Issue Archive

Seymour and colleagues investigated the adverse event (AE) burdens of continuous acalabrutinib vs ibrutinib treatment during follow-up of a phase 3 randomized trial for chronic lymphocytic leukemia that demonstrated noninferiority in efficacy with acalabrutinib. The authors report exposure-adjusted incidence rates of AEs and AE-related discontinuation rates. This post hoc analysis indicates a higher AE-driven discontinuation rate for ibrutinib and a higher overall AE burden.

Preventing graft-versus-host disease (GVHD) without increasing rates of leukemia relapse remains the holy grail of allogeneic hematopoietic cell transplantation (HCT). Abatacept interrupts a key T-cell costimulatory signal and reduces acute GVHD in unrelated donor HCTs. Through pharmacokinetic (PK) data, Takahashi and colleagues describe how higher abatacept exposures correlate with lower occurrence of acute GVHD without increasing the risk of relapse or serious infection. The authors suggest that future trials should evaluate PK-driven adjustments in abatacept dosing during HCT.

Pediatric acute lymphoblastic leukemia with intrachromosomal amplification of chromosome 21 (iAMP21-ALL) has been recognized as a distinct entity for 20 years. iAMP21-ALL is associated with an older age at diagnosis and relatively unfavorable outcomes, although survival is improved when patients are treated on higher-intensity treatment regimens. Gao et al report in detail its genomic landscape across 124 cases, revealing it comprises multiple subgroups and pinpointing iAMP21 as an early event that evolves progressively over time.

Acute trauma-induced coagulopathy can be catastrophic. Han et al report on in vitro studies and an in vivo rat model of severe multisite trauma, demonstrating that leukocyte inflammation contributes to trauma-induced coagulopathy via oxidation and digestion of fibrinogen. A novel melanocortin fusion protein is demonstrated to reduce leukocyte-derived inflammation, protect fibrinogen, and prevent coagulopathy; these data suggest a potential preemptive strategy for future clinical evaluation.

Why ABO blood group antigens influence susceptibility to COVID-19 has been incompletely understood. Wu et al discovered that the receptor binding domain of SARS-CoV-2 has ABO blood group binding similarity with human galectins and exhibits specificity for blood group A, leading to a preference for infecting blood group A cells. These data provide a direct link between blood group A expression and increased infection rates.