Glioblastoma (GBM) is the most common primary malignancy of the brain with a poor prognosis. Despite advances in therapeutics, the gold standard of treatment remains maximal safe resection followed by temozolomide and radiation therapy, with the inter- and intratumoral heterogeneity of GBM making effective management challenging. As a result, the search for mechanisms underlying this heterogeneity has been paramount. The immunosuppressive and anti-inflammatory microenvironment of GBM has been of particular interest in recent years. Inflammasomes are protein complexes responsible for initiation of pro-inflammatory cascades and a specialized form of regulated cell death known as pyroptosis in response to noxious cellular stimuli. Inflammasomes play a critical role in several disease processes, including multiple sclerosis and traumatic brain injury. However, their role in GBM pathogenesis and regulation in the tumor microenvironment remains poorly understood. Here, we describe the current status of investigations into inflammasomes, their role in GBM pathogenesis, and their potential as therapeutic targets.
Govindarajan et al. (Wed,) studied this question.