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, and Deputy Editor Nancy Berliner, MD. If you would like a PDF copy of any of the manuscripts highlighted below or would like to request an interview with the author, please email email@example.com
Inflammatory neovascularization during graft-versus-host disease is regulated by αv integrin and miR-100, Leonhardt et al.
In this week’s Plenary Paper, Leonhardt and colleagues propose that neovascularization may play a significant role in the development of acute graft-versus-host disease (aGVHD) involving the gut. Using a mouse model of aGVHD, researchers demonstrate a correlation between blocking endothelial integrin expression and preventing the accumulation of endothelial cells with decreased neovascularization and aGVHD severity. Furthermore, researchers identify the microRNA miR-100 as being downregulated in intestinal tissue in the setting of aGVHD. This research provides an entry point for new interventions targeting angiogenesis for the treatment of aGVHD.
A European collaborative study of treatment outcomes in 346 patients with cardiac stage III AL amyloidosis, Wechalekar et al.
The prognosis for patients with amyloidosis and advanced cardiac failure is poor, and most of these patients are excluded from clinical trials. In this multi-center study of a large cohort of patients with cardiac stage III AL amyloidosis, Wechalekar and colleagues report the surprising result that, despite advanced disease, these patients may respond to chemotherapy, with 33 percent hematologic responses and 12 percent complete responses. This is testimony to the impact of the effective chemotherapeutic agents that have been developed for plasma cell dyscrasias and suggests that all patients with amyloidosis should be considered for therapy.
Mi2β-mediated silencing of the fetal γ-globin gene in adult erythroid cells, Amaya et al.
Increasing γ -globin expression is an effective strategy for the treatment of sickle cell disease. During hemoglobin switching, γ -globin gene expression is silenced through the activity of the transcription factor BCL11A. In this week’s issue of Blood, Amaya and colleagues further elucidate the molecular mechanism of hemoglobin switching and identify a potential target for increasing γ -globin gene expression. They demonstrate that Mi2β, a component of the NuRD chromatin modifying complex, binds directly to BCL11A and KLF1 and increases their activity. Investigators also demonstrate that reducing the expression of Mi2 β increases γ -globin expression, suggesting that it may be a potential target for the induction of fetal hemoglobin.
Reporters who wish to receive a copy of any of the manuscripts highlighted above or would like to request an interview with the authors may contact Amanda Szabo at 202-552-4914 or firstname.lastname@example.org
Blood (www.bloodjournal.org), 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) (www.hematology.org), the world’s largest professional society concerned with the causes and treatment of blood disorders.
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