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Current Issue
Volume 136,
Issue 16,
October 15, 2020

Issue Highlights

Latest in Blood
Free Articles
Stephen P. Hunger; Elizabeth A. Raetz
DOI: 10.1182/blood.2019004043
Plenary Papers
T. R. L. Klei; J. Dalimot; B. Nota; M. Veldthuis; F. P. J. Mul; T. Rademakers; M. Hoogenboezem; S. Q. Nagelkerke; W. F. J. van IJcken; E. Oole; P. Svendsen; S. K. Moestrup; F. P. J. van Alphen; A. B. Meijer; T. W. Kuijpers; R. van Zwieten; R. van Bruggen
DOI: 10.1182/blood.2020005351
First Edition
Barbara A Konkle; Christopher Walsh; Miguel A Escobar; Neil C Josephson; Guy Young; Annette von Drygalski; Scott W. J. McPhee; R. Jude Samulski; Ivan Bilic; Maurus De La Rosa; Birgit Reipert; Hanspeter Rottensteiner; Friedrich Scheiflinger; John Chapin; Bruce M. Ewenstein; Paul Edward Monahan
DOI: 10.1182/blood.2019004625
Clinical Trials and Observations
Erica Brivio; Franco Locatelli; Marta Lopez-Yurda; Andrea Malone; Cristina Diaz de Heredia; Bella Bielorai; Claudia Rossig; Vincent H.J. van der Velden; Anneke CJ Ammerlaan; Adriana Thano; Inge Margriet van der Sluis; Monique L. Den Boer; Ying Chen; Barbara Sleight; Benoit Brethon; Karsten Nysom; Lucie Sramkova; Ingrid ├śra; Luciana Vinti; Christiane Chen-Santel; Christian Michel Zwaan
DOI: 10.1182/blood.2020007848


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Authors and Reviewers: New COVID-19 Announcement

Featured Content

Blood Podcast: Season 1, Episode 42

In this week’s episode, we will review a study that utilized whole-genome sequencing to define the mutational spectrum and clonal architecture of myelodysplastic/ myeloproliferative neoplasms, learn more about the association between plasma levels of growth differentiation factor 15 and the risk of venous thromboembolism, and examine the role of microenvironment myeloid cells in supporting the growth of T-cell acute lymphoblastic leukemia.

Tumor-associated myeloid cells provide critical support for T-ALL

Lyu et al investigated the role of the microenvironment in T-cell ALL (T-ALL), demonstrating that monocyte-macrophages are necessary for supporting the survival and proliferation of T-ALL cells in vitro and in vivo in murine models. In addition, they demonstrated that an enriched macrophage signature in human pediatric T-ALL is associated with inferior outcomes, suggesting that tumor-associated myeloid cells might offer a novel target for T-ALL therapy.

Molecular landscape and clonal architecture of adult myelodysplastic/myeloproliferative neoplasms

Myelodysplastic/myeloproliferative (MDS/MPN) neoplasms are a heterogeneous set of syndromes, including chronic myelomonocytic leukemia, atypical chronic myeloid leukemia, MDS/MPN with ring sideroblasts and thrombocytosis, and MDS/MPN unclassifiable (MDS/MPN-U). Using genome-wide sequencing, the authors defined gene signatures underlying genotype-phenotype associations and demonstrated that many patients with MDS/MPN-U have signatures that mimic other subtypes.

How I treat relapsed acute lymphoblastic leukemia in the pediatric population

Although 85% of pediatric patients with ALL have long-term remission following chemotherapy, the prognosis of relapsed ALL remains poor. Hunger and Raetz use multiple scenarios involving 3 illustrative patients to highlight advances in therapy for relapsed ALL and discuss appropriate sequencing of hematopoietic stem cell transplantation and novel immunotherapies.

Plasma levels of growth differentiation factor 15 are associated with future risk of venous thromboembolism

Growth differentiation factor 15 (GDF-15) is elevated in inflammation and a biomarker for arterial cardiovascular disease. The authors examined the association between GDF-15 and venous thromboembolism (VTE). They demonstrated that elevated plasma levels of GDF-15 are associated with increased VTE risk, with Mendelian randomization suggesting that it is a biomarker of potential VTE risk but not causal.

VEGF-C protects the integrity of the bone marrow perivascular niche in mice

The bone marrow stem cell niche is critical for hematopoietic stem cell development. The authors demonstrate that vascular endothelial growth factor C (VEGF-C) is critical for maintaining the niche: elimination of VEGF-C leads to delayed hematopoietic recovery posttransplant, and exogenous VEGF-C accelerates hematopoietic recovery from irradiation.

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