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EDITORIAL

Diagnosis and treatment of acquired hemolytic anemia can be challenging. In this How I Treat series, edited by Mario Cazzola, clinical experts discuss their approaches to the treatment of patients with 4 different classes of acquired hemolytic anemia.

BLOOD COMMENTARIES

HOW I TREAT SERIES

Acquired Hemolytic Anemia

Diagnosis and treatment of acquired hemolytic anemia can be challenging. In this How I Treat series, edited by Mario Cazzola, clinical experts discuss their approaches to the treatment of patients with 4 different classes of acquired hemolytic anemia.

Diagnosis and treatment of acquired hemolytic anemia can be challenging. In this How I Treat series, edited by Mario Cazzola, clinical experts discuss their approaches to the treatment of patients with 4 different classes of acquired hemolytic anemia.

Diagnosis and treatment of acquired hemolytic anemia can be challenging. In this How I Treat series, edited by Mario Cazzola, clinical experts discuss their approaches to the treatment of patients with 4 different classes of acquired hemolytic anemia.

Diagnosis and treatment of acquired hemolytic anemia can be challenging. In this How I Treat series, edited by Mario Cazzola, clinical experts discuss their approaches to the treatment of patients with 4 different classes of acquired hemolytic anemia.

CLINICAL TRIALS AND OBSERVATIONS

Blockade of programmed death 1 (PD-1) is now established as a standard treatment for relapsed Hodgkin lymphoma, and how this approach can be incorporated into first line therapies is an important question. Allen et al report an early-phase trial of single agent pembrolizumab for an initial 3 cycles followed by 4 to 6 cycles of chemotherapy. They demonstrate encouraging single-agent activity and excellent efficacy and tolerability for the sequential therapy in previously untreated patients with either unfavorable early-stage or advanced-stage disease.

HEMATOPOIESIS AND STEM CELLS

IMMUNOBIOLOGY AND IMMUNOTHERAPY

Congenital neutropenias (CNs) are characterized by defective neutrophil maturation caused by mutations in any one of more than 20 different genes, including the signal recognition particle 54 gene (SRP54). Schürch et al show that SRP54 mutations found in CN act in a dominant negative manner in zebrafish models, causing neutropenia due to impaired splicing of the transcription factor Xbox-binding protein 1 (XBP1).

LYMPHOID NEOPLASIA

T-cell/histiocyte-rich large B-cell lymphoma has a unique tumor microenvironment with an extensive infiltrate of T cells and histiocytes. Using multiparameter immunophenotyping studies with sophisticated spatial image analyses, Griffin and colleagues report that the unique cellular architecture of this lymphoma’s microenvironment appears to be an important contributor to immune escape of the lymphoma cells.

MYELOID NEOPLASIA

Xiao et al describe a subset of acute myeloid leukemias (AMLs) that displays expansion of mature plasmacytoid dendritic cells (pDCs). This subset is enriched for RUNX1 mutations and has a poor prognosis. The authors also show that AML blasts with RUNX1 mutations have a propensity to make pDCs, suggesting unappreciated leukemia biology and a possible therapeutic target for further exploration.

THROMBOSIS AND HEMOSTASIS

Plasma microvesicles are a heterogeneous collection of membranous cell-derived microparticles that are released in response to various insults and are typically prothrombotic. Obermayer and colleagues report the discovery of naturally occurring immunoglobulin M (IgM) antibodies that bind to microvesicles and inhibit their contribution to the propagation of coagulation. Their work reveals a specific endogenous means to counter the prothrombotic effect of microvesicles and an anticoagulant role for innate immunity.

TRANSPLANTATION

LETTERS TO BLOOD

BLOOD WORK

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