Joanne Britto, Audrey Y. H. Dong, Gregory Pond, Tobias Berg, Kylie Lepic, Tom Kouroukis, Gwynivere A. Davies, Graeme Fraser, Ronan Foley, Amaris K. Balitsky
Introduction
Chimeric antigen receptor T-cell (CART) therapy has shown clinical efficacy in relapsed and refractory large B-cell malignancies. There is emerging data on the long-term complications including risk of secondary malignancies. We aimed to describe the incidence and characteristics of secondary malignancies following CART therapy.
Methods
We performed a single-center retrospective analysis of a prospectively collected cohort of 87 patients who received CART therapy for relapsed/refractory B-cell malignancies between January 2020 and August 2023.
Results
Seven patients (8.0%) developed a secondary malignancy, with a median age of 57 years (40–77) and mean time to onset of 16.9 months (3–34.5 months). Two patients were diagnosed with MDS and five with AML. Six patients had cytogenetic abnormalities at diagnosis of MDS/AML. Five patients received hypomethylating agents and two received an allogeneic stem cell transplant as treatment for their myeloid malignancy. Two patients were alive at 12 months after diagnosis of their myeloid malignancy. The 12-month cumulative incidence function (CIF) was 2.3% (95% CI, 0.4%–7.3%) and the 24-month CIF was 6.9% (95% CI, 2.4%–14.4%).
Conclusion
Development of a secondary malignancy is a potential complication following CART therapy. Results of this single-center study should be confirmed with larger multicenter studies.
Trial Registration: The authors have confirmed clinical trial registration is not needed for this submission.
{"title":"Secondary Malignancies Following CAR T-Cell Therapy for B-Cell Malignancies: A Retrospective Analysis","authors":"Joanne Britto, Audrey Y. H. Dong, Gregory Pond, Tobias Berg, Kylie Lepic, Tom Kouroukis, Gwynivere A. Davies, Graeme Fraser, Ronan Foley, Amaris K. Balitsky","doi":"10.1002/jha2.70164","DOIUrl":"10.1002/jha2.70164","url":null,"abstract":"<div>\u0000 \u0000 \u0000 <section>\u0000 \u0000 <h3> Introduction</h3>\u0000 \u0000 <p>Chimeric antigen receptor T-cell (CART) therapy has shown clinical efficacy in relapsed and refractory large B-cell malignancies. There is emerging data on the long-term complications including risk of secondary malignancies. We aimed to describe the incidence and characteristics of secondary malignancies following CART therapy.</p>\u0000 </section>\u0000 \u0000 <section>\u0000 \u0000 <h3> Methods</h3>\u0000 \u0000 <p>We performed a single-center retrospective analysis of a prospectively collected cohort of 87 patients who received CART therapy for relapsed/refractory B-cell malignancies between January 2020 and August 2023.</p>\u0000 </section>\u0000 \u0000 <section>\u0000 \u0000 <h3> Results</h3>\u0000 \u0000 <p>Seven patients (8.0%) developed a secondary malignancy, with a median age of 57 years (40–77) and mean time to onset of 16.9 months (3–34.5 months). Two patients were diagnosed with MDS and five with AML. Six patients had cytogenetic abnormalities at diagnosis of MDS/AML. Five patients received hypomethylating agents and two received an allogeneic stem cell transplant as treatment for their myeloid malignancy. Two patients were alive at 12 months after diagnosis of their myeloid malignancy. The 12-month cumulative incidence function (CIF) was 2.3% (95% CI, 0.4%–7.3%) and the 24-month CIF was 6.9% (95% CI, 2.4%–14.4%).</p>\u0000 </section>\u0000 \u0000 <section>\u0000 \u0000 <h3> Conclusion</h3>\u0000 \u0000 <p>Development of a secondary malignancy is a potential complication following CART therapy. Results of this single-center study should be confirmed with larger multicenter studies.</p>\u0000 \u0000 <p><b>Trial Registration</b>: The authors have confirmed clinical trial registration is not needed for this submission.</p>\u0000 </section>\u0000 </div>","PeriodicalId":72883,"journal":{"name":"EJHaem","volume":"6 6","pages":""},"PeriodicalIF":1.2,"publicationDate":"2025-10-28","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12560101/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145403215","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
<p>A 54-year-old man with an apparently unremarkable previous medical history presented from an outside hospital with abdominal pain and unintentional weight loss. A computerized tomography scan revealed splenomegaly and generalized lymphadenopathy. The clinical impression of lymphoma led to a cervical lymph node (LN) biopsy. Hematoxylin and eosin-stained histological images of this biopsy demonstrated distortion of architecture by interfollicular vaguely nodular expanses (evident on low power, indicated by white circles) of small to medium-sized cytologically monotonous cells with moderately dispersed chromatin (high-power inset) (Figure 1). These cells were surrounded by a heterogeneous mixture of lymphocytes and non-lymphoid hematopoietic elements, including megakaryocytes (labeled EMH, extramedullary hematopoiesis). The nodular infiltrates expressed CD123 and TCL1, indicating that they were plasmacytoid dendritic cells (pDCs). Extraneous to the nodules, CD163 decorated monocytes while myeloperoxidase, E-cadherin, and CD61 highlighted myeloid, erythroid, and megakaryocytic cells, respectively, indicative of EMH. Next-generation sequencing on the LN revealed <i>NRAS</i>, <i>ZRSR2</i>, and biallelic <i>TET2</i> disease-associated variants. Following the LN biopsy, the full blood count (FBC) and differential became available, showing an absolute (8.5 × 10<sup>9</sup>/L) and relative (28.3%) monocytosis in the setting of anemia (hemoglobin 100 g/L) and thrombocytopenia (platelets 90 × 10<sup>9</sup>/L). A follow-up in-house bone marrow aspirate and biopsy revealed marked hypercellularity with an increased myeloid:erythroid ratio (6.7:1), monocytosis (12%), myeloid left shift with increased blasts and promonocytes (8%), and trilineage cytologic atypia. There was no abnormal increase in reticulin fibrosis. Bone marrow flow cytometry showed increased monocytes (10.1%) that co-expressed CD56, and a minor but discrete population of myeloblasts (2.3%). Cytogenetics showed a normal male karyotype.