Jeffrey K. Harrison

The paper identifies treatment-resistant persister cells in glioblastoma that exploit macrophage lipid metabolism to sustain tumor growth and immune evasion, suggesting lipid-targeted therapies could improve outcomes.

This study shows that disrupting DR5 disulfide bonds activates pro-apoptotic signaling and reveals DR5 disulfide bonding as a sensor and effector of ER stress in cancer cells.

This paper optimizes combination immunotherapy regimens for glioblastoma using a virtual murine cohort and finds personalized treatment improves survival.

This study identifies M-CSF and IL-34 as drivers of M-MDSC differentiation and T cell suppression in glioblastoma, with NOS involvement and microenvironmental niches contributing to M-MDSC heterogeneity.

This study validates a murine model of glioblastoma stem cells that recapitulate human features and enables investigation of their interactions with the immune system.

This study examines how hydroxyl dendrimers are taken up by M-MDSCs in tumor and lymphoid organs, showing differential uptake based on dendrimer functionality and serum proteins.