American Journal of Hematology最新文献

{"title":"Multicenter Retrospective Evaluation of Treatment for High‐Risk Acute Promyelocytic Leukemia: Real‐World Outcomes From the HERO Consortium","authors":"Lydia L. Benitez, Kayleigh R. Marx, Caitlin R. Rausch, Kaitlyn M. Buhlinger, Stephen M. Clark, Justin H. Reid, Mimi Lo, Katie S. Gatwood, Sarah Profitt, Richa Shah, Jenna Ciervo, Jeffrey Baron, Bernard L. Marini, Anthony J. Perissinotti, Ashley Soule, Madeline Waldron, Benyam Muluneh","doi":"10.1002/ajh.27667","DOIUrl":"https://doi.org/10.1002/ajh.27667","url":null,"abstract":"","PeriodicalId":7724,"journal":{"name":"American Journal of Hematology","volume":"183 1","pages":""},"PeriodicalIF":12.8,"publicationDate":"2025-03-26","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143702661","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":1,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Sézary Syndrome—Eosinophilia Explained by a Blood Film","authors":"Merel T. A. Soeterik, Joris Janssen, Leo M. Budel, Anton W. Langerak, Yorick Sandberg, Barbara J. Bain","doi":"10.1002/ajh.27673","DOIUrl":"https://doi.org/10.1002/ajh.27673","url":null,"abstract":"<div>\u0000<figure>\u0000<div><picture>\u0000<source media=\"(min-width: 1650px)\" srcset=\"/cms/asset/e6d81656-5778-4c1c-b3d8-11da987a6fef/ajh27673-gra-0001-m.jpg\"/><img alt=\"image\" data-lg-src=\"/cms/asset/e6d81656-5778-4c1c-b3d8-11da987a6fef/ajh27673-gra-0001-m.jpg\" loading=\"lazy\" src=\"/cms/asset/bea8d614-6dff-40e4-927d-0531b119246b/ajh27673-gra-0001-m.png\" title=\"image\"/></picture><p></p>\u0000</div>\u0000</figure>\u0000</div>\u0000<p>A 61-year-old man, with no significant medical history, presented with a six-month history of fatigue, pruritus, night sweats, and weight loss. Physical examination revealed erythroderma and generalized lymphadenopathy. Laboratory tests showed prominent eosinophilia (white blood cell count 10.6 × 10⁹/L, eosinophils 2.9 × 10⁹/L). There was no lymphocytosis (lymphocyte count 1.1 × 10⁹/L). Lactate dehydrogenase (LDH) was elevated at 469 U/L. A peripheral blood smear (top left and top right, May–Grünwald–Giemsa [MGG], ×100 objective) highlighted marked eosinophilia alongside large, atypical lymphocytes with convoluted and grooved nuclei. Lymph node biopsy confirmed infiltration by an aberrant T-cell population. Bone marrow examination showed atypical large T cells accounting for 14% of the total cell population and an eosinophil fraction of 25% (bottom left, MGG, ×100). A skin punch biopsy (bottom right, hematoxylin and eosin, ×20) demonstrated superficial perivascular lymphocytic and eosinophilic dermatitis, with no spongiosis or epidermotropism. Immunohistochemical analysis identified abnormal lymphocytes expressing CD4 with a CD4:CD8 ratio ≥ 10 and concurrent loss of CD5 and partial loss of CD7. Subsequent immunophenotyping of peripheral blood, bone marrow, and lymph nodes confirmed the presence of an identical clonal T-cell population with loss of CD26 expression also being shown.</p>\u0000<p>Based on these peripheral blood and histopathological findings in the context of erythroderma, the diagnosis of Sézary syndrome was established. Sézary syndrome is an aggressive form of mature T-cell leukemia, characterized by refractory symptoms and a poor prognosis. Eosinophilia occurs frequently [<span>1</span>] and is believed to result from the secretion of specific Th2-associated cytokines by neoplastic cells [<span>2</span>].</p>\u0000<p>There are innumerable causes of eosinophilia. Sézary syndrome is one of a number of causes that may be revealed by peripheral blood examination. This may be so even when the lymphocyte count is not increased. In addition, the eosinophil count may be of prognostic significance in cutaneous T-cell lymphomas [<span>1</span>].