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EDITORIAL

In this commissioned How I Treat series introduced by Associate Editor Mario Cazzola, experts review relevant pathophysiology and provide guidance regarding the treatment of patients with anemia in common general medical settings.

BLOOD COMMENTARIES

HOW I TREAT SERIES

Anemia

In this commissioned How I Treat series introduced by Associate Editor Mario Cazzola, experts review relevant pathophysiology and provide guidance regarding the treatment of patients with anemia in common general medical settings.

In this commissioned How I Treat series introduced by Associate Editor Mario Cazzola, experts review relevant pathophysiology and provide guidance regarding the treatment of patients with anemia in common general medical settings.

Professional illustration by Patrick Lane, ScEYEnce Studios

In this commissioned How I Treat series introduced by Associate Editor Mario Cazzola, experts review relevant pathophysiology and provide guidance regarding the treatment of patients with anemia in common general medical settings.

In this commissioned How I Treat series introduced by Associate Editor Mario Cazzola, experts review relevant pathophysiology and provide guidance regarding the treatment of patients with anemia in common general medical settings.

CLINICAL TRIALS AND OBSERVATIONS

Röllig and colleagues used data from a large German registry to demonstrate that variation in time to commencement of induction therapy for acute myeloid leukemia is not associated with survival. This has important implications for assignment of clinically stable patients to genetic test–guided therapy in both standard and clinical trial settings.

HEMATOPOIESIS AND STEM CELLS

Using the new technology of RNA tomography to provide spatially resolved genome-wide transcriptomics at given time points in development across vertebrate species, Yvernogeau et al identified the molecular landscape of the hematopoietic stem cell (HSC) microenvironment in the embryonic aorta and identified evolutionarily conserved extrinsic regulators of HSC development. Zhu and colleagues used single-cell analyses and multiomics to investigate how hemogenic endothelial cells in the embryo become precursors of hematopoietic stem cells, defining a Runx1-regulated bottleneck and 2 waves of CD45+ cells.

Using the new technology of RNA tomography to provide spatially resolved genome-wide transcriptomics at given time points in development across vertebrate species, Yvernogeau et al identified the molecular landscape of the hematopoietic stem cell (HSC) microenvironment in the embryonic aorta and identified evolutionarily conserved extrinsic regulators of HSC development. Zhu and colleagues used single-cell analyses and multiomics to investigate how hemogenic endothelial cells in the embryo become precursors of hematopoietic stem cells, defining a Runx1-regulated bottleneck and 2 waves of CD45+ cells.

IMMUNOBIOLOGY AND IMMUNOTHERAPY

LYMPHOID NEOPLASIA

Watanabe and colleagues identify that cumulative methylation of DNA at sites differentially determined by human T-cell leukemia virus 1 infection is correlated with the development and progression of adult T-cell leukemia-lymphoma (ATL). Consistent with this being functionally important, they demonstrate potent activity of hypomethylating agents in patient- and cell line–derived xenografts.

MYELOID NEOPLASIA

Deficiencies in regulatory T cells (Tregs) are a pathogenic feature of idiopathic aplastic anemia (AA). Lim et al reveal two mechanisms leading to skewed Treg composition in AA and provide an example of how this new knowledge could be used for therapeutic gain.

THROMBOSIS AND HEMOSTASIS

Chen et al made use of a cell-based screening system and an in vivo bleeding model to identify drugs that can perturb the vitamin K–dependent carboxylation machinery in a clinically impactful manner. Bleeding caused by drugs inhibiting the reduction of vitamin K epoxide but not vitamin K can be rescued by vitamin K administration.

LETTER TO BLOOD

In this phase 1 trial, inhibition of granulocyte-macrophage colony-stimulating factor (GM-CSF) was associated with clinically meaningful responses in 5 of 15 patients with relapsed or refractory chronic myelomonocytic leukemia (CMML). Preliminary data suggest that this approach may be tractable in CMML bearing activating NRAS mutations.

BLOOD WORK

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