</p><p>This case demonstrates a mature pDC proliferation associated with chronic myelomonocytic leukemia (CMML), a diagnosis initially, and somewhat unusually, considered on this LN biopsy. Extramedullary involvement by CMML can be seen and may include LN involvement or nodal extramedullary hematopoiesis [<span>1</span>]. CMML is frequently associated with the presence of nodules of mature pDCs, both in the marrow and when it presents in LNs [<span>2-4</span>]. This seems particularly common in <i>RAS</i>-mutated CMML [<span>2, 3</span>], as is evident in this case. The <i>TET2</i> mutations (occurring in ∼60% of cases) and RAS pathway mutations (occurring in ∼30% of cases) seen in our case are supportive of the diagnosis [<span>5</span>]. Biallelic <i>TET2</i> mutations, as in this case, are particularly frequent in CMML [<span>6</span>]. The pDC nodules were the prominent morphological feature in the LN in this case, which was performed before bone marrow stud
{"title":"A Perplexing Predominance of Plasmacytoid Dendritic Cells: Chronic Myelomonocytic Leukemia Initially Considered on a Lymph Node Biopsy","authors":"Jaryse Harris, Elena Fenu, Adam Bagg","doi":"10.1002/jha2.70157","DOIUrl":"10.1002/jha2.70157","url":null,"abstract":"<p>A 54-year-old man with an apparently unremarkable previous medical history presented from an outside hospital with abdominal pain and unintentional weight loss. A computerized tomography scan revealed splenomegaly and generalized lymphadenopathy. The clinical impression of lymphoma led to a cervical lymph node (LN) biopsy. Hematoxylin and eosin-stained histological images of this biopsy demonstrated distortion of architecture by interfollicular vaguely nodular expanses (evident on low power, indicated by white circles) of small to medium-sized cytologically monotonous cells with moderately dispersed chromatin (high-power inset) (Figure 1). These cells were surrounded by a heterogeneous mixture of lymphocytes and non-lymphoid hematopoietic elements, including megakaryocytes (labeled EMH, extramedullary hematopoiesis). The nodular infiltrates expressed CD123 and TCL1, indicating that they were plasmacytoid dendritic cells (pDCs). Extraneous to the nodules, CD163 decorated monocytes while myeloperoxidase, E-cadherin, and CD61 highlighted myeloid, erythroid, and megakaryocytic cells, respectively, indicative of EMH. Next-generation sequencing on the LN revealed <i>NRAS</i>, <i>ZRSR2</i>, and biallelic <i>TET2</i> disease-associated variants. Following the LN biopsy, the full blood count (FBC) and differential became available, showing an absolute (8.5 × 10<sup>9</sup>/L) and relative (28.3%) monocytosis in the setting of anemia (hemoglobin 100 g/L) and thrombocytopenia (platelets 90 × 10<sup>9</sup>/L). A follow-up in-house bone marrow aspirate and biopsy revealed marked hypercellularity with an increased myeloid:erythroid ratio (6.7:1), monocytosis (12%), myeloid left shift with increased blasts and promonocytes (8%), and trilineage cytologic atypia. There was no abnormal increase in reticulin fibrosis. Bone marrow flow cytometry showed increased monocytes (10.1%) that co-expressed CD56, and a minor but discrete population of myeloblasts (2.3%). Cytogenetics showed a normal male karyotype.</p><p>This case demonstrates a mature pDC proliferation associated with chronic myelomonocytic leukemia (CMML), a diagnosis initially, and somewhat unusually, considered on this LN biopsy. Extramedullary involvement by CMML can be seen and may include LN involvement or nodal extramedullary hematopoiesis [<span>1</span>]. CMML is frequently associated with the presence of nodules of mature pDCs, both in the marrow and when it presents in LNs [<span>2-4</span>]. This seems particularly common in <i>RAS</i>-mutated CMML [<span>2, 3</span>], as is evident in this case. The <i>TET2</i> mutations (occurring in ∼60% of cases) and RAS pathway mutations (occurring in ∼30% of cases) seen in our case are supportive of the diagnosis [<span>5</span>]. Biallelic <i>TET2</i> mutations, as in this case, are particularly frequent in CMML [<span>6</span>]. The pDC nodules were the prominent morphological feature in the LN in this case, which was performed before bone marrow stud","PeriodicalId":72883,"journal":{"name":"EJHaem","volume":"6 6","pages":""},"PeriodicalIF":1.2,"publicationDate":"2025-10-27","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12558439/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145395799","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Stephen P. Hibbs, Yosef Joseph Rene Amel Riazat-Kesh, Funmi Oyesanya, Matthew L. Smith, Jeff K. Davies