</p>","PeriodicalId":7724,"journal":{"name":"American Journal of Hematology","volume":"183 1","pages":""},"PeriodicalIF":12.8,"publicationDate":"2025-03-26","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143703040","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":1,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Update in GVHD Prophylaxis: Novel Pharmacologic and Graft Manipulation Strategies","authors":"Elizabeth O. Hexner,&nbsp;Zachariah DeFilipp","doi":"10.1002/ajh.27597","DOIUrl":"10.1002/ajh.27597","url":null,"abstract":"<div>\u0000 \u0000 <p>Prevention of graft-versus-host disease (GVHD) is critical to successful allogeneic hematopoietic cell transplantation (HCT), but for many years was difficult to achieve. Advances in the understanding of allogeneic HCT biology and immunology have paved the way for novel clinical approaches to GVHD prophylaxis, highlighted by the broad adoption of posttransplant cyclophosphamide and the approval of abatacept by the US Food and Drug Administration to prevent acute GVHD. Patients undergoing allogeneic HCT are now experiencing severe acute GVHD at historically low rates, and significant improvements in preventing chronic GVHD are also being achieved. This review highlights key pharmacological approaches and graft manipulation strategies being used or investigated for GVHD prophylaxis. Furthermore, we discuss the ongoing unmet needs in GVHD prevention and the challenges in addressing these areas in future clinical trials.</p>\u0000 </div>","PeriodicalId":7724,"journal":{"name":"American Journal of Hematology","volume":"100 S3","pages":"30-39"},"PeriodicalIF":10.1,"publicationDate":"2025-03-24","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143678336","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":1,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Steroid Refractory Acute GVHD: The Hope for a Better Tomorrow","authors":"Portia Smallbone,&nbsp;Rohtesh S. Mehta,&nbsp;Amin Alousi","doi":"10.1002/ajh.27592","DOIUrl":"10.1002/ajh.27592","url":null,"abstract":"<div>\u0000 \u0000 <p>Steroid-refractory acute graft-versus-host disease (SR-AGVHD) presents a significant barrier to successful outcomes following allogeneic hematopoietic cell transplantation (HCT), despite advancements in GVHD prophylaxis and management. While ruxolitinib therapy has shown improved response rates, survival benefits remain elusive. This review explores the definitions and proposed distinct pathophysiology and treatment landscape of SR-AGVHD. Emerging therapies offer potential, yet further research is critical to better define steroid-refractory populations, improve treatment precision with biomarkers, and overcome resistance, particularly in ruxolitinib-refractory cases.</p>\u0000 </div>","PeriodicalId":7724,"journal":{"name":"American Journal of Hematology","volume":"100 S3","pages":"14-29"},"PeriodicalIF":10.1,"publicationDate":"2025-03-24","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143678335","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":1,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Prediction and Prognostication of Acute Graft-Versus-Host Disease by MAGIC Biomarkers","authors":"John E. Levine","doi":"10.1002/ajh.27594","DOIUrl":"10.1002/ajh.27594","url":null,"abstract":"<div>\u0000 \u0000 <p>Recent advancements in prophylaxis for acute graft-versus-host disease (GVHD) have successfully reduced the incidence of severe cases; however, overall survival rates have not significantly improved, and GVHD continues to be a major cause of mortality. The severity of gastrointestinal (GI) damage is especially critical, as it strongly correlates with treatment failure and non-relapse mortality, but clinical symptoms do not reliably predict peak severity in its early stages. Biomarker-based algorithms, such as the Mount Sinai Acute GVHD International Consortium (MAGIC) algorithm, leverage serum levels of GI GVHD biomarkers (ST2 and REG3α) to quantify intestinal crypt damage, providing more accurate predictions of GVHD outcomes compared to clinical assessments. Clinical trials have investigated the use of biomarkers as entry criteria for treatment, with notable success in guiding treatment de-escalation, which is increasingly important as the presentation of GVHD shifts towards milder forms. The recently developed MAGIC composite scores further enhance prediction accuracy by integrating clinical symptom severity with biomarker assessments. Future clinical trials that employ these composite scores or similar algorithms are anticipated to be more efficient by identifying patients who are most likely to benefit from specific therapies and ultimately improving the management of GVHD.