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Hematopoietic stem cell transplantation remains the only curative therapy for certain genetic diseases of the hematopoietic system, including some inheritable deficiencies in red blood cells (RBC). Recent advances in induced pluripotent stem cells may open a new era for the cure of such severe genetic RBC diseases.
The BRAF inhibitors (BRAFi) induce anti-tumor responses in nearly 60% of patients with advanced V600BRAF-mutant melanomas but only 5% of patients with V600BRAF-mutant colorectal carcinomas. Earlier studies of how a subset of melanoma that initially responds to BRAFi but later acquires drug resistance pointed to the importance of receptor tyrosine kinases (RTKs) in drug escape. In a pair of recent reports, this RTK-mediated mechanism of acquired BRAFi resistance in melanoma is re-surfacing in the context of innate or primary BRAFi resistance in V600BRAF-mutant colorectal carcinomas, suggesting potential upfront therapeutic strategies to prevent BRAFi resistance.
Pre-leukemic MLL-AF4 fusions arise prenatally and typically lead to overt acute lymphoblastic leukemia (ALL) at or shortly after birth. In a recent study, Bueno and colleagues explored the effects of MLL-AF4 expression in human embryonic stem cells (hESCs), with a focus on early hemato-endothelial development.
Macrophage migration inhibitory factor (MIF) is overexpressed in numerous tumors and has been correlated with the development of breast cancer, but the mechanism(s) have largely remained unknown. Suppression of autophagy has now been unraveled as a pivotal mechanism underlying MIF's role in breast cancer. Strikingly, the study demonstrates that MIF phenocopies the anti-autophagic effects of steroid receptor coactivator-3 (SRC-3), a known oncogene, which in turn drives MIF gene expression.