<p>Sociodemographic disparities in access to and outcomes from allogeneic haematopoietic stem cell transplants (HSCT) are well-documented, particularly in the USA [<span>1</span>]. In the USA context, the absence of universal access to specialist healthcare and the close association between racial minoritisation and socioeconomic deprivation create significant barriers to equitable care. With a different history of racial and ethnic minoritisation and a National Health Service (NHS) that offers free healthcare at the point of use, the UK provides a contrasting context to examine access to allogeneic HSCT.</p><p>Despite this different context, a recent UK study across 13,978 transplants found that patient ethnicity predicted survival following allogeneic HSCT receipt [<span>2</span>]. The authors noted that their analysis was limited to patients who received HSCT, preventing assessment of potential inequities in access. To our knowledge, no UK studies have examined the impact of sociodemographic factors on access to allogeneic HSCT.</p><p>We present our data assessing how sociodemographic factors influence the likelihood of receiving HSCT for patients with acute leukaemia in the UK. Beyond donor availability and universal health coverage, we suggest other factors as to why patients do or do not receive HSCT, including the decisions of doctors and patients themselves.</p><p>In 2021, we conducted a retrospective review at our transplant centre (St Bartholomew's Hospital, London, UK), examining 260 cases of acute leukaemia identified from MDT meeting minutes. These meetings included all new cases diagnosed across the regional network and transplants completed over the preceding three years. For this analysis, we included all patients discussed between 2018 and 2019, of whom 112 (43%) received allogeneic HSCT. We excluded six patients with lymphoblastic lymphoma (LBL) without bone marrow involvement, in whom HSCT would rarely be indicated, leaving 254 in the analytical cohort. Demographics for patients included in the analysis are shown in Table 1. All statistical analyses were conducted using Python 3.8.</p><p>Using multivariable logistic regression, we analysed the odds of receiving HSCT, adjusting for age, HCT-comorbidity index (HCT-CI), and baseline disease risk [<span>3, 4</span>] (Table 2). Our findings showed that living in a wealthier area (measured by the index of multiple deprivation, IMD) was associated with higher odds of receiving HSCT (odds ratio 1.24, 95% CI 1.11–1.38). Conversely, patients living in more deprived areas (by IMD decile) had lower odds of receiving HSCT. Ethnicity was not associated with odds of HSCT receipt within this limited model.</p><p>Given that all patients were treated within a publicly funded healthcare system, it is notable that individuals from wealthier areas were more likely to receive HSCT than those from more deprived areas. Our methods could not determine whether the differences in HSCT receipt among indiv
异体造血干细胞移植（HSCT）的可及性和结果在社会人口统计学上存在差异，尤其是在美国。在美国，缺乏普遍获得专业医疗保健的机会，以及种族少数化与社会经济贫困之间的密切联系，为公平护理创造了重大障碍。英国有着不同的种族和少数民族历史，国家卫生服务（NHS）在使用点提供免费医疗保健，这为检查同种异体造血干细胞移植提供了一个截然不同的背景。尽管存在这种不同的背景，但英国最近一项针对13978例移植的研究发现，患者的种族预测了同种异体造血干细胞移植后的生存。作者指出，他们的分析仅限于接受HSCT的患者，因此无法评估获得HSCT的潜在不公平。据我们所知，英国没有研究调查社会人口因素对获得同种异体造血干细胞移植的影响。我们展示了我们的数据，评估社会人口因素如何影响英国急性白血病患者接受造血干细胞移植的可能性。除了供体可用性和全民健康覆盖之外，我们还提出了其他因素，包括医生和患者自己的决定，来解释患者是否接受造血干细胞移植。2021年，我们在我们的移植中心（英国伦敦圣巴塞洛缪医院）进行了回顾性审查，检查了从MDT会议记录中确定的260例急性白血病。这些会议包括在区域网络中诊断的所有新病例和在过去三年中完成的移植。在这项分析中，我们纳入了2018年至2019年期间讨论的所有患者，其中112例（43%）接受了同种异体造血干细胞移植。我们排除了6例没有骨髓受累的淋巴母细胞淋巴瘤（LBL）患者，这些患者很少需要HSCT，在分析队列中留下254例。纳入分析的患者人口统计资料见表1。所有统计分析均使用Python 3.8进行。使用多变量逻辑回归，我们分析了接受HSCT的几率，调整了年龄、hct合并症指数（HCT-CI）和基线疾病风险[3,4]（表2）。我们的研究结果显示，生活在较富裕的地区（以多重剥夺指数（IMD）衡量）接受HSCT的几率较高（优势比1.24,95% CI 1.11-1.38）。相反，生活在更贫困地区的患者（按IMD十分位数计算）接受造血干细胞移植的几率更低。在这个有限的模型中，种族与接受HSCT的几率无关。考虑到所有患者都在公共资助的医疗系统中接受治疗，值得注意的是，来自富裕地区的患者比来自贫困地区的患者更有可能接受造血干细胞移植。我们的方法不能确定不同社会经济地位的个体在HSCT接受量上的差异是由于供体可得性、转诊模式、健康评估还是患者决策。后两个因素值得进一步反思和考虑。移植医生评估病人是否适合接受细胞治疗。这些评估通常涉及对谁是“移植候选人”的主观判断，这可能受到种族或社会经济地位等社会人口因素的影响。例如，一个坐在轮椅上进行临床评估的病人可能会被他们的医生认为不适合，尤其是当他们第一次见面的时候。然而，对于一些家庭来说，在医院使用轮椅的决定可能与医生的决定有不同的含义，这意味着个人的痛苦和家庭的支持，而不是严重的功能损伤。这种误解可能会使某些群体的患者在健身决策中处于不利地位。当患者选择是否进行细胞治疗时，他们的决策过程受到许多因素的影响。这些因素包括对卫生保健系统的信任、支持网络的可用性、财务和家庭责任，以及他们是否能够在会诊期间进行有效沟通。我们的研究有几个局限性。IMD是一项强有力的、由政府支持的措施，它整合了多个数据来源，以评估英国小地区的贫困状况。然而，它反映的是地理区域的总体特征，而不是个体特征，因此可能不能准确地代表每个患者的社会经济地位。此外，社会经济地位与其他因素交叉，如健康素养、住房不安全感和英语熟练程度，这些因素可能会影响接受HSCT的可能性。这些变量在临床记录中记录不一致，因此无法纳入我们的分析，但值得进一步调查。 临床医生和患者的决策因素与社会人口分组交叉，需要更仔细的检查。进一步的研究跨越细胞治疗评估，决定，转诊和接收是必要的，并可能阐明直接可改变的因素。SPH, YJRAR-K， FO和MLS对项目进行了概念化。YJRAR-K收集和分析数据。JKD提供监督。SPH撰写了初稿，YJRAR-K、FO、MLS和JKD对手稿进行了严格的审查和编辑。Stephen P. Hibbs由惠康信托基金资助的HARP博士研究奖学金（资助号223500/Z/21/Z）支持。本研究未收到任何资金。本研究作为一项服务评估项目进行，旨在评估和改进现有的临床实践。因此，它不需要研究伦理委员会的审查。作者没有什么可报告的。作者声明无利益冲突。
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Phillip LR Nicolson, Midhat Asif, Richard J Buka, Peter Dyer, Eman Hassan, Claire N Harrison, Bernard D Maybury, Andrew J Doyle
Introduction
Secondary and idiopathic polycythaemia is far more common than polycythaemia vera. Whilst venesection for polycythaemia vera has a robust evidence base, the data supporting this treatment for secondary and/or idiopathic polycythaemia are limited to small single-arm studies showing transient improvement in symptoms or physiologic endpoints. As a result the British Society for Haematology Guideline for the management of specific situations in polycythaemia vera and secondary erythrocytosis suggests considering venesection in patients with hypoxic lung disease with Hct > 0.56 or to a target Hct < 0.55 in those with idiopathic polycythaemia. We hypothesised that this paucity of evidence results in widespread variation in management of secondary polycythaemia.