</p>\u0000 </div>","PeriodicalId":7724,"journal":{"name":"American Journal of Hematology","volume":"100 S3","pages":"5-13"},"PeriodicalIF":10.1,"publicationDate":"2025-03-24","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143678334","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":1,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Introduction to American Journal of Hematology Supplement: Improving Initial Care for Acute GVHD Patients","authors":"Corey Cutler","doi":"10.1002/ajh.27653","DOIUrl":"10.1002/ajh.27653","url":null,"abstract":"","PeriodicalId":7724,"journal":{"name":"American Journal of Hematology","volume":"100 S3","pages":"3-4"},"PeriodicalIF":10.1,"publicationDate":"2025-03-24","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143678333","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":1,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Identifying Microbiota and Immune Host Factors Associated With Bleeding Risk in Children With Immune Thrombocytopenia","authors":"Shelly Saini, Parastoo Sabaeifard, Laura Coughlin, Nicole Poulides, Shuheng Gan, Xiaowei Zhan, Mary Dang, Andrew Y. Koh, Ayesha Zia","doi":"10.1002/ajh.27669","DOIUrl":"https://doi.org/10.1002/ajh.27669","url":null,"abstract":"&lt;p&gt;The hallmark of immune thrombocytopenia (ITP) is a decrease in the number of platelets in the blood, leading to excessive bruising and bleeding. While most clinically significant bleeding events in ITP occur at platelet counts &lt; 30,000/uL, patients with comparable platelet counts may have variable bleeding phenotypes. Inflammation has been shown to promote thrombosis through increasing pro-coagulant factors and inhibiting anticoagulant pathways. The gut microbiome is critical in host immune system education and thrombotic pathways, but its role in bleeding risk in ITP has not been studied. For example, lipopolysaccharide (LPS), the outer membrane glycoprotein found in gram-negative bacteria, increases coagulability by activating the toll-like receptor-4 (TLR4)-induced coagulation pathway [&lt;span&gt;1&lt;/span&gt;]. In contrast, the gut microbiota-derived metabolite butyrate induces immune tolerance, mitigates inflammation, and minimizes LPS translocation in the intestines [&lt;span&gt;1&lt;/span&gt;]. Systemic cytokine production correlates with specific gut microbiota, as evidenced by lower TNF- levels in humans with high levels of &lt;i&gt;Bifidobacterium adolescentis&lt;/i&gt; bacteria [&lt;span&gt;1&lt;/span&gt;]. We aimed to investigate the role of the microbiome and cytokine production in ITP patients with mild versus moderate–severe bleeding phenotype. We hypothesized that children with ITP with a moderate–severe bleeding phenotype would have increased levels of gut microbiota associated with mitigating local and systemic inflammation and increased anti-inflammatory systemic cytokines, as inflammation has been shown to promote thrombosis.&lt;/p&gt;\u0000&lt;p&gt;Our prospective IRB-approved cohort study included patients &lt; 18 years of age with acute ITP within 3 months of diagnosis and with platelet counts ≤ 30,000/uL at diagnosis at the University of Texas Southwestern (UTSW) Medical Center and Children's Health. Fecal and blood samples were obtained in inpatient and outpatient settings and stored de-identified with study-specific sample IDs. Stool samples were obtained within 36 h of inpatient IVIG or steroid initiation and prior to outpatient steroid treatment. 16S rRNA genes (variable region 4, V4) were amplified, sequenced, and analyzed from each sample. Alpha diversity metrics (Simpson diversity, Shannon diversity, Chao1 and Faith richness) were calculated. Output matrices were further analyzed by principal coordinate analysis (PCoA) using weighted UniFrac and Bray–Curtis, along with linear discriminant analysis (LDA) effect size (LEfSe) to identify differences in relative abundance at taxonomic levels. Blood samples were loaded into the MAGPIX system (Luminex corporation, Austin, Texas, USA) for cytokine analysis in the UTSW Genomics and Microarray Core Facility.