Benjamin Posorske

This study identifies MAFG as a driver of melanoma progression by interacting with MITF to alter gene expression and promote a dedifferentiated melanoma phenotype.

This paper develops a genetically engineered mouse model of uveal melanoma that recapitulates human disease progression and immune microenvironment features, revealing phenotypic plasticity and cooperative genetic drivers.

This study identifies PHGDH induction via MAPK and mTORC1 pathways as essential for melanoma formation and shows that combining BRAFV600E inhibition with serine restriction can target this vulnerability.