Methods
To assess attitudes and practice in the treatment of secondary and idiopathic polycythaemia we designed an international clinician survey to evaluate current practice and define the point of clinical equipoise at which clinicians would be content to enter patients into a randomised venesection study. This survey was distributed using the wide-reaching HaemSTAR research network.
Results
A total of 123 clinicians responded, of which 90 were experienced senior clinicians. 62% reported not routinely offering regular venesection whereas 38% of respondents did. Those considering venesection rose to ∼2/3 of respondents in specific circumstances such as polycythaemia-related symptoms, previous arterial or unprovoked venous thrombosis. Respondents were more likely to offer venesection to patients with idiopathic- compared to androgen- or hypoxia-driven polycythaemia. Of those who would venesect, most would use a threshold Hct ≥ 0.55, with a target Hct < 0.55 but there was significant variability.
Conclusions
Our survey showed considerable variability in venesection practice for patients with secondary or idiopathic polycythaemia, probably reflecting the paucity of the evidence base. There was widespread support for a trial of venesection vs observation in secondary polycythaemia and this survey has helped to define the threshold Hct at which clinical equipoise exists.
{"title":"Common Themes and Uncertainties in Management of Secondary Polycythaemia: An International Clinician Survey of Practice","authors":"Phillip LR Nicolson, Midhat Asif, Richard J Buka, Peter Dyer, Eman Hassan, Claire N Harrison, Bernard D Maybury, Andrew J Doyle","doi":"10.1002/jha2.70171","DOIUrl":"10.1002/jha2.70171","url":null,"abstract":"<div>\u0000 \u0000 \u0000 <section>\u0000 \u0000 <h3> Introduction</h3>\u0000 \u0000 <p>Secondary and idiopathic polycythaemia is far more common than polycythaemia vera. Whilst venesection for polycythaemia vera has a robust evidence base, the data supporting this treatment for secondary and/or idiopathic polycythaemia are limited to small single-arm studies showing transient improvement in symptoms or physiologic endpoints. As a result the British Society for Haematology Guideline for the management of specific situations in polycythaemia vera and secondary erythrocytosis suggests <i>considering</i> venesection in patients with hypoxic lung disease with Hct > 0.56 or to a target Hct < 0.55 in those with idiopathic polycythaemia. We hypothesised that this paucity of evidence results in widespread variation in management of secondary polycythaemia.</p>\u0000 </section>\u0000 \u0000 <section>\u0000 \u0000 <h3> Methods</h3>\u0000 \u0000 <p>To assess attitudes and practice in the treatment of secondary and idiopathic polycythaemia we designed an international clinician survey to evaluate current practice and define the point of clinical equipoise at which clinicians would be content to enter patients into a randomised venesection study. This survey was distributed using the wide-reaching HaemSTAR research network.</p>\u0000 </section>\u0000 \u0000 <section>\u0000 \u0000 <h3> Results</h3>\u0000 \u0000 <p>A total of 123 clinicians responded, of which 90 were experienced senior clinicians. 62% reported not routinely offering regular venesection whereas 38% of respondents did. Those considering venesection rose to ∼2/3 of respondents in specific circumstances such as polycythaemia-related symptoms, previous arterial or unprovoked venous thrombosis. Respondents were more likely to offer venesection to patients with idiopathic- compared to androgen- or hypoxia-driven polycythaemia. Of those who would venesect, most would use a threshold Hct ≥ 0.55, with a target Hct < 0.55 but there was significant variability.</p>\u0000 </section>\u0000 \u0000 <section>\u0000 \u0000 <h3> Conclusions</h3>\u0000 \u0000 <p>Our survey showed considerable variability in venesection practice for patients with secondary or idiopathic polycythaemia, probably reflecting the paucity of the evidence base. There was widespread support for a trial of venesection vs observation in secondary polycythaemia and this survey has helped to define the threshold Hct at which clinical equipoise exists.</p>\u0000 </section>\u0000 </div>","PeriodicalId":72883,"journal":{"name":"EJHaem","volume":"6 6","pages":""},"PeriodicalIF":1.2,"publicationDate":"2025-10-27","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12558438/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145395747","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Li Yuan Chan, Simon O'Connor, Dima El-Sharkawi, Sunil Iyengar
Background
Patients with relapsed/refractory post-transplant lymphoproliferative disorder (R/R PTLD) following solid-organ transplants (SOT) or hematopoietic stem cell transplants (HSCT) after frontline chemoimmunotherapy have dismal outcomes. There is no standard of care for this group of patients, and they are generally excluded or ineligible for clinical trials. Several effective novel agents have been licensed in recent years for the treatment of diffuse large b-cell lymphoma (DLBCL), including CD19 CAR-T cell therapy and CD3xCD20 bispecific antibody.
