Blood
Articles in this Issue
From breakthroughs to blueprints: evolving evidence and future directions in relapsed and refractory large B-cell lymphoma
Abstract The therapeutic landscape for relapsed or refractory large B-cell lymphoma (R/R LBCL) has undergone rapid and profound change, driven by cellular therapies, bispecific ant...
The inflammatory “death-to-life” loop in VEXAS syndrome
A step towards guided complement-targeted therapy in ITP?
Transfusing HPA-mismatched platelets to mimic fetomaternal hemorrhage elicits fetal/neonatal alloimmune thrombocytopenia
Abstract Fetal/neonatal alloimmune thrombocytopenia (FNAIT) is a bleeding disorder in which maternal antibodies target fetal and neonatal platelet alloantigens, most commonly human...
Minimal residual disease in CLL: when does it really matter?
Hitting AML where it breathes: the peroxisome fat trap
Inflammatory cell death and monocyte dysfunction in VEXAS syndrome
Abstract VEXAS (vacuoles, E1 enzyme, X-linked, autoinflammatory, somatic) syndrome is a severe adult-onset autoinflammatory disease caused by somatic mutations in the UBA1 gene, di...
Bridging the gap to pregnancy for modeling FNAIT prophylaxis
Bone marrow endothelial injury by venetoclax and azacitidine
Grabow S, Delbridge ARD, Valente LJ, Strasser A. MCL-1 but not BCL-XL is critical for the development and sustained expansion of thymic lymphoma in p53-deficient mice. <i>Blood</i> . 2014;124(26):3939-3946.
Ellis L, Bots M, Lindemann RK, et al. The histone deacetylase inhibitors LAQ824 and LBH589 do not require death receptor signaling or a functional apoptosome to mediate tumor cell death or therapeutic efficacy. <i>Blood</i> . 2009;114(2):380-393.
MYB builds leukemic enhancers
Study of NSD2 using a dTAG system reveals its molecular mechanism and oncogenic implications in t(4;14) multiple myeloma
Abstract The histone H3 lysine 36 dimethylation (H3K36me2) methyltransferase NSD2 is deleted in Wolf-Hirschhorn syndrome and is aberrantly expressed in 10% to 15% of patients with...
MYB activity drives emergent enhancer activation and enhancer-promoter interactions in acute lymphoblastic leukemia
Abstract Aberrant enhancer usage is a defining feature of oncogenic transcriptional reprogramming. Therapeutic strategies that disrupt enhancer-driven gene regulation may offer new...
Remodeling of the bone marrow vasculature induced by venetoclax and azacitidine damage
Abstract The Bcl2 inhibitor venetoclax in combination with the hypomethylating agent azacitidine (ven/aza) has become increasingly used clinically for the treatment of many hematol...
Fixed-duration VenO vs FCR/BR in fit patients with untreated CLL: primary analysis of the phase 3 CRISTALLO trial
Abstract The phase 3 CRISTALLO trial compared first-line fixed-duration venetoclax-obinutuzumab (VenO) vs fludarabine, cyclophosphamide, and rituximab (FCR)/bendamustine-rituximab...
Magnificent Seven? CD7 CARTs take a surprise shot at AML
Targeting ABCD1 inhibits peroxisomal fatty acid oxidation to selectively eliminate acute myeloid leukemia cells
Abstract Altered lipid metabolism enables growth of acute myeloid leukemia (AML) cells. Although mitochondrial lipid oxidation is well characterized, the contribution of peroxisoma...
Complement activation profile in adult primary immune thrombocytopenia
Abstract Complement activation has been reported in primary immune thrombocytopenia (ITP); however, its clinical relevance remains poorly understood. This study aimed to clarify th...
Acquisition of Philadelphia chromosome at relapse in a case of Ph-like B-ALL
How does NSD2 fuel multiple myeloma?
Anti-CD7 fratricide-resistant chimeric antigen receptor T cells for relapsed/refractory acute myeloid leukemia
Abstract Autologous second-generation CD7-directed chimeric antigen receptor T cells, expressing an anti-CD7 protein expression blocker to prevent self-killing fratricide, were inf...