Issue Archive

Edited by Associate Editor Robert Zeiser, this Review Series presents the current understanding of the pathophysiology of and therapeutic approaches to acute graft-versus-host disease (aGVHD). The articles discuss the role of the microbiome in contributing to aGVHD and review how novel cellular therapies, biologicals, and small-molecule inhibitors may advance its treatment.

In a Plenary Paper, the authors describe their investigation of targets of nucleoporin 98 (NUP98) fusion oncogenes, the products of recurrent translocations found in poor-prognosis acute myeloid leukemia (AML). Using mouse models and transcriptomic analysis, they found multiple transcriptional targets of NUP98 fusions and identified CDK6 as a potential candidate for targeted therapy for this subset of AML.

Edited by Associate Editor Robert Zeiser, this Review Series presents the current understanding of the pathophysiology of and therapeutic approaches to acute graft-versus-host disease (aGVHD). The articles discuss the role of the microbiome in contributing to aGVHD and review how novel cellular therapies, biologicals, and small-molecule inhibitors may advance its treatment.

Edited by Associate Editor Robert Zeiser, this Review Series presents the current understanding of the pathophysiology of and therapeutic approaches to acute graft-versus-host disease (aGVHD). The articles discuss the role of the microbiome in contributing to aGVHD and review how novel cellular therapies, biologicals, and small-molecule inhibitors may advance its treatment.

Edited by Associate Editor Robert Zeiser, this Review Series presents the current understanding of the pathophysiology of and therapeutic approaches to acute graft-versus-host disease (aGVHD). The articles discuss the role of the microbiome in contributing to aGVHD and review how novel cellular therapies, biologicals, and small-molecule inhibitors may advance its treatment.

Edited by Associate Editor Robert Zeiser, this Review Series presents the current understanding of the pathophysiology of and therapeutic approaches to acute graft-versus-host disease (aGVHD). The articles discuss the role of the microbiome in contributing to aGVHD and review how novel cellular therapies, biologicals, and small-molecule inhibitors may advance its treatment.

Radiation and chemotherapy damage hematopoietic stem and progenitor cells. Chute et al demonstrated that epidermal growth factor receptor promotes stem cell regeneration through activation of DNA repair pathways in both mouse and human stem cells.

Tumor-associated antigens (TAAs) targeted by immunotherapy are predominantly self-antigens that are overexpressed or aberrantly expressed in malignancy. Roex et al examined the T-cell repertoire in normal donors and report that naturally occurring T cells directed against TAAs are almost entirely of low reactivity, requiring priming to become active against their target antigens.

The high protein load in multiple myeloma cells renders them sensitive to proteasome inhibitors. The authors demonstrate that the chaperone protein 14-3-3ε regulates protein synthesis in myeloma cells and its expression correlates with sensitivity to proteasome inhibition.

The authors present a large retrospective analysis of 232 patients with cold agglutinin disease. They demonstrate higher prevalence of symptomatic disease in colder climates and confirm a high rate of durable responses with rituximab or rituximab-bendamustine therapy.

The authors present a retrospective analysis of bleeding and thrombosis in 400 patients hospitalized with COVID-19. They report venous thromboembolism and bleeding rates of 9.5% and 4.8%, respectively, and confirm the predictive value of elevated D-dimer levels for thrombosis, bleeding, and death.

The gut microbiome has become established as a contributor to graft-versus-host disease (GVHD). Using a mouse model, the authors demonstrated that choline-metabolized trimethylamine N-oxide (TMAO) produced in the gut worsens GVHD through activation of the NLRP3 inflammasome and modulation of macrophage polarization. A high-choline diet or TMAO enhances GVHD, which is reversed by inhibition of the NLRP3 inflammasome.