Case Report
Acknowledging the limited data and extrapolating the evidence from trials in DLBCL, we report a case of R/R PTLD successfully treated with CD3xCD20 bispecific antibody, Epcoritamab, with good tolerability and long-term response.
Trial Registration
The authors have confirmed clinical trial registration is not needed for this submission.
{"title":"Epcoritamab for Relapsed/Refractory EBV+ Post-Transplant Lymphoproliferative Disorder of DLBCL-Type","authors":"Li Yuan Chan, Simon O'Connor, Dima El-Sharkawi, Sunil Iyengar","doi":"10.1002/jha2.70156","DOIUrl":"https://doi.org/10.1002/jha2.70156","url":null,"abstract":"<div>\u0000 \u0000 \u0000 <section>\u0000 \u0000 <h3> Background</h3>\u0000 \u0000 <p>Patients with relapsed/refractory post-transplant lymphoproliferative disorder (R/R PTLD) following solid-organ transplants (SOT) or hematopoietic stem cell transplants (HSCT) after frontline chemoimmunotherapy have dismal outcomes. There is no standard of care for this group of patients, and they are generally excluded or ineligible for clinical trials. Several effective novel agents have been licensed in recent years for the treatment of diffuse large b-cell lymphoma (DLBCL), including CD19 CAR-T cell therapy and CD3xCD20 bispecific antibody.</p>\u0000 </section>\u0000 \u0000 <section>\u0000 \u0000 <h3> Case Report</h3>\u0000 \u0000 <p>Acknowledging the limited data and extrapolating the evidence from trials in DLBCL, we report a case of R/R PTLD successfully treated with CD3xCD20 bispecific antibody, Epcoritamab, with good tolerability and long-term response.</p>\u0000 </section>\u0000 \u0000 <section>\u0000 \u0000 <h3> Trial Registration</h3>\u0000 \u0000 <p>The authors have confirmed clinical trial registration is not needed for this submission.</p>\u0000 </section>\u0000 </div>","PeriodicalId":72883,"journal":{"name":"EJHaem","volume":"6 6","pages":""},"PeriodicalIF":1.2,"publicationDate":"2025-10-25","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://onlinelibrary.wiley.com/doi/epdf/10.1002/jha2.70156","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145367157","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Silvia Neri, Corien L. Eckhardt, Boukje M. Beuger, Folman Folman, Eva Rettenbacher, Hanke L. Matlung, Taco W. Kuijpers, Josephine M. I. Vos, Robin van Bruggen
Introduction
IgA-mediated autoimmune hemolytic anemia (AIHA) is a rare condition associated with severe hemolysis and limited therapeutic response. Bortezomib, a proteasome inhibitor, targets plasma cells responsible for autoantibody production. Here, we describe a case of refractory IgA-mediated AIHA in a 13-year-old boy presenting with severe hemolysis, who was successfully treated with bortezomib.
Methods:
Blood samples were collected at different time points throughout the disease course for immunohematology testing.
Results
The patient showed significant hematologic improvement following four doses of Bortezomib with reduction in hemolysis and recovery of hemoglobin levels. Laboratory tests revealed complement-negative, Coombs-positive blood tests combined with altered RBC morphology. Phagocytosis of patient's RBC was absent at all timepoints. Notably, despite hematologic improvement, IgA-positive RBC remained present, accompanied by compensated hemolysis.
Conclusions
The present case demonstrates the potential of bortezomib as a treatment option for refractory AIHA cases, particularly in children.
Trial Registration: The authors have confirmed clinical trial registration is not needed for this submission
{"title":"Successful Treatment of Refractory IgA-Mediated Autoimmune Hemolytic Anemia With Bortezomib","authors":"Silvia Neri, Corien L. Eckhardt, Boukje M. Beuger, Folman Folman, Eva Rettenbacher, Hanke L. Matlung, Taco W. Kuijpers, Josephine M. I. Vos, Robin van Bruggen","doi":"10.1002/jha2.70162","DOIUrl":"https://doi.org/10.1002/jha2.70162","url":null,"abstract":"<div>\u0000 \u0000 \u0000 <section>\u0000 \u0000 <h3> Introduction</h3>\u0000 \u0000 <p>IgA-mediated autoimmune hemolytic anemia (AIHA) is a rare condition associated with severe hemolysis and limited therapeutic response. Bortezomib, a proteasome inhibitor, targets plasma cells responsible for autoantibody production. Here, we describe a case of refractory IgA-mediated AIHA in a 13-year-old boy presenting with severe hemolysis, who was successfully treated with bortezomib.</p>\u0000 </section>\u0000 \u0000 <section>\u0000 \u0000 <h3> Methods:</h3>\u0000 \u0000 <p>Blood samples were collected at different time points throughout the disease course for immunohematology testing.</p>\u0000 </section>\u0000 \u0000 <section>\u0000 \u0000 <h3> Results</h3>\u0000 \u0000 <p>The patient showed significant hematologic improvement following four doses of Bortezomib with reduction in hemolysis and recovery of hemoglobin levels. Laboratory tests revealed complement-negative, Coombs-positive blood tests combined with altered RBC morphology. Phagocytosis of patient's RBC was absent at all timepoints. Notably, despite hematologic improvement, IgA-positive RBC remained present, accompanied by compensated hemolysis.</p>\u0000 </section>\u0000 \u0000 <section>\u0000 \u0000 <h3> Conclusions</h3>\u0000 \u0000 <p>The present case demonstrates the potential of bortezomib as a treatment option for refractory AIHA cases, particularly in children.</p>\u0000 \u0000 <p><b>Trial Registration</b>: The authors have confirmed clinical trial registration is not needed for this submission</p>\u0000 </section>\u0000 </div>","PeriodicalId":72883,"journal":{"name":"EJHaem","volume":"6 6","pages":""},"PeriodicalIF":1.2,"publicationDate":"2025-10-25","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://onlinelibrary.wiley.com/doi/epdf/10.1002/jha2.70162","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145367156","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Natsumi Kawasaki, Sei Shu, Mayu Tomita, Xiaoxiao Liu, Shigeki Yoshiura, Yoriko Yamashita-Kashima
Background
Aggressive non-Hodgkin lymphoma (aNHL) often relapses after first-line treatment. Clinical data supports the safety and efficacy of the combination of mosunetuzumab, a CD20×CD3 bispecific antibody, and polatuzumab vedotin, an anti-CD79b antibody drug conjugate (Mosun-Pola) in relapsed/refractory aNHL. This study investigated the molecular mechanism behind the combination effect of Mosun-Pola in human diffuse large B-cell lymphoma (DLBCL) cell lines.
