Growth factor receptors signaling in glioblastoma cells: therapeutic implications

Carapancea, M; Alexandru, Oana; Fetea, Ani S.; Dragutescu, Laura; Castro, Juan; Georgescu, Ada Maria; Popa‐Wagner, Aurel; Bäcklund, L. Magnus; Lewensohn, Rolf; Dricu, Anica

doi:10.1007/s11060-008-9753-8

Cited by 27 publications

(26 citation statements)

References 57 publications

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“…It has been demonstrated that many growth factor receptor families, such as epithelial growth factor receptor (EGF-R), platelet derived growth factor receptor (PDGF-R), and vascular endothelium growth factor receptor (VEGF-R), and their mutations, are involved in pathogenesis of GBM 6–12. There is evidence that primary and secondary GBM have a different molecular-genetic basis, however, treatment has not been stratified by these findings so far 2,13–15…”

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confidence: 99%

Temozolomide in malignant glioma

Dresemann¹

2010

OTT

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Glioblastoma multiforme WHO grade IV (GBM) is the most aggressive malignant glioma and the most frequent primary tumor of the central nervous system. The median survival of newly diagnosed GBM patients was between 9 to 12 months prior to treatment with temozolomide being introduced. Primary resection that is as complete as possible is recommended for malignant glioma. Conventional fractionated irradiation 55 to 60 gy with concomitant temozolomide followed by standard temozolomide 6 cycles (5/28) (EORTC/NCIC-regime published by R Stupp in 2005) is the standard of care for newly diagnosed GBM after surgery, independent of the methylation status of the MGM-T gene promoter. Age is no contraindication for treatment with temozolomide, although comorbidity and performance status have to be considered. For temozolomide naive GBM and astrocytoma grade III patients with disease progression, temozolomide is still the treatment of choice outside of clinical studies. A general consensus regarding the schedule of choice has not yet been achieved; so far the 5 out of 28 days regimen (5/28) is the standard of care in most countries. Patients with disease progression after standard temozolomide (5/28) are candidates for clinical studies. Outside of clinical studies, dose-dense (7/7), prolonged (21/28), or metronomic (28/28) temozolomide, or alternatively a nitrosourea-based regimen can be an option. The excellent toxicity profile of temozolomide allows for various combinations with antitumor agents. None of these combinations, however, have been demonstrated to be statistically significantly superior compared to temozolomide alone. The role of lower dosed, dose-dense, or continuous regimen with or without drug combination and the role of temozolomide for newly diagnosed astrocytoma grade III and low grade glioma still has to be determined.

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confidence: 99%

Temozolomide in malignant glioma

Dresemann¹

2010

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“…Empirical in vitro experimental data indicates these must all be inhibited [40,41] . The proposed intervention -cathepsin B inhibition with auranofi n -would be a small link in that long chain.…”

Section: Discussionmentioning

confidence: 99%

Glioblastoma Invasion, Cathepsin B, and the Potential for Both to be Inhibited by Auranofin, an Old Anti-Rheumatoid Arthritis Drug

Re¹

2010

Cen Eur Neurosurg

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“…Although advances have been achieved in cancer therapy by using modern techniques and therapeutic approaches such as personalized targeted therapy, the solid tumor cells are generally resistant to treatment and patients continue to exhibit a poor prognosis [91]. The concept that tumor development and progression depends on the evolution of CSCs dramatically changes the possibilities in which cancer can be cured.…”

Section: Targeted Therapy Against Cancer Stem Cells (Cscs)mentioning

confidence: 99%

Cancer Stem Cells: Biological Functions and Therapeutically Targeting

Ciurea

Georgescu

Purcaru

et al. 2014

IJMS

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Almost all tumors are composed of a heterogeneous cell population, making them difficult to treat. A small cancer stem cell population with a low proliferation rate and a high tumorigenic potential is thought to be responsible for cancer development, metastasis and resistance to therapy. Stem cells were reported to be involved in both normal development and carcinogenesis, some molecular mechanisms being common in both processes. No less controversial, stem cells are considered to be important in treatment of malignant diseases both as targets and drug carriers. The efforts to understand the role of different signalling in cancer stem cells requires in depth knowledge about the mechanisms that control their self-renewal, differentiation and malignant potential. The aim of this paper is to discuss insights into cancer stem cells historical background and to provide a brief review of the new therapeutic strategies for targeting cancer stem cells.

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Growth factor receptors signaling in glioblastoma cells: therapeutic implications

Cited by 27 publications

References 57 publications

Temozolomide in malignant glioma

Temozolomide in malignant glioma

Glioblastoma Invasion, Cathepsin B, and the Potential for Both to be Inhibited by Auranofin, an Old Anti-Rheumatoid Arthritis Drug

Cancer Stem Cells: Biological Functions and Therapeutically Targeting

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