Volume 131, Issue 4



January 25, 2018 – 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, PhD, and Deputy Editor Nancy Berliner, MD.

Cover Figure: Suppression of erythropoiesis in iron deficiency is coordinated by HRI through eIF2αP and mTORC1. See the article by Zhang et al.

A phase 1 study of romidepsin and pralatrexate reveals marked activity in relapsed and refractory T-cell lymphoma
Amengual and colleagues report a phase 1 study of romidepsin and pralatrexate in relapsed/refractory lymphoma, including 14 patients with peripheral T-cell lymphoma (PTCL). They report a high rate of response among PTCL patients, suggesting a possible new backbone for future therapy of T-cell lymphoma.

Somatic mutations and clonal hematopoiesis in congenital neutropenia
Both severe congenital neutropenia and Shwachman-Diamond syndrome (SDS) are associated with the development of acute myeloid leukemia (AML). Xia et al used exome sequencing to demonstrate that clonal hematopoiesis does not reflect an increase in total somatic mutations, but rather the clonal selection of cells carrying specific mutations. They report that over half of patients with SDS carry somatic mutations in TP53, suggesting that acquisition of TP53 mutations is an early event in AML development.

HRI coordinates translation by eIF2αP and mTORC1 to mitigate ineffective erythropoiesis in mice during iron deficiency
Zhang and colleagues elucidate the mechanism by which erythropoiesis is suppressed in iron deficiency (ID). Using mouse models of ID, they demonstrate that heme-regulated eIF2α kinase (HRI) is upregulated by heme deficiency, leading to several intermediary steps that ultimately suppress erythropoiesis through the mTORC1 pathway.

Mutant JAK3 signaling is increased by loss of wild-type JAK3 or by acquisition of secondary JAK3 mutations in T-ALL
The JAK3 kinase is mutated in 10% to 16% of cases of T-cell acute lymphoblastic leukemia (T-ALL). Degryse et al observed that one-third of these cases harbor 2 JAK3 mutations and that second mutations increase the oncogenic potential of mutant JAK3.

How I treat CLL patients with ibrutinib
The Bruton tyrosine kinase inhibitor ibrutinib has been a major addition to the chronic lymphocytic leukemia (CLL) armamentarium. However, its known toxicities in real-world use have resulted in increased drug discontinuation and inferior survival in comparison with early trials. This How I Treat article provides detailed and helpful guidance for the management of expected toxicities that maximizes the potential positive impact of ibrutinib on CLL therapy.

Single-board hematology fellowship track: a 10-year institutional experience
In the United States, there is growing concern about the decline in the number of dedicated hematologists in hematology-oncology fellowship programs. In a Letter to Blood, Naik and colleagues examine the impact over 10 years of a single-board hematology track within the Johns Hopkins hematology-oncology fellowship, demonstrating a high rate of retention in academic hematology.


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