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Current Issue
Volume 142,
Issue 22,
November 30 2023

Issue Highlights

Latest in Blood
Plenary Papers
Sruthi Cheloor Kovilakam; Muxin Gu; William G. Dunn; Ludovica Marando; Clea Barcena; Serena Nik-Zainal; Irina Mohorianu; Siddhartha P. Kar; Margarete A. Fabre; Pedro M. Quiros; George S. Vassiliou
First Edition
Ethan Andrew Mack; Meaghan C. Dougher; Ashley Ginda; Caitlin Q Cahill; Melissa Murter; Kevin Schell; Yvette C Tanhehco; Vijay Bhoj; Andrew D Fesnak; Don L Siegel; Taku Kambayashi; Nicole Aqui; Una O'Doherty
Clinical Trials and Observations
Mattia D'Agostino; Giuseppe Bertuglia; Delia Rota-Scalabrini; Angelo Belotti; Sonia Morè; Paolo Corradini; Stefania Oliva; Antonio Ledda; Mariella Grasso; Vincenzo Pavone; Sonia Ronconi; Iolanda Donatella Vincelli; Stelvio Ballanti; Cristina Velluti; Claudia Cellini; Alessandro Gozzetti; Angelo D. Palmas; Barbara Gamberi; Katia Mancuso; Laura Paris; Renato Zambello; Maria Teresa Petrucci; Benedetto Bruno; Pellegrino Musto; Francesca Gay


Featured Content

High-risk cytogenetics in solitary bone plasmacytomas; complement activation in vaso-occlusive pain episodes; platelet reactivity to predict thrombotic disease risk

On today’s podcast we'll discuss high-risk cytogenetic abnormalities in solitary bone plasmacytomas. Then, we'll consider complement activation in vaso-occlusive pain episodes and how targeting C5a generation inhibited those effects. Finally we'll explore the genetics of platelet reactivity and how researchers used this data to develop a genetic score that was associated with risk of thrombotic diseases.

Impact of cytogenetic abnormalities on the risk of disease progression in solitary bone plasmacytomas

Solitary bone plasmacytoma (SBP) is generally considered a low-risk disease condition, and radiation therapy is curative for roughly half of the patients. However, Yadav and colleagues show that this paradigm does not hold true for SBP presenting with 1 or more high-risk cytogenetic markers: +1q or del(17p). Despite radiation therapy, median time to progression to symptomatic myeloma was only 8 months, demonstrating that there is a group of patients who need immediate systemic treatment to prevent further end-organ damage

A signature of platelet reactivity in CBC scattergrams reveals genetic predictors of thrombotic disease risk

Genetically determined platelet reactivity is postulated to modulate the risk of thrombotic diseases, including coronary artery disease, ischemic stroke, and venous thromboembolism, but assessing this at population-scale has not been possible. Verdier et al pioneered a novel method to predict platelet reactivity from complete blood count (CBC) data and applied it to identify associated genetic variants and find associations with thrombotic diseases. This new approach has exciting potential to discover novel targets to reduce thrombosis.

Cold exposure induces vaso-occlusion and pain in sickle mice that depend on complement activation

Patients with sickle cell disease (SCD) may have more severe symptoms, especially pain, after cold exposure, but this has not been well explained. Ivy et al show that the alternative complement pathway drives vaso-occlusion and pain after cold exposure in a mouse model of SCD. Inhibition of C5a generation with anti-C5 or signaling with anti-C5aR antibody inhibits cold-induced vaso-occlusive episodes and hyperalgesia, suggesting therapeutic avenues for clinical evaluation.

O-linked sialic acid residues on platelet membrane glycoprotein IIb mask the human HPA-9b alloepitope

Accurate diagnosis of fetal/neonatal alloimmune thrombocytopenia is important and requires the presence of both fetomaternal (parental) platelet antigen incompatibility and maternal antibodies specific to the incompatible antigen. Using induced pluripotent stem cells, Zhang and colleagues show that maternal alloantibodies in sera can be either sialylation-dependent or independent. This opens new ways to enhance antibody detection and reveal alloantibodies that would otherwise be missed.

EGR1-mediated metabolic reprogramming to oxidative phosphorylation contributes to ibrutinib resistance in B-cell lymphoma

Resistance to ibrutinib is a cause of treatment failure in mantle cell lymphoma (MCL). Liu et al describe a new route to acquired ibrutinib resistance via the transcription factor early growth response gene 1 (EGR1) which induces metabolic changes towards oxidative phosphorylation (OXPHOS) in MCL and also activated B-cell–like diffuse large B-cell lymphoma. Targeting OXPHOS with IM156, a novel chemical derivative of metformin, overcomes ibrutinib resistance, suggesting a future strategy for testing in clinical trials.

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