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Table of Contents

BLOOD COMMENTARIES

REVIEW ARTICLE

TET2 is frequently mutated in lymphoid and myeloid malignancy. Lio et al review the current understanding of the role of TET enzymes in lymphoid and myeloid malignancy, highlighting that loss of TET protein function can occur either by mutation or as a result of metabolic alteration.

CLINICAL TRIALS AND OBSERVATIONS

Yacoub et al report excellent responses to pegylated interferon alfa-2a in patients with hydroxyurea-resistant/intolerant polycythemia vera or essential thrombocythemia.

IMMUNOBIOLOGY AND IMMUNOTHERAPY

Somekh and colleagues identify CD137, a member of the tumor necrosis factor superfamily, as a novel cause of immunodeficiency associated with a risk of autoimmunity and lymphoid malignancy.

LYMPHOID NEOPLASIA

Iyer and colleagues used deep sequencing of T-cell receptor genes to demonstrate clonal heterogeneity of mycosis fungoides, with repeated seeding of disparate clones from the blood.

MYELOID NEOPLASIA

Sun et al identify a circular RNA, circMYBL2, that upregulates FLT3 translation to promote FLT3-ITD acute myeloid leukemia (AML) progression, suggesting a novel therapeutic target for FLT3-ITD AML.

RED CELLS, IRON, AND ERYTHROPOIESIS

Xavier-Ferrucio and colleagues elucidate the mechanism of thrombocytosis in iron deficiency anemia, using murine and human cell models to demonstrate that iron deficiency attenuates ERK signaling and biases the commitment of megakaryocyte-erythrocyte progenitors toward the megakaryocytic lineage.

LETTER TO BLOOD

BLOOD WORK

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