Issue Archive

In a Plenary Paper, Merlet et al report a provocative and elegant study demonstrating that exercise training leads to muscle capillary growth in patients with sickle cell disease, a finding with potential to improve their lives.

In a Blood Spotlight that is also this month’s CME article, the authors review the current understanding of the biology underpinning mutant CALR-driven myeloproliferative neoplasms, discuss its clinical implications, and highlight future therapeutic approaches.

Hematopoietic stem cell transplantation can be curative for sickle cell disease, but decision-making is often complex. This How I Treat provides a perspective on how to negotiate this process for an individual patient.

This article reports a novel mechanism by which Epstein-Barr virus (EBV) microRNA (miRNA) plays a role to fine-tune the expression of LMP1-driven amplification of inhibitory checkpoint programmed death ligand 1 (PD-L1) and PD-L2 in EBV⁺ diffuse large B-cell lymphoma. Identification and understanding of the immune checkpoint regulation via miRNA may enable potential novel RNA-based therapies to emerge.

This article reports the largest series of patients with systemic AL amyloidosis to date treated with first-line bortezomib. With relatively mature follow-up, the data indicate the importance of a stringent dFLC response (difference in involved and uninvolved light chains) as a predictor of prolonged response.

These complementary papers by Borrow et al report persuasive but indirect evidence that the lymphoid enzyme terminal deoxynucleotidyl transferase (TdT) is the mutagen responsible for 2 common pathogenic genetic changes in acute myeloid leukemia (AML): FLT3-ITD and NPM1.

These complementary papers by Borrow et al report persuasive but indirect evidence that the lymphoid enzyme terminal deoxynucleotidyl transferase (TdT) is the mutagen responsible for 2 common pathogenic genetic changes in acute myeloid leukemia (AML): FLT3-ITD and NPM1.

The bleeding diathesis in patients with Noonan syndromes due to germline mutations in SHP2 has been described by others previously, but its mechanism has been elusive. In this article, Bellio et al demonstrate that there are distinct thrombocytopathic diatheses related to specific mutations and provide important insights relevant to the medical care of affected patients in situations where bleeding risk is heightened.