HSC interactions with the niche are regulated by Wnt–β-catenin signaling. Expression of a Wnt antagonist from BM osteoblasts leads to HSC exhaustion,10 whereas activation of β-catenin within niche cells (MSCs and possibly osteoblasts or endothelial cells) induces the transformation to MDS or AML. Inhibitors of Wnt–β-catenin signaling may prevent the development of anemia and prolong survival in MDS. Illustration by Madeleine Flynn, QIMR Berghofer Medical Research Institute.