Methods
The in vitro Mosun-Pola efficacy in DLBCL cells (SU-DHL-8 and HT) was evaluated by T cell-dependent cellular cytotoxicity (TDCC) assay. CD20-stable-knockdown SU-DHL-8 cells were established using lentiviral short hairpin RNA. Surface and T-cell activation marker proteins expression were determined by flow cytometry. Human T-cell-injected mice or humanized NOD/Shi-scid, IL-2Rγnull (huNOG) mice were used for an in vivo study.
Results
An in vitro TDCC assay showed a synergistic effect in SU-DHL-8 and HT cells. Based on our experimental results of suppressing CD20 expression, it was suggested that this combination effect could be caused by an increase in CD20 expression by polatuzumab vedotin. In addition, examining the effects of CD20 upregulation in tumor cells on T-cell activation demonstrated that the combination of Mosun-Pola enhanced T-cell activation markers in both CD4+ and CD8+ T cells during the TDCC reaction. In vivo studies, using human immune system-reconstituted mouse models confirmed that polatuzumab vedotin enhanced CD20 expression in tumors, and the combination of Mosun-Pola showed significantly improved anti-tumor effects compared with single-drug treatments.
Conclusion
These findings suggest that polatuzumab vedotin-induced CD20 upregulation provides a molecular rationale to explain the synergistic effect of this combination therapy.
Trial Registration
The authors have confirmed clinical trial registration is not needed for this submission.
{"title":"Polatuzumab Vedotin Induced CD20 Upregulation Contributes to the Efficacy of Mosunetuzumab in Combination With Polatuzumab Vedotin in Diffuse Large B-Cell Lymphoma Preclinical Models","authors":"Natsumi Kawasaki, Sei Shu, Mayu Tomita, Xiaoxiao Liu, Shigeki Yoshiura, Yoriko Yamashita-Kashima","doi":"10.1002/jha2.70169","DOIUrl":"https://doi.org/10.1002/jha2.70169","url":null,"abstract":"<div>\u0000 \u0000 \u0000 <section>\u0000 \u0000 <h3> Background</h3>\u0000 \u0000 <p>Aggressive non-Hodgkin lymphoma (aNHL) often relapses after first-line treatment. Clinical data supports the safety and efficacy of the combination of mosunetuzumab, a CD20×CD3 bispecific antibody, and polatuzumab vedotin, an anti-CD79b antibody drug conjugate (Mosun-Pola) in relapsed/refractory aNHL. This study investigated the molecular mechanism behind the combination effect of Mosun-Pola in human diffuse large B-cell lymphoma (DLBCL) cell lines.</p>\u0000 </section>\u0000 \u0000 <section>\u0000 \u0000 <h3> Methods</h3>\u0000 \u0000 <p>The in vitro Mosun-Pola efficacy in DLBCL cells (SU-DHL-8 and HT) was evaluated by T cell-dependent cellular cytotoxicity (TDCC) assay. CD20-stable-knockdown SU-DHL-8 cells were established using lentiviral short hairpin RNA. Surface and T-cell activation marker proteins expression were determined by flow cytometry. Human T-cell-injected mice or humanized NOD/Shi-scid, IL-2Rγnull (huNOG) mice were used for an in vivo study.</p>\u0000 </section>\u0000 \u0000 <section>\u0000 \u0000 <h3> Results</h3>\u0000 \u0000 <p>An in vitro TDCC assay showed a synergistic effect in SU-DHL-8 and HT cells. Based on our experimental results of suppressing CD20 expression, it was suggested that this combination effect could be caused by an increase in CD20 expression by polatuzumab vedotin. In addition, examining the effects of CD20 upregulation in tumor cells on T-cell activation demonstrated that the combination of Mosun-Pola enhanced T-cell activation markers in both CD4+ and CD8+ T cells during the TDCC reaction. In vivo studies, using human immune system-reconstituted mouse models confirmed that polatuzumab vedotin enhanced CD20 expression in tumors, and the combination of Mosun-Pola showed significantly improved anti-tumor effects compared with single-drug treatments.</p>\u0000 </section>\u0000 \u0000 <section>\u0000 \u0000 <h3> Conclusion</h3>\u0000 \u0000 <p>These findings suggest that polatuzumab vedotin-induced CD20 upregulation provides a molecular rationale to explain the synergistic effect of this combination therapy.</p>\u0000 </section>\u0000 \u0000 <section>\u0000 \u0000 <h3> Trial Registration</h3>\u0000 \u0000 <p>The authors have confirmed clinical trial registration is not needed for this submission.</p>\u0000 </section>\u0000 </div>","PeriodicalId":72883,"journal":{"name":"EJHaem","volume":"6 5","pages":""},"PeriodicalIF":1.2,"publicationDate":"2025-10-24","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://onlinelibrary.wiley.com/doi/epdf/10.1002/jha2.70169","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145367016","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
A. Alraddadi, J. P. Smalley, W. Alzahrani, et al. “Targeted Degradation of Class 1 HDACs With PROTACs is Highly Effective at Inducing DLBCL Cell Death,” EJHaem 6, no. 4 (2025): e70127, https://doi.org/10.1002/jha2.70127.
