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Another characteristic feature of GBM is the presence of palisading cells around the area of necrosis (Figure 2C, arrows), which is widely regarded as a poor prognostic hallmark of GBM ( 10, 11). The presence of central necrosis (Figure 2A, arrows) and marginal proliferation of endothelial cells (microvascular hyperplasia) (Figure 2B, arrows) are hallmark histological features that separate GBM from lower grade glial tumors. This review examines the current knowledge on the CSC markers SALL4, OCT-4, SOX2, STAT3, NANOG, c-Myc, KLF4, CD133, CD44, nestin, and glial fibrillary acidic protein, specifically focusing on their use and validity in GBM research and how they may be utilized for investigations into GBM’s cancer biology. This is compounded further by the presence of multiple GBM and glioblastoma cancer stem cell subtypes, making investigation and establishment of a universal treatment difficult. Studies of many cancer types have identified CSCs using specific markers, but it is still unclear as to where in the stem cell hierarchy these markers fall. CSCs possess the ability for perpetual self-renewal and proliferation, producing downstream progenitor cells that drive tumor growth.
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Glioblastoma multiforme (GBM), an aggressive tumor that typically exhibits treatment failure with high mortality rates, is associated with the presence of cancer stem cells (CSCs) within the tumor. 3Centre for Biodiscovery, School of Biological Sciences, Victoria University of Wellington, Wellington, New Zealand.2Department of Neurosurgery, Wellington Regional Hospital, Wellington, New Zealand.
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