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SRSF2-mutated MDS: bortezomib STAT?

In this issue of Blood, Takashima et al show that reduced STAT1 abundance in SRSF2-mutant myelodysplastic syndrome (MDS) cells confers protection against interferon (IFN)-driven cell suppression relative to normal wild-type (WT) cells.1 Importantly, the authors demonstrate that treatment with the proteasome inhibitor bortezomib in vitro increases STAT1 abundance and sensitizes SRSF2-mutant cells to IFN. These findings provide potential rationale for using bortezomib therapy in SRSF2-mutated MDS, which is characterized by poor outcomes.