemotherapy with temozolomide and a COX-II inhibitor, a presumably anti-angiogenic therapy. RESULTS: While anti-tumour activity of this therapy regimen was excellent with a mean overall time to progression of 10.4 (+/-0.9) months and a mean overall survival of 17.8 (+/-1.5) months, an unusually high rate of distant recurrences was observed (62.5%). CONCLUSION: Patients treated with an anti-angiogenic chemotherapy experience distant recurrences at a higher rate than reported for conventional therapies. This may reflect an anti-angiogenic therapy-induced activation of glioma invasion confirming similar recently published experimental results.
PURPOSE:Glioblastoma multiforme is the prototype of an angiogenic tumour. Under experimental conditions, anti-angiogenic therapy strategies lead to an increased invasion. Here we report on the pattern of tumour recurrence in glioblastomapatients treated with an anti-angiogenic chemotherapy. PATIENTS AND METHODS: A total of 32 patients with glioblastoma multiforme and a residual tumour mass after operation were treated with a continuous low-dose chemotherapy with temozolomide and a COX-II inhibitor, a presumably anti-angiogenic therapy. RESULTS: While anti-tumour activity of this therapy regimen was excellent with a mean overall time to progression of 10.4 (+/-0.9) months and a mean overall survival of 17.8 (+/-1.5) months, an unusually high rate of distant recurrences was observed (62.5%). CONCLUSION:Patients treated with an anti-angiogenic chemotherapy experience distant recurrences at a higher rate than reported for conventional therapies. This may reflect an anti-angiogenic therapy-induced activation of glioma invasion confirming similar recently published experimental results.
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