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Glioblastoma multiforme (GBM) stands out as the most tremendous brain tumor, constituting 60% of primary brain cancers, accompanied by dismal survival rates. Despite advancements in research, therapeutic options remain limited to chemotherapy and surgery. GBM molecular heterogeneity, the intricate interaction with the tumor microenvironment (TME), and non-selective treatments contribute to the neoplastic relapse. Diagnostic challenges arise from GBM advanced-stage detection, necessitating the exploration of novel biomarkers for early diagnosis. Using data from the literature and a bioinformatic tool, the current manuscript delineates the molecular interplay between human GBM, astrocytes, and myeloid cells, underscoring selected protein pathways belonging to astroglia and myeloid lineage, which can be considered for targeted therapies. Moreover, the pivotal role of extracellular vesicles (EVs) in orchestrating a favorable microenvironment for cancer progression is highlighted, suggesting their utility in identifying biomarkers for GBM early diagnosis. [ABSTRACT FROM AUTHOR]

Glioblastoma multiforme (GBM) is the most common primary brain tumor, characterized by a remarkable inner complexity and inter-tumor variability. Moreover, it is very aggressive and resistant to conventional treatments, so that it rapidly relapse. Therefore, there is an immediate need for experimental strategies to enhance our comprehension of GBM, aiming to mitigate its economic and social impact. Here, we described different in vivo and in vitro strategies currently used for the study of GBM. First, we gave a brief and general overview of the classical in vivo models, including xenograft mouse and zebrafish models and canine models, offering a wide range of advantages but also presenting a series of strong limitations. Thus, we described in vitro models, starting from more traditional 2D culture models, comparing different approaches, and critically exposing the advantages and disadvantages of using one or the other methods. We also briefly described GBM 2D culture systems that allow recreating multiple cell-cell and cell-extracellular matrix contacts but still do not reflect the complexity of in vivo tumors. We finally described the intricacies of the more novel 3D in vitro models, e.g., spheroids and organoids. These sophisticated models have demonstrated exceptional suitability across a wide spectrum of applications in cancer research, ranging from fundamental scientific inquiries to applications in translational research. Their adaptability and three-dimensional architecture render them invaluable tools, offering new insights and paving the way for advancements in both basic and applied research. [ABSTRACT FROM AUTHOR]

Glioblastoma multiforme (GBM) is a primary brain tumor that is very aggressive, resistant to treatment, and characterized by a high degree of anaplasia and proliferation. Routine treatment includes ablative surgery, chemotherapy, and radiotherapy. However, GMB rapidly relapses and develops radioresistance. Here, we briefly review the mechanisms underpinning radioresistance and discuss research to stop it and install anti-tumor defenses. Factors that participate in radioresistance are varied and include stem cells, tumor heterogeneity, tumor microenvironment, hypoxia, metabolic reprogramming, the chaperone system, non-coding RNAs, DNA repair, and extracellular vesicles (EVs). We direct our attention toward EVs because they are emerging as promising candidates as diagnostic and prognostication tools and as the basis for developing nanodevices for delivering anti-cancer agents directly into the tumor mass. EVs are relatively easy to obtain and manipulate to endow them with the desired anti-cancer properties and to administer them using minimally invasive procedures. Thus, isolating EVs from a GBM patient, supplying them with the necessary anti-cancer agent and the capability of recognizing a specified tissue-cell target, and reinjecting them into the original donor appears, at this time, as a reachable objective of personalized medicine. [ABSTRACT FROM AUTHOR]