Issue Archive

In this How I Treat article, Wierda and Tambaro discuss the rationale for use of venetoclax in patients with chronic lymphocytic leukemia (CLL) in both the first-line and relapsed and refractory treatment settings. They provide practical guidance for the use of this novel agent that targets BCL2.

Rowan and colleagues investigated biomarkers in a prospective multicenter cohort study of nonrelapse mortality after allogeneic stem cell transplantation, identifying plasma levels of stimulation-2 (ST2) prior to transplant as prognostic, independent of significant clinical covariates.

In an international effort examining large prospective data sets, Enshaei et al demonstrate that by using a continuous variable analytical approach, a limited set of well-established prognostic factors in childhood acute lymphoblastic leukemia can improve prediction of outcomes compared to current risk stratification approaches.

Human herpesvirus 6B (HHV-6B) frequently reactivates after allogeneic hematopoietic cell transplantation (HCT). In a post hoc analysis of a randomized trial of cytomegalovirus prophylaxis, Hill et al found that brincidofovir prophylaxis reduces HHV-6B reactivation after allogeneic HCT.

Common variable immunodeficiency is usually considered to be an intrinsic disorder of B-cell development. Troilo and colleagues convincingly show that, in some patients, the defect lies within the bone marrow niche and causes defective B-cell development.

Treating pediatric acute lymphoblastic leukemia is a challenge in resource-limited countries. Pedrosa and colleagues describe the success of an approach that identifies patients at very low risk of relapse and employs a low-intensity chemotherapy regimen for these patients, achieving excellent efficacy and minimal toxicity.

Yoshida and colleagues report identification of recurrent fusion genes involving CD28 in more than one-third of young Japanese patients with adult T-cell leukemia/lymphoma (ATLL). They suggest that CTLA4-CD28 fusion may be a pathway amenable to therapeutic targeting with CTLA4 blockade.

Long and colleagues demonstrate that histone deacetylase 8 (HDAC8) upregulation is an important mechanism through which FLT3-ITD⁺ acute myeloid leukemia cells can persist during tyrosine kinase inhibitor (TKI) therapy. Their data suggest that combining HDAC8 inhibition with TKI treatment could be a promising strategy to treat tyrosine kinase mutation–harboring leukemias.

Seth Chhabra et al describe a new factor VIII (FVIII) variant created through protein engineering that has similar functional activity to recombinant or plasma-derived FVIII but with considerably enhanced pharmacokinetic properties. This may enable convenient scheduling to achieve protection against bleeding in conditions of severe hemostatic challenge.