Primary glial tumor patients treated by combining cis-platin and etoposide

Abstract

Thirty eight patients with malignant gliomas (27 GBM and 11 AA) were treated with up to 7 cycles of CDDP + VP16 every month after surgery. Chemotherapy was planned as two cycles before and 5 cycles after radiation (42 Gy) using a three times daily fractionation schedule. No severe toxicity was observed. The object of our study was to investigate the antitumor effectiveness by combining CDDP plus VP16 against primary malignant glial tumors. The time to tumor progression (TTP) and survival time (ST) of the GBM patients in the present study were 38.5 and 68.5 weeks respectively. The TTP of the AA patients was 73 weeks and the ST was not calculated as most patients are still alive. By the 18th. month after surgery, 38% of GBM and 74% of AA patients treated with (CDDP + VP16) are still alive. This study demonstrates that the combination of CDDP and VP16 is effective in patients with malignant gliomas.

Drug resistance of human glioblastoma cells conferred by a tumor-specific mutant epidermal growth factor receptor through modulation of Bcl-X L and caspase-3-like proteases

“…Because ⌬EGFR expression in glioma cells has been shown to decrease the rate of apoptosis both under serum-starved culture conditions and in implanted tumors derived from such cells (16), we tested the sensitivity of ⌬EGFR-expressing glioma cells to the chemotherapeutic drug, CDDP, a DNA-damaging agent known to induce apoptosis in tumor cells and that often has been used in glioma therapy (21,22). Endogenous and exogenous wt EGFR were moderately autophosphorylated under the culture condition used (10% serum), suggesting that wt EGFR was constantly stimulated by ligand in the serum (Fig.…”

A peptide derived from the non-receptor-binding region of urokinase plasminogen activator inhibits glioblastoma growth and angiogenesis in vivo in combination with cisplatin

“…We therefore wanted to determine whether it was more effective in vitro if administered in combination with a cytotoxic agent that could retard the proliferation of the tumor cells. We chose to use CDDP because this compound has been used in the clinical treatment of GBM (19,27,28). We first tested the ability of Å6 to directly inhibit the in vitro proliferation of a panel of GBM cell lines that included U87MG, U251MG, U178MG, LN229, A1207, and LNZ308.…”

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

“…A recent study showed the activity of a CBCDA (carboplatin) -VP-16 (etoposide)-based therapy in the treatment of low-grade gliomas in children (Massimino et al, 2002). The efficacy of CBCDA or cisplatin (CDDP) in combination with etoposide has been evaluated in various schedules in other trials in high-grade gliomas with various results (Buckner et al, 1990;Boiardi et al, 1991;Jeremic et al, 1992). The role of topoisomerase IIa in glioma cancer cells is still unclear.…”