&lt;/p&gt;\u0000&lt;p&gt;We assigned study participants to two groups, mild or moderate–severe, using the Buchanan-Adix bleeding score, with mild participants having a score ≤ 3a and moderate–severe a score ≥ 3b [&lt;span&gt;2&lt;/span&gt;]. Score cutoffs ","PeriodicalId":7724,"journal":{"name":"American Journal of Hematology","volume":"24 1","pages":""},"PeriodicalIF":12.8,"publicationDate":"2025-03-20","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143661120","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":1,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"A Novel Method for a Precise Identification of Human Erythroblast Subpopulations by Flow Cytometry","authors":"Julien M. P. Grenier, Auria Godard, Robert Seute, Alexandra Grimaldi, Barbara Peyrard, Jacques Chiaroni, Narla Mohandas, Wassim El Nemer, Maria De Grandis","doi":"10.1002/ajh.27668","DOIUrl":"https://doi.org/10.1002/ajh.27668","url":null,"abstract":"&lt;p&gt;Erythropoiesis is a complex multistep process encompassing the differentiation of hematopoietic stem cells (HSCs) to mature red blood cells (RBCs). Three distinct phases are identified: erythroid progenitors, terminal erythroid differentiation, and reticulocyte maturation. A detailed understanding of physiological and pathological erythropoiesis requires careful monitoring and characterization of these distinct differentiation stages. Recent technological advances such as single-cell transcriptomics have enabled unprecedented insights into cellular heterogeneity [&lt;span&gt;1&lt;/span&gt;]. Nevertheless, these techniques are expensive and require specialized expertise, limiting their accessibility and broad use [&lt;span&gt;1&lt;/span&gt;]. Consequently, flow cytometry (FACS) remains the gold standard for studying erythroid differentiation [&lt;span&gt;2, 3&lt;/span&gt;].&lt;/p&gt;\u0000&lt;p&gt;Two staining and gating strategies, referred to as “waterfalls” are currently used to study human terminal erythroid differentiation. While both approaches utilize glycophorin A (GPA), one panel is based on the expression of CD49d and Band3 [&lt;span&gt;2&lt;/span&gt;], while the other relies on CD105 [&lt;span&gt;3&lt;/span&gt;]. As these strategies utilize different marker sets, it is likely that the identified populations do not completely overlap due to variations in sample sources, that is, peripheral or cord blood and bone marrow, and in experimental conditions used in different studies. As such, there is a need for establishing consensus immunophenotyping for terminally differentiating erythroblast subpopulations.&lt;/p&gt;\u0000&lt;p&gt;In this study, we performed in vitro erythroid differentiation with FACS monitoring, integrating both “waterfalls” within the same experimental setup to compare their ability to resolve different cell subsets and their limitations. Using bioinformatics tools for dimensionality reduction (UMAPs) and unsupervised clustering, we show that while the two “waterfalls” are complementary, they are also distinct. We report a new gating strategy combining GPA, CD105, and CD49d that enhances the resolution and ensures panel harmonization for studying erythroblast subpopulations during terminal erythroid differentiation.&lt;/p&gt;\u0000&lt;p&gt;We isolated CD34&lt;sup&gt;Pos&lt;/sup&gt; cells from three healthy donors and cultured them for 18 days using a four-phase protocol previously described [&lt;span&gt;4&lt;/span&gt;]. Phenotypic expression profiles were monitored every other day using an antibody panel composed of CD123, CD49d, CD71, GPA, and Band3 to characterize both “waterfalls.” We then employed the gating strategy shown in Figure 1A to define the erythroblast subpopulations.&lt;/p&gt;\u0000&lt;figure&gt;&lt;picture&gt;\u0000&lt;source media=\"(min-width: 1650px)\" srcset=\"/cms/asset/590abce2-a303-4f50-8f49-5bb245176829/ajh27668-fig-0001-m.jpg\"/&gt;&lt;img alt=\"Details are in the caption following the image\" data-lg-src=\"/cms/asset/590abce2-a303-4f50-8f49-5bb245176829/ajh27668-fig-0001-m.jpg\" loading=\"lazy\" src=\"/cms/asset/92480b05-39ac-4d22-a5c2-70738342f6e8/ajh27668-fig-0001-m.png","PeriodicalId":7724,"journal":{"name":"American Journal of Hematology","volume":"33 1","pages":""},"PeriodicalIF":12.8,"publicationDate":"2025-03-18","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143641136","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":1,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Waldenström Macroglobulinemia: 2025 Update on Diagnosis, Risk Stratification, and Management","authors":"Morie A. Gertz","doi":"10.1002/ajh.27666","DOIUrl":"https://doi.org/10.1002/ajh.27666","url":null,"abstract":"Waldenström macroglobulinemia (WM) is a lymphoplasmacytic lymphoma