Blood Reviews最新文献

Neonates represent a distinct population within the context of transfusion medicine. Blood transfusions in neonates are vital interventions for multiple conditions, despite their inherent risks and potential complications. Differences in physiology and other transfusion risk factors unique to this group require careful adaptation of transfusion guidelines. This article seeks to offer a thorough overview of the current evidence-based practices for RBC administration in neonates. It covers the collection, processing and storage of RBCs and discusses the research underpinning the most recent transfusion guidelines. Furthermore, it emphasizes the challenges in establishing precise cut-off values for these conditions in both preterm and critically ill neonates and discusses indications for transfusion, thresholds, current guidelines, and potential complications. Finally, it highlights gaps in critical areas of transfusion related research and proposes future targets for research.

The global infrastructure supporting nearly 100 million transfusions annually relies on the ability to store red cell concentrates (RCCs) for up to 42 days at hypothermic temperatures or indefinitely at low sub-zero temperatures. While these methods are generally effective, there is both an opportunity and, in specific settings, a need to refine storage techniques that have remained largely unchanged since the 1980s. Recent research has identified ways to address limitations that were not fully understood when these methods were first implemented in blood banks, with much of it focusing on modifying conventional storage strategies, while some studies explore alternative approaches. In this review, we explore the current state of RBC preservation and the future prospects for advancing both short- and long-term storage strategies.

Bruton tyrosine kinase inhibitors (BTKi) have shown prominent clinical efficacy in patients with B cell malignancies, such as chronic lymphocytic leukemia, mantle cell lymphoma, diffuse large B cell lymphoma, and Waldenström's macroglobulinemia. Nevertheless, numerous factors contribute to BTKi resistance, encompassing genetic mutations, chromosomal aberrations, dysregulation of protein expression, tumor microenvironment, and metabolic reprogramming. Accordingly, potential therapeutic strategies have been explored to surmount BTKi resistance, including noncovalent BTKi, BTK proteolysis-targeting chimeras, and combination therapies. Herein, we summarize the mechanisms responsible for BTKi resistance as well as the current preclinical and clinical strategies to address BTKi resistance in B cell malignancies treatment.

Immune monitoring of cell therapies is a complex and evolving topic, particularly in the rapid expanding field of chimeric antigen receptor T (CAR-T) cell applications. Defining essential, recommended, and optional immune monitoring data post-CAR-T cell infusion is crucial to improve patient outcomes and inform post-treatment decisions. To address this gap, we conducted a survey-based study across centers affiliated with the European Society for Blood and Marrow Transplantation (EBMT), focusing on patients treated with European Medicines Agency (EMA)-approved CAR-T products. Building on a thorough review of the literature, we mapped the current landscape of immune monitoring practices and assessed their impact on clinical management. By defining the state of the art in the field, this work marks an initial step towards a structured harmonization process potentially able to enhance the management and outcomes of patients undergoing these immune cell therapies.

Classic Hodgkin lymphoma (cHL) is defined by distinctive Hodgkin Reed-Sternberg (HRS) cells, which are CD30+/CD15+ multinucleated tumor cells lacking typical B-cell markers. These cells comprise <5 % of tumor mass but orchestrate an extensive immunosuppressive tumor microenvironment (TME). Classic HL was curable with radiation therapy and multi-agent chemotherapy. Despite high cure rates, treatment-related toxicities remain significant. The goals of multimodality therapy are to achieve a cure while minimizing treatment-associated toxicity. Advances in molecular insights into HRS cells have led to transformative therapies, including checkpoint inhibitors, antibody-drug conjugates like brentuximab vedotin, which have shown remarkable efficacy, especially in relapsed or refractory disease. However, challenges persist due to the heterogeneity of cHL, driven by the complex biology of HRS cells and their surrounding tumor microenvironment. Novel approaches such as single-cell RNA sequencing and circulating tumor DNA profiling provide promising strategies to address these challenges. This review examines the origin, morphology, phenotype, and genetic profiles of HRS cells, highlighting key pathobiological features, including biomarkers and Epstein-Barr Virus involvement. It also explores the biological mechanisms underlying HRS cell survival and evaluates standard and emerging therapies, offering insights into the rationale for novel treatment strategies.

The strength of evidence supporting use of PET in the evaluation of suspected histological transformation (HT) of follicular lymphoma (FL) is unknown. We conducted a systematic review of studies reporting the diagnostic performance of ≥1 PET parameters for the detection of HT in patients with known FL. We searched PubMed for any study reporting ≥1 diagnostic performance metrics. Risk of bias was evaluated with the QUADAS2 tool. We included 7 studies encompassing 152 patients with a biopsy showing FL (or indolent non-Hodgkin lymphoma) and 111 with a biopsy confirming HT. Study designs and study populations differed substantially. PET methods were poorly reported and ¹⁸F-FDG dose was highly variable. Most studies were judged to be at high risk of bias in the patient and index test domains of QUADAS2. The diagnostic performance of 5 PET parameters were reported in at least one study but only SUVmax (n = 7) was reported in >2. Median SUVmax ranged from 9.2 to 10.9 in FL/iNHL and from 13.7 to 24.4 in HT. While SUVmax was consistently higher in the HT group, there was considerable overlap between the two groups and significant variability between studies. Area under the ROC curve for SUVmax to distinguish between FL/iNHL and HT ranged from 0.68 to 0.97. Sensitivity and specificity of the proposed cutoffs also varied widely (sensitivity ∼0.6 to 1, specificity ∼0.4 to 1). In conclusion, few studies - mostly small and potentially biased - have addressed this question. Although SUVmax is generally higher in HT than in FL, the diagnostic performance and optimal cutoffs remain unclear. Proposed SUVmax cutoffs should not be used to determine whether a patient has HT or to decide whether a biopsy should be obtained. For now, we encourage physicians to evaluate results of their own practice to devise a prudent workup of suspected.