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Current Issue
Volume 136,
Issue 5,
July 30, 2020

Issue Highlights

Latest in Blood
Free Articles
Oliver Weigert
DOI: 10.1182/blood.2020005591
Plenary Papers
Karl C. Desch; Ayse B. Ozel; Matt Halvorsen; Paula M. Jacobi; Krista Golden; Mary Underwood; Marine Germain; David-Alexandre Tregouet; Pieter H. Reitsma; Clive Kearon; Lauren Mokry; J. Brent Richards; Frances Williams; Jun Z. Li; David Goldstein; David Ginsburg
DOI: 10.1182/blood.2019004161
First Edition
Sarah Gooding; Naser Ansari-Pour; Fadi Towfic; Maria Ortiz Estevez; Philip P Chamberlain; Kao-Tai Tsai; Erin Flynt; Marissa Hirst; Dan Rozelle; Paula Dhiman; Paola Neri; Karthik Ramasamy; Nizar J Bahlis; Paresh Vyas; Anjan Thakurta
DOI: 10.1182/blood.2020007081
Clinical Trials and Observations
Yiwei Liu; John Carl Panetta; Wenjian Yang; Seth E. Karol; Cheng Cheng; Jun J. Yang; William E. Evans; Hiroto Inaba; Ching-Hon Pui; Sima Jeha; Mary V. Relling
DOI: 10.1182/blood.2020006214


Message from ASH President on Diversity, Equity, and Inclusion

Authors and Reviewers: New COVID-19 Announcement

Featured Content

Blood Podcast: Season 1, Episode 31

In this week's episode we will review a study that demonstrates how the impaired hematopoietic stem cells (HSCs) observed in β-thalassemia can be rescued by administration of parathyroid hormone, learn more about genetic variants that can increase the risk of venous thromboembolism, and explore the identification of two DNA methylation subtypes of Waldenström’s macroglobulinemia.

Functional and genetic testing in adults with HLH reveals an inflammatory profile rather than a cytotoxicity defect

While primary hemophagocytic lymphohistiocytosis (HLH) is explained by genetic deficiencies in lymphocyte cytotoxicity, the role of intrinsic cytotoxicity defects in the more common secondary HLH has not been defined. Carvelli and colleagues reveal that no major intrinsic cytotoxicity dysfunction is seen in secondary HLH when appropriate comparisons are made with patients having the same precipitating diseases but without HLH.

MDH1-mediated malate-aspartate NADH shuttle maintains the activity levels of fetal liver hematopoietic stem cells

Gu et al used a transgenic mouse model that reports mitochondrial respiration to explore how energy metabolism and stemness interrelate between different stages of developmental hematopoiesis. Their work reveals that fetal liver stem cells principally use mitochondrial respiration as their main energy source and demonstrates how this is tightly regulated.

Identification of 2 DNA methylation subtypes of Waldenström macroglobulinemia with plasma and memory B-cell features

The B cells of 35 patients with MYD88-mutated Waldenström macroglobulinemia (WM) were studied by Roos-Weil et al, using integrated genome-wide DNA methylation, transcriptome, and mutation profiling. Their data suggest that WM can be subdivided into 2 major groups (memory B-cell–like and plasma cell–like) based on patterns of DNA methylation, each associating with different genetic and phenotypic features.

Hematopoietic stem cell function in β-thalassemia is impaired and is rescued by targeting the bone marrow niche

Aprile et al report bone marrow niche defects in a well-established murine model of β-thalassemia and suggest that the niche renders stem cells more proliferative due to reduced parathormone (PTH) expression and impaired osteolineage niche regulation. Importantly, the stem cell defect can be corrected by PTH treatment, suggesting possibilities for targeting this niche in clinical care.

Whole-exome sequencing identifies rare variants in STAB2 associated with venous thromboembolic disease

In this Plenary Paper, Desch and colleagues describe whole-exome sequencing of patients with venous thromboembolic disease (VTE) vs controls and novel analytic techniques to identify rare STAB2 variants associated with VTE, each of which reduces the surface expression of the gene product stabilin-2. Stabilin-2 enhances clearance of von Willebrand factor (VWF), and elevated levels of VWF are observed in patients with STAB2 variants, suggesting a mechanism for the elevated VTE risk. This work establishes STAB2 as a thrombophilia gene.

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