with immunoglobulin M (IgM) monoclonal protein. Clinical features include anemia, thrombocytopenia, hepatosplenomegaly, lymphadenopathy, and rarely hyperviscosity.","PeriodicalId":7724,"journal":{"name":"American Journal of Hematology","volume":"55 1","pages":""},"PeriodicalIF":12.8,"publicationDate":"2025-03-17","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143635319","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":1,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Cyclophosphamide Abrogates Immune Effector Cell-Associated Neurotoxicity Syndrome Associated With CAR-T Cell Therapy","authors":"Zhengfeng Hou, Yanli Jiang, Yi Fu, Min Ruan, Danchen Meng, Yuxin Li, Dinghui Zhao, Jichun Yang, Zhangbiao Long, Jian Ge","doi":"10.1002/ajh.27671","DOIUrl":"https://doi.org/10.1002/ajh.27671","url":null,"abstract":"&lt;p&gt;The patient was a 50-year-old woman diagnosed with acute lymphoblastic leukemia 6 years before the current presentation. After two cycles of VDCLP induction chemotherapy (vincristine, daunorubicin, cyclophosphamide, L-asparaginase, and prednisone), bone marrow examination indicated complete remission, with flow cytometry showing a minimal residual disease (MRD) level of &lt; 1 × 10&lt;sup&gt;−4&lt;/sup&gt;. The patient had undergone multiple consolidation treatments over the following 5 years. One year before the current presentation, a follow-up bone marrow flow cytometry revealed that abnormal immature lymphoblasts accounted for 24.4%, indicating leukemia relapse. After the failure of VDLP chemotherapy (vincristine, daunorubicin, L-asparaginase, and prednisone) and MA chemotherapy (methotrexate and cytarabine), and given the lack of a suitable donor for bone marrow transplantation, the patient enrolled in a chimeric antigen receptor T (CAR-T) clinical trial at our hospital (NCT06532630) in March 2024. This CAR-T cell therapy targets CD19 and is manufactured using a nonviral electroporation platform. It incorporates a scFv that directly binds to CD19, linked to a CD8α transmembrane domain, and integrates CD28 and CD3ζ signaling domains to activate and enhance T cell cytotoxicity. Given the patient's high initial tumor burden (49.5% blasts in the bone marrow), bridging chemotherapy with the VIP regimen (vincristine, idarubicin, and prednisone) was administered 20 days prior to CAR-T cell infusion to reduce tumor burden (Figure 1A).&lt;/p&gt;\u0000&lt;figure&gt;&lt;picture&gt;\u0000&lt;source media=\"(min-width: 1650px)\" srcset=\"/cms/asset/ffc4b216-2292-42ec-b45d-bf4d2dd5b894/ajh27671-fig-0001-m.jpg\"/&gt;&lt;img alt=\"Details are in the caption following the image\" data-lg-src=\"/cms/asset/ffc4b216-2292-42ec-b45d-bf4d2dd5b894/ajh27671-fig-0001-m.jpg\" loading=\"lazy\" src=\"/cms/asset/2b591e4d-2eab-465e-a0c6-0377ad5efa00/ajh27671-fig-0001-m.png\" title=\"Details are in the caption following the image\"/&gt;&lt;/picture&gt;&lt;figcaption&gt;\u0000&lt;div&gt;&lt;strong&gt;FIGURE 1&lt;span style=\"font-weight:normal\"&gt;&lt;/span&gt;&lt;/strong&gt;&lt;div&gt;Open in figure viewer&lt;i aria-hidden=\"true\"&gt;&lt;/i&gt;&lt;span&gt;PowerPoint&lt;/span&gt;&lt;/div&gt;\u0000&lt;/div&gt;\u0000&lt;div&gt;Timeline of the patient (A). Measures of cytokine levels related to cell infusion (B). Measure of CAR-T cell copies related to cell infusion, according to the study protocol, if the CAR-T cell copies fall below the limit of quantification for two consecutive tests, further testing is not required (C). T lymphocyte subset changes over time (D). Brain magnetic resonance imaging and CT scan. The images in the first row show the cranial CT scan results on Day 12 following CAR-T cell therapy, revealing mild cerebral edema. The images in the second row show the cranial MRI results on Day 32, indicating partial resolution of the edema. These images confirm the effectiveness of our treatment (E). Improvement of the patient since the use of cyclophosphamide. The first photo captures the condition on Day 12 after CAR-T cells infu","PeriodicalId":7724,"journal":{"name":"American Journal of Hematology","volume":"9 1","pages":""},"PeriodicalIF":12.8,"publicationDate":"2025-03-17","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143635363","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":1,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}