Co-author Martin J. S. Dyer was incorrectly listed as Martin Dyer.
We apologize for this error.
[更正文章DOI: 10.1002/jha2.70127.]。
{"title":"Correction to “Targeted Degradation of Class 1 HDACs With PROTACs is Highly Effective at Inducing DLBCL Cell Death”","authors":"","doi":"10.1002/jha2.70159","DOIUrl":"10.1002/jha2.70159","url":null,"abstract":"<p>A. Alraddadi, J. P. Smalley, W. Alzahrani, et al. “Targeted Degradation of Class 1 HDACs With PROTACs is Highly Effective at Inducing DLBCL Cell Death,” <i>EJHaem</i> 6, no. 4 (2025): e70127, https://doi.org/10.1002/jha2.70127.</p><p>Co-author Martin J. S. Dyer was incorrectly listed as Martin Dyer.</p><p>We apologize for this error.</p>","PeriodicalId":72883,"journal":{"name":"EJHaem","volume":"6 5","pages":""},"PeriodicalIF":1.2,"publicationDate":"2025-10-21","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12538633/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145350081","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
<p>A 69-year-old man complained of melena. He was diagnosed with gastric primary nasal-type extranodal natural killer/T-cell lymphoma (ENKTL) in October 2017. On <sup>18</sup>F-fluorodeoxyglucose positron emission tomography/computed tomography (<sup>18</sup>F-FDG-PET/CT), accumulations were observed in the stomach and small intestine, indicating stage IV disease. He received combination chemotherapy including alkylating agents, topoisomerase 2 inhibitors, dexamethasone, a nucleoside metabolic inhibitor, and a programmed death-ligand 1 inhibitor, with repeated recurrences and remissions up to September 2022. <sup>18</sup>F-FDG-PET/CT showed a complete metabolic response in November 2022. There was no bone marrow invasion by lymphoma cells during this period. The following March, he contracted COVID-19 and was treated with nirmatrelvir. After recovering from the infection, he presented with pancytopenia without blasts. Although pancytopenia might be due to viral infection, bone marrow examination was performed since he had a long history of chemotherapy including alkylating agents and topoisomerase 2 inhibitors.</p><p>Bone marrow showed hypocellularity with 9.2% blasts (Figure 1a), and dysplasia was detected in myeloid (pseudo-Pelger-Huët anomaly and giant neutrophil: Figures 1b,c), erythroid (nuclear budding: Figure 1d), and megakaryocytic (micromegakaryocyte, multinucleated megakaryocyte: Figures 1e,f) lineages. Flow cytometry showed that the leukemic blasts were positive for CD13, CD33, CD34, CD56, and myeloperoxidase. Cytogenetic analysis demonstrated a complicated karyotype with deletion of chromosomes 5q and 7. Based on these findings, myeloid neoplasm post cytotoxic therapy (MN-pCT) was diagnosed.</p><p>In bone marrow, there was an increase in eosinophils (14.7%), in addition to blasts, and some eosinophils were dysplastic with large basophilic granules of purple-violet color (Figures 2a,b), which are referred to as harlequin cells [<span>1</span>].</p><p>ENKTL is associated with Epstein–Barr virus infection and rarely involves the gastrointestinal tract. Advances in ENKTL treatment have led to an increase in the number of survivors. Consequently, the risk of patients developing MN-pCT may have increased.</p><p>Two cases of MN-pCT with harlequin cells have been reported. Although the primary cancers were different (thymoma and colon adenocarcinoma), alkylating agents were administered in both cases [<span>2, 3</span>].</p><p>The harlequin cells are classified as Code 9 by the International Working Group on Morphology of MDS [<span>4</span>] and are more frequently observed in de novo acute myeloid leukemia harboring <i>CBFB::MYH11</i> fusion [<span>1, 4</span>]. Harlequin cells are observed not only in hematologic malignancies but also in patients with non-hematologic diseases [<span>1, 4</span>]. However, in AML with the <i>CBFB::MYH11</i> fusion, these eosinophils are considered part of the neoplastic clone [<span>4</span>].</p><p>The app
{"title":"Harlequin Cells in Myeloid Neoplasm Post Cytotoxic Therapy for Gastric Primary Nasal-Type Extranodal Natural Killer/T-Cell Lymphoma","authors":"Sachi Tanaka, Hiromi Kinoshita, Naoki Takahashi, Yasuhiro Ebihara","doi":"10.1002/jha2.70167","DOIUrl":"https://doi.org/10.1002/jha2.70167","url":null,"abstract":"<p>A 69-year-old man complained of melena. He was diagnosed with gastric primary nasal-type extranodal natural killer/T-cell lymphoma (ENKTL) in October 2017. On <sup>18</sup>F-fluorodeoxyglucose positron emission tomography/computed tomography (<sup>18</sup>F-FDG-PET/CT), accumulations were observed in the stomach and small intestine, indicating stage IV disease. He received combination chemotherapy including alkylating agents, topoisomerase 2 inhibitors, dexamethasone, a nucleoside metabolic inhibitor, and a programmed death-ligand 1 inhibitor, with repeated recurrences and remissions up to September 2022. <sup>18</sup>F-FDG-PET/CT showed a complete metabolic response in November 2022. There was no bone marrow invasion by lymphoma cells during this period. The following March, he contracted COVID-19 and was treated with nirmatrelvir. After recovering from the infection, he presented with pancytopenia without blasts. Although pancytopenia might be due to viral infection, bone marrow examination was performed since he had a long history of chemotherapy including alkylating agents and topoisomerase 2 inhibitors.