Volume 131, Issue 18



May 3, 2018 – Welcome to “This Week in Blood,” a weekly snapshot of the hottest studies from each week’s issue of Blood, the official journal of the American Society of Hematology (ASH), hand-picked by Blood Editor-in-Chief Bob Löwenberg, MD, PhD, and Deputy Editor Nancy Berliner, MD.

Cover Figure: Ruxolitinib protects skin stem cells and improves cutaneous manifestations of murine GVHD.
See the article by Takahashi et al.

Stable lines and clones of long-term proliferating normal, genetically unmodified murine common lymphoid progenitors
Kawano and colleagues develop a culture system allowing the long-term proliferation of unmanipulated lymphoid progenitor cells. These cells retain the ability to differentiate into all lymphoid lineages in vitro and in vivo.

High-grade B-cell lymphoma with MYC and BCL2 and/or BCL6 rearrangements with diffuse large B-cell lymphoma morphology
Scott and colleagues use a large cohort of diffuse large B-cell lymphoma samples to delineate the challenges of developing screening strategies to identify double-hit lymphomas while limiting the extent of fluorescence in situ hybridization testing required to successfully identify this high-risk population.

Epigenetic regulation of NFE2 overexpression in myeloproliferative neoplasms
Myeloproliferative neoplasms (MPNs) are associated with upregulation of the NFE2, and induced overexpression of NFE2 induces an MPN phenotype. Peeken et al examine the mechanism of NFE2 upregulation in MPNs, demonstrating two epigenetic regulatory pathways that cooperate to increase NFE2 expression.

Ruxolitinib protects skin stem cells and maintains skin homeostasis in murine graft-versus-host disease
Takahashi et al report that while topical steroids worsen skin stem cell loss in a murine model of graft-versus-host disease, ruxolitinib protects skin stem cells, restores hair growth, and promotes wound healing.

BTKCys481Ser drives ibrutinib resistance via ERK1/2, and protects BTKwild-type MYD88-mutated cells by a paracrine mechanism
Chen et al investigate the mechanism of ibrutinib resistance in MYD88-mutated cells mediated by the acquisition of a BTKCys481Ser mutation. The mutation leads to upregulation of ERK1/2 and upregulation of cytokine production. The authors make the novel observation that this pathway can confer resistance on BTKwild-type cells by a paracrine mechanism.

Coagulopathy induced by traumatic brain injury: systemic manifestation of a localized injury
In a Blood Spotlight, Zhang and colleagues review the current understanding of the pathophysiology of coagulopathy in the setting of traumatic brain injury, discussing how disruption of the blood-brain barrier allows systemic propagation of coagulation and fibrinolysis in response to localized brain injury.


View this week's complete table of contents

Why Submit to Blood?


Blood (, the most cited peer-reviewed publication in the field of hematology, is available weekly in print and online. Blood is the official journal of the American Society of Hematology (ASH) (, the world’s largest professional society concerned with the causes and treatment of blood disorders.

ASH’s mission is to further the understanding, diagnosis, treatment, and prevention of disorders affecting blood, bone marrow, and the immunologic, hemostatic, and vascular systems by promoting research, clinical care, education, training, and advocacy in hematology.

blood® is a registered trademark of the American Society of Hematology.