Pub Date : 2026-03-13DOI: 10.1182/blood.2025032050
Michael Oertel,Bouthaina S Dabaja,Dennis Görlich,Bjorn R Thomas,Van Sim,Philippa Johnstone,Ayesha Hashmi,Mario Levis,Bradley Ackerson,Christina Hague,Christopher R Weil,John Plastaras,Daniel Edward Roos,Youlia Kirova,Rainer Fietkau,Penny Q Fang,Andrea K Ng,Felix Bock,Yolanda D Tseng,Philipp Linde,Jürgen Dunst,Stephanie A Terezakis,Teresa Easwaran,Jan C Peeken,Andrea Wittig,Hong In Yoon,Randa Tao,Timothy M Illidge,Chris R Kelsey,Umberto Ricardi,Michael S Binkley,Belinda A Campbell,