Abstract
Glioblastoma (GBM) is the most deadly primary brain tumour and is a paradigmatic example of heterogeneous cancer. Although expanding data propose the phenotypic plasticity exhibited by glioblastoma cells, as a critical feature involved in the tumour development and posttherapy recurrence, the central machinery responsible for their aggressiveness remains elusive. Despite decades of research, the complex biology of the glioblastoma is still unknown. Progress in genetic and epigenetic discoveries has improved diagnostic classification, prognostic information, and therapeutic planning. In the complex model of intercellular signalling, several studies have shown that extracellular vesicles have a key role in the intercellular communication among GBM cells and the tumour microenvironment modulation. The purpose of this review is to summarize the role of the EV-mediated intercellular crosstalk in the glioblastoma physiopathology.
Highlights
Glioblastoma (GBM) is the most common and malignant brain tumour in adults [1]
Despite aggressive treatments used in GBM, such as surgical resection followed by radiotherapy and temozolomide therapy and in tumour regrowth/recurrence, salvage therapy options, including repeat surgical resection, antiangiogenic therapy, and immunotherapy, the limited success of current treatment leads to poor prognosis [2]
The major transforming event occurring in the 50% of GBM cases is the amplification, rearrangement, or point mutations of the oncogenic receptor tyrosine kinases, known as epidermal growth factor receptor (EGFR), whereas a large proportion of cases is positive for a distinct mutant known as EGFRvIII [45]
Summary
Glioblastoma (GBM) is the most common and malignant brain tumour in adults [1]. Despite aggressive treatments used in GBM, such as surgical resection followed by radiotherapy and temozolomide therapy and in tumour regrowth/recurrence, salvage therapy options, including repeat surgical resection, antiangiogenic therapy (bevacizumab), and immunotherapy, the limited success of current treatment leads to poor prognosis [2]. E GBM therapy resistance is linked both to intrinsically aggressive traits as well as to its heterogeneity [2]. Such heterogeneity derives from the accumulation of mutations and from the dynamic changes in the cell status, stemming from the clonal genomic selection and the phenotypic modifications [4, 5]. Aside from the heterogeneity linked to distinct genetic mutation, studies on GBM stem-like cells have shown that the functional cell diversification can be described within an unchanged genomic background [3, 8]. E purpose of this review is to summarize the EV role in the intercellular crosstalk, underling the advances in the knowledge of genetic profiling and epigenetic plasticity in the glioblastoma physiopathology
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