SIGLEC9 inhibition for glioblastoma; plus Long COVID genetic risks and more

Two independent teams found deletion of the mouse homolog of SIGLEC9, SIGLECE, delayed tumor growth and prolonged survival in models of glioblastoma.

A University of Basel group, including InCephalo AG co-founder Gregor Hutter, revealed in Science Translational Medicine high expression of SIGLEC9 correlated with reduced survival in patients with glioblastoma. Microglia- and monocyte-derived cell-specific knockout of SIGLECE increased T cell activation and improved survival of anti-CD47 and anti-PD-1 co-treated mice with glioblastoma...