Temozolomide and oral VP‐16 for children and young adults with recurrent or treatment‐induced malignant gliomas

Korones, David N.; Smith, Amy; Foreman, Nicholas K.; Bouffet, Éric

doi:10.1002/pbc.20510

Cited by 25 publications

(12 citation statements)

References 30 publications

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“…Co-treatment with roscovitine enhanced the response of TuBECs to VP-16, paclitaxel, and thapsigargin. VP-16 is used for treating gliomas, 43 and so combined administration of this drug with roscovitine may be more efficient in treating brain tumors because of the additional anti-angiogenic effects. Our data are consistent with previous reports using other Cdk1 inhibitors, such as Purvalanol A and NU6140, which enhanced apoptosis in paclitaxel-treated HeLa cells.…”

Section: Discussionmentioning

confidence: 99%

Increased Survivin Expression Confers Chemoresistance to Tumor-Associated Endothelial Cells

Virrey

Guan

et al. 2008

The American Journal of Pathology

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Growing evidence suggests that survivin, a member of the inhibitor of apoptosis gene family, is responsible for drug resistance in cancer cells, yet little is known about its role in the endothelial cells of the tumor vasculature. We have previously reported that tumor-associated endothelial cells derived from gliomas (TuBECs) are resistant to anticancer chemotherapy whereas normal brain endothelial cells (BECs) are sensitive. The focus of this study is to investigate the mechanism behind this chemoresistance. Here we show that survivin is constitutively overexpressed in the glioma vasculature but not in the blood vessels of normal brain. To determine whether survivin contributes to TuBEC chemoresistance, we used a lentiviral siRNA system or the drug roscovitine to down-regulate survivin expression. Reduced levels of survivin sensitized TuBECs to the chemotherapeutic agents VP-16, paclitaxel, thapsigargin, and temozolomide. This cell death was mediated through caspases 7 and 4. Conversely, forced expression of survivin in BECs was protective against drug cytotoxicity. These data suggest that overexpression of survivin in endothelial cells serves as a protective mechanism that defends the vasculature from drug cytotoxicity. Our studies demonstrate that targeting survivin may be an effective approach to chemosensitization and anti-vascular therapy for brain tumors.

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Section: Discussionmentioning

confidence: 99%

Increased Survivin Expression Confers Chemoresistance to Tumor-Associated Endothelial Cells

Virrey

Guan

et al. 2008

The American Journal of Pathology

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“…Though few paediatric series have been reported [9,38,72,73,74,75], in children significant myelosuppression [38] can be observed at a higher frequency than in most trials of adulthood with an incidence of grade 3-4 neutropenia, thrombocytopenia, and anemia in 33%, 29%, and 7% off all cycles, respectively [72].…”

Section: Paediatric Administrationmentioning

confidence: 97%

“…If the paediatric incidence of severe haematologic toxicity [73,74] has been described as relatively low, prolunged thrombocytopenia and neutropenia resulted in both delays to treatment and dose reduction. The 22% of cycles were administrated at reduced dose and 17% were delayed by 7 days or more.…”

Section: Paediatric Administrationmentioning

confidence: 99%

The Safety of the Temozolomide in Patients with Malignant Glioma

Dario¹,

Tomei

2006

CDS

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The temozolomide is a promising orally cytotoxic agent used in malignant glioma. The survival curve improvement after drug administration appears to be statistically significant. The review of temozolomide side effects is carried out by search on literature data found on web and is divided on the 4 grades of toxicity according to the National Cancer Institute Common Toxicity Criteria, version 2.0. The adverse effects related with TMZ administration are divided in three categories: myelosuppression, non haematologic toxicity, and infections. The main adverse effect is the myelosuppression that appears to be rather low and reversible as well as the vomiting or nausea. The different schedules of administration are analysed. The frequency of concomitant infections is underlined. In particular, if available, the relationship between temozolomide and other cytotoxic agents or anticonvulsivant drugs is analysed to clarify the possibility of increase of toxicity. The temozolomide is used also in children but the toxicity could be more frequent.

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“…The effects of etoposide have been shown to be synergistic to the cisplatin analogue carboplatin, and this combination has been shown to be effective in recurrent GBM. 55,68,69 More recently the safety of combining temozolomide and etoposide has been evaluated in Phase I trials in GBM; 70,71 however, the efficacy of this combination still needs to be elucidated. It would be interesting to see if measurable TopoIIa levels in patients could be used as a predictive marker for patient responsiveness to TopoII inhibitors.…”

Section: Topoisomerase IImentioning

confidence: 99%

Contribution of DNA repair mechanisms to determining chemotherapy response in high-grade glioma

Parkinson

Wheeler

McDonald

2008

Journal of Clinical Neuroscience

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Temozolomide and oral VP‐16 for children and young adults with recurrent or treatment‐induced malignant gliomas

Abstract: These data suggest there is activity of temozolomide in combination with oral VP-16 for children and young adults with recurrent malignant gliomas.

Cited by 25 publications

References 30 publications

Increased Survivin Expression Confers Chemoresistance to Tumor-Associated Endothelial Cells

Increased Survivin Expression Confers Chemoresistance to Tumor-Associated Endothelial Cells

The Safety of the Temozolomide in Patients with Malignant Glioma

Contribution of DNA repair mechanisms to determining chemotherapy response in high-grade glioma

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