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glioblastoma/tyrosine
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A combination of tyrosine kinase inhibitors, crizotinib and dasatinib for the treatment of glioblastoma multiforme.
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Glioblastoma multiforme (GBM) is the most common and aggressive primary brain tumor. Despite the advances in surgery, radiotherapy and chemotherapy, patient survival averages only 14.6 months. In most GBM tumors, tyrosine kinases show increased activity and/or expression and actively contribute to
The effects of ponatinib, a multi-targeted tyrosine kinase inhibitor, against human U87 malignant glioblastoma cells.
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Glioblastoma is one of the most common malignant tumors in the nervous system in both adult and pediatric patients. Studies suggest that abnormal activation of receptor tyrosine kinases contributes to pathological development of glioblastoma. However, current therapies targeting tyrosine kinase
DDR1 (discoidin domain receptor tyrosine kinase 1) drives glioblastoma therapy resistance by modulating autophagy.
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Therapy resistance of tumor cells is a major obstacle for efficient anticancer treatment approaches and has been attributed to tumor heterogeneity as well as genetic and epigenetic changes. Accumulating evidence demonstrates that tumor cell adhesion to the extracellular matrix acts as an additional
Mer receptor tyrosine kinase inhibition impedes glioblastoma multiforme migration and alters cellular morphology.
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Glioblastoma multiforme (GBM) is an aggressive brain tumor, fatal within 1 year from diagnosis in most patients despite intensive multimodality therapy. The migratory and microscopically invasive nature of GBM as well as its resistance to chemotherapy renders conventional therapies inadequate in its
Extracellular Hyaluronic Acid Influences the Efficacy of EGFR Tyrosine Kinase Inhibitors in a Biomaterial Model of Glioblastoma.
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3D biomaterial models have potential to explore the influence of the tumor microenvironment on aberrant signaling pathways and compensatory signals using patient-derived cells. Glioblastoma (GBM) tumors are highly heterogeneous, with both cell composition and extracellular matrix biophysical factors
Quantitative Analysis of Tyrosine Kinase Signaling Across Differentially Embedded Human Glioblastoma Tumors.
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Glioblastoma is the most aggressive primary brain tumor with a poor mean survival even with the current standard of care. Kinase signaling analyses of clinical glioblastoma samples provide a physiologically relevant view of oncogenic signaling networks. Here, we describe the methods that enable the
Analysis of copy number loss of the ErbB4 receptor tyrosine kinase in glioblastoma.
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Current treatments for glioblastoma multiforme (GBM)-an aggressive form of brain cancer-are minimally effective and yield a median survival of 14.6 months and a two-year survival rate of 30%. Given the severity of GBM and the limitations of its treatment, there is a need for the discovery of novel
Fusicoccin a, a phytotoxic carbotricyclic diterpene glucoside of fungal origin, reduces proliferation and invasion of glioblastoma cells by targeting multiple tyrosine kinases.
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Glioblastoma multiforme (GBM) is a deadly cancer that possesses an intrinsic resistance to pro-apoptotic insults, such as conventional chemotherapy and radiotherapy, and diffusely invades the brain parenchyma, which renders it elusive to total surgical resection. We found that fusicoccin A, a fungal
Receptor protein tyrosine phosphatase zeta as a therapeutic target for glioblastoma therapy.
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Astrocytomas are the most frequent brain tumour type in adults. The most common astrocytoma is the glioblastoma (GBM), which is also the most malignant and refractory to treatment--ultimately leading to the patient's death within a year of diagnosis. Neither the classical nor more experimental
No Sugar Added: A New Strategy to Inhibit Glioblastoma Receptor Tyrosine Kinases.
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A novel inhibitor of N-linked glycosylation (NGI-1) inhibits the glycosylation and phosphorylation of multiple receptor tyrosine kinases in glioblastoma (GBM). NGI-1 sensitizes multiple models of GBM to chemotherapy and radiation in vitro and in vivo and may be especially effective in GBMs that
Preferential inhibition of glioblastoma cells with wild-type epidermal growth factor receptors by a novel tyrosine kinase inhibitor ethyl-2,5-dihydroxycinnamate.
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Epidermal growth factor receptor (EGFR) gene overexpression and mutations play an important role in the pathogenesis of a variety of malignant human cancers. In this study, we tested the effects of a novel EGFR tyrosine kinase inhibitor, ethyl-2,5-dihydroxycinnamate (EtDHC), against related human
Small tyrosine kinase inhibitors interrupt EGFR signaling by interacting with erbB3 and erbB4 in glioblastoma cell lines.
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Signaling through the epidermal growth factor receptor (EGFR) is relevant in glioblastoma. We have determined the effects of the EGFR inhibitor AG1478 in glioblastoma cell lines and found that U87 and LN-229 cells were very sensitive to this drug, since their proliferation diminished and underwent a
Glioblastoma: Targeting Angiogenesis and Tyrosine Kinase Pathways
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Angiogenesis is a hallmark of glioblastoma (GBM) and remains an important therapeutic target in its treatment, especially for recurrent GBM. GBMs are characterized by the release of vascular endothelial growth factor (VEGF), an important regulator and promoter of angiogenesis. Therefore,
Sequence survey of receptor tyrosine kinases reveals mutations in glioblastomas.
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It is now clear that tyrosine kinases represent attractive targets for therapeutic intervention in cancer. Recent advances in DNA sequencing technology now provide the opportunity to survey mutational changes in cancer in a high-throughput and comprehensive manner. Here we report on the sequence
Analysis of EGFR gene amplification, protein over-expression and tyrosine kinase domain mutation in recurrent glioblastoma.
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Gefitinib and erlotinib are both selective EGFR tyrosine kinase inhibitors (EGFR-TKIs) that have produced responses in a small subgroup of lung cancer patients. The strongest evidence for a role of EGFR in the biology of glioblastoma stems from clinical trials in which 15-20% of recurrent
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