Abstract
The histone-modifying PRC2 complex has an ambiguous role in cancer, bearing both oncogenic and tumor-suppressive features depending on cell type. Studies of malignant peripheral nerve sheath tumors (MPNSTs) have now identified loss-of-function mutations altering PRC2 subunits, leading to the amplification of Ras-driven transcription and conferring vulnerability to BRD4 inhibitors.
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