</p><p>Bone marrow showed hypocellularity with 9.2% blasts (Figure 1a), and dysplasia was detected in myeloid (pseudo-Pelger-Huët anomaly and giant neutrophil: Figures 1b,c), erythroid (nuclear budding: Figure 1d), and megakaryocytic (micromegakaryocyte, multinucleated megakaryocyte: Figures 1e,f) lineages. Flow cytometry showed that the leukemic blasts were positive for CD13, CD33, CD34, CD56, and myeloperoxidase. Cytogenetic analysis demonstrated a complicated karyotype with deletion of chromosomes 5q and 7. Based on these findings, myeloid neoplasm post cytotoxic therapy (MN-pCT) was diagnosed.</p><p>In bone marrow, there was an increase in eosinophils (14.7%), in addition to blasts, and some eosinophils were dysplastic with large basophilic granules of purple-violet color (Figures 2a,b), which are referred to as harlequin cells [<span>1</span>].</p><p>ENKTL is associated with Epstein–Barr virus infection and rarely involves the gastrointestinal tract. Advances in ENKTL treatment have led to an increase in the number of survivors. Consequently, the risk of patients developing MN-pCT may have increased.</p><p>Two cases of MN-pCT with harlequin cells have been reported. Although the primary cancers were different (thymoma and colon adenocarcinoma), alkylating agents were administered in both cases [<span>2, 3</span>].</p><p>The harlequin cells are classified as Code 9 by the International Working Group on Morphology of MDS [<span>4</span>] and are more frequently observed in de novo acute myeloid leukemia harboring <i>CBFB::MYH11</i> fusion [<span>1, 4</span>]. Harlequin cells are observed not only in hematologic malignancies but also in patients with non-hematologic diseases [<span>1, 4</span>]. However, in AML with the <i>CBFB::MYH11</i> fusion, these eosinophils are considered part of the neoplastic clone [<span>4</span>].</p><p>The app","PeriodicalId":72883,"journal":{"name":"EJHaem","volume":"6 5","pages":""},"PeriodicalIF":1.2,"publicationDate":"2025-10-18","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://onlinelibrary.wiley.com/doi/epdf/10.1002/jha2.70167","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145317712","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Van Tuong Nguyen, Lina Han, Jing Xu, Miguel Cantu, Franklin Fuda, Samuel John, Tamra Slone, Weina Chen
Background
NUP98::BPTF rearranged (r) leukaemia is rare with only five reported cases, including acute myeloid leukemia and T-lymphoblastic leukemia (T-ALL).
Results
Herein, we report a case of NUP98::BPTF-r mixed phenotype acute leukemia (MPAL), B/T with T-lineage-predominance in a 15-year-old female. Cytogenetic and molecular studies revealed a t(11;17)(p15;q23)/NUP98::BPTF fusion and cooperative gene alterations characteristic of T-ALL (NOTCH1, FBXW7, and PHF6). Our patient had a primary induction failure with T-ALL-directed chemotherapy and achieved complete remission following consolidation.
Conclusion
This is the first case study characterizing the clinicopathological and genomic features of B/T MPAL harboring NUP98::BPTF fusion and providing insights into molecular pathogenesis.
Trial Registration
The authors have confirmed clinical trial registration is not needed for this submission.
背景：BPTF重排(r)白血病是罕见的，仅有5例报道，包括急性髓系白血病和t淋巴母细胞白血病（T-ALL）。结果：在此，我们报告了一例15岁女性的NUP98::BPTF-r混合表型急性白血病（MPAL）， B/T伴T谱系优势。细胞遗传学和分子生物学研究显示t(11;17)(p15;q23)/NUP98::BPTF融合和t - all （NOTCH1、FBXW7和PHF6）的协同基因改变特征。我们的患者在接受t - all定向化疗时出现了原发性诱导失败，并在巩固后完全缓解。结论：这是第一个描述含有NUP98::BPTF融合的B/T MPAL的临床病理和基因组特征的病例研究，并为分子发病机制提供了新的见解。试验注册：作者已确认本次提交不需要临床试验注册。
{"title":"B/T Mixed Phenotype Acute Leukaemia Harbouring NUP98::BPTF Fusion","authors":"Van Tuong Nguyen, Lina Han, Jing Xu, Miguel Cantu, Franklin Fuda, Samuel John, Tamra Slone, Weina Chen","doi":"10.1002/jha2.70166","DOIUrl":"10.1002/jha2.70166","url":null,"abstract":"<div>\u0000 \u0000 \u0000 <section>\u0000 \u0000 <h3> Background</h3>\u0000 \u0000 <p><i>NUP98</i>::<i>BPTF</i> rearranged (r) leukaemia is rare with only five reported cases, including acute myeloid leukemia and T-lymphoblastic leukemia (T-ALL).</p>\u0000 </section>\u0000 \u0000 <section>\u0000 \u0000 <h3> Results</h3>\u0000 \u0000 <p>Herein, we report a case of <i>NUP98::BPTF</i>-r mixed phenotype acute leukemia (MPAL), B/T with T-lineage-predominance in a 15-year-old female. Cytogenetic and molecular studies revealed a t(11;17)(p15;q23)/<i>NUP98::BPTF</i> fusion and cooperative gene alterations characteristic of T-ALL (<i>NOTCH1</i>, <i>FBXW7</i>, and <i>PHF6</i>). Our patient had a primary induction failure with T-ALL-directed chemotherapy and achieved complete remission following consolidation.</p>\u0000 </section>\u0000 \u0000 <section>\u0000 \u0000 <h3> Conclusion</h3>\u0000 \u0000 <p>This is the first case study characterizing the clinicopathological and genomic features of B/T MPAL harboring <i>NUP98::BPTF</i> fusion and providing insights into molecular pathogenesis.</p>\u0000 </section>\u0000 \u0000 <section>\u0000 \u0000 <h3> Trial Registration</h3>\u0000 \u0000 <p>The authors have confirmed clinical trial registration is not needed for this submission.</p>\u0000 </section>\u0000 </div>","PeriodicalId":72883,"journal":{"name":"EJHaem","volume":"6 5","pages":""},"PeriodicalIF":1.2,"publicationDate":"2025-10-14","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12519876/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145304804","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
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