How does the oncogene astrocyte elevated gene-1 (AEG-1) augment glioma progression?

摘要: Gliomas are common primary brain tumors in adults that for the most part lethal. Recent studies suggest gliomas can arise from adult neural stem cells or multipotential progenitor exist subventricular and subgranular zone [1]. According to WHO, classified into four malignancy grades (I–IV) based on their histological features; among these, grade I II considered low-grade with better prognosis, while glioblastoma multiforme ([GBM], malignant glioma, IV) has worst prognosis. Patients diagnosed glioma display a median survival of approximately 12–15 months even multimodal therapeutic approaches including maximal tolerated surgery, chemotherapy radiotherapy [2]. exhibit strong propensity invade healthy tissue by migrating through convoluted extracellular spaces parenchyma, eventually develop at distant locations. Due this invasive nature human it is difficult define borders between normal tumor, which leads incomplete surgical excision tumors. As such, following surgery as combination therapies standard care management Malignant highly heterogeneous both genetically pathologically, makes selection diagnostic markers targeted challenging. The Cancer Genome Atlas (TCGA) network established three essential signaling pathways important progression RTK/RAS/PI3K, p53 Rb [3]. Additionally, several hallmark tumorigenesis features relevant progression, uncontrolled proliferation, invasion, angiogenesis chemo-radio resistance. Consequently, imperative understand Luni Emdad‡,1,2,3, Bin Hu1, Timothy P Kegelman1, Swadesh K Das1,2,3, Devanand Sarkar1,2,3 & Paul B Fisher*,‡,1,2,3 “The multifaceted role AEG-1 implies inhibition would be an appropriate end point counter pathogenesis dismal disease, particularly conjunction other current treatment modalities.”