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We undertook this study to understand how the transcription factor Sox2 contributes to the malignant phenotype of glioblastoma multiforme (GBM), the most aggressive primary brain tumor.
The frequency of CC genotype for CDKN2 p16 540 C>G was significantly two-fold higher (p<0.001) and possessing a C allele conferred a ~7-fold increased risk (p=0.005) of primary brain tumor.
Amplification of the epidermal growth factor receptor (EGFR) and its mutant EGFRvIII are among the most common genetic alterations in glioblastoma (GBM), the most frequent and most aggressive primary brain tumor.
To suppress the growth and invasive effects of CD44 expression on primary brain tumors we have designed two hammerhead ribozymes as potential gene therapeutic agents.
The lack of expression of larger molecular weight CD44 variants by primary brain tumors may also partially explain why these tumors rarely metastasize to distant sites.
A frequent genetic alteration in primary brain tumors such as gliomas is an in-frame deletion in the epidermal growth factor receptor (EGFR) gene EGFRvIII, which brings together what were normally distant polypeptide sequences in the intact receptor.
Erlotinib (Tarceva<sup>®</sup>), a potent small molecule inhibitor of the epidermal growth factor receptor tyrosine kinase, has been evaluated to treat infants and children with primary brain tumors.
The Epidermal Growth Factor Receptor gene has been reported to be involved in the progression of gliomas which is one of the deadliest primary brain tumors in humans.
Mutations in the isocitrate dehydrogenase 1 and 2 (IDH1 and IDH2) genes suggest a role for this abnormal metabolic pathway in the pathogenesis and progression of these primary brain tumors.
The aim of this study is to investigate the staining pattern of mIDH1R132H, an antibody specific to mutant IDH1 protein, in primary brain tumors and non-neoplastic systemic organs.
Primary brain tumors with KIAA1549-BRAF fusion should not be treated with first-generation BRAFi due to paradoxical activation of the Ras-Raf-MEK-ERK pathway.
After her death, a review of her past medical history and comprehensive analysis of her primary brain tumor and aspiration biopsy/autopsy bone marrow samples with glial immunohistochemical markers, fluorescence in situ hybridization examination, and immunohistochemical/sequencing analyses of mutant IDH1 revealed the accurate diagnosis.
We also summarize clinical experience with RAF and MEK inhibitors in patients with primary brain tumors and describe ongoing clinical trials of RAF inhibitors in glioma.