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.
Invasive fungal infection and impaired neutrophil killing in human CARD9 deficiency, Drewniak et al.
This week’s Plenary Paper reports on the mechanism of invasive fungal infections in individuals with Caspase recruitment domain-containing protein 9 (CARD9) deficiency. Such fungal infections (candida) can be either mucosal or systemic, and the pathways governing their development are distinct; patients generally contract either one or the other. Mucosal candida is controlled by adaptive immunity by IL-17 producing lymphocytes, while systemic infection is blocked by innate immunity through the activity of neutrophils. This manuscript reports that because CARD9 sits at the intersection of these fungal infection pathways, patients with CARD9 deficiency display both decreased TH17 lymphocytes and impaired phagocyte function and consequently suffer from both mucosal and systemic fungal infection.
Hyperdiploidy with 58-66 chromosomes in childhood B-acute lymphoblastic leukemia is highly curable: 58951 CLG-EORTC results, Dastague et al.
While it has been known for some time that hyperdiploidy is a good prognostic feature of childhood acute lympocytic leukemia (ALL), the outcome for patients with chromosomal numbers of 50 or higher remains a subject of debate. In this week’s issue of Blood, Dastugue and colleagues report results of an analysis of a large group of patients enrolled in a Children’s Leukemia Group-European Organisation for Research and Treatment of Cancer clinical trial (CLG-EORTC cohort 58951) to determine if specific chromosomal gains or other features indicated good prognosis. Data from the analysis show that the strongest predictor of survival was not specific chromosomal gain, but rather a modal chromosome number of 58-66, as patients with a modal chromosome number within this range experienced 100 percent survival with therapy.
Glucose metabolism impacts the spatio-temporal onset and magnitude of HSC induction in vivo, Harris et al.
In this week’s issue of Blood, Harris and colleagues report on the metabolic modulation of hematopoietic stem cell (HSC) development. In this manuscript, investigators demonstrate that glucose uptake enhances HSC development and metabolic inhibitors diminish stem cell numbers in a zebrafish model and propose a mechanism by which this metabolic modulation occurs. They also demonstrate that glucose modulates hif1α expression, which has a downstream effect on HSC-relevant gene expression.
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 Andrea Slesinski at 202-552-4927 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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