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Fig. 3 | Experimental Hematology & Oncology

Fig. 3

From: Mechanistic insights and the clinical prospects of targeted therapies for glioblastoma: a comprehensive review

Fig. 3

Schematic representation of alternate treatment modalities investigated in GBM. (A) Neural and mesenchymal stem cells (NSCs and MSCs) exhibit chemotactic migratory capabilities and will migrate to GBM tumours where elevated levels of chemoattractants are present. NSCs and MSCs elicit cell death in GBM tumours by secreting proinflammatory chemokines and TRAILs into the tumour microenvironment. Additionally, NSCs and MSCs can be loaded with oncolytic viruses, or co-administered with drugs to facilitate specific delivery of these anti-cancer agents to tumours. NSCs and MSCs developed against GBM tumours are listed in the red box. (B) Chimeric antigen receptor (CAR) T cells (in red boxes) have been engineered to bind to tumour-associated receptors commonly expressed in GBM tumours, such as EGFRvIII and IL-13Rα2, allowing for the induction of tumour-specific T cell cytotoxicity. (C) Oncolytic virotherapy has been developed for the specific targeting of GBM tumours by inducing oncolytic lysis of the tumour cells. During which, immunostimulatory cytokines are released into the tumour microenvironment. Consequently, various immune cells are trafficked to the tumour to mount an anti-tumour immune response. Various oncolytic viruses have been engineered and are investigated for the treatment of GBM (in the red box)

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