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Learn MoreThe underlying mechanisms responsible for the competitive advantage of MDS HSPC in an inflammatory milieu remains poorly defined. Here, we show that MDS HPSC are protected from low-grade chronic inflammation, and that the adaptive response of these cells to the inflammatory milieu via the non-canonical NF-B pathway contributes to sustained myeloid expansion and a competitive advantage. These findings uncover the mechanistic basis for the clonal dominance of functionally impaired MDS HSPC and reveal the therapeutic potential of interfering with non-canonical NF-B signaling. SOURCE: Kwangmin Choi Cincinnati Children's Hospital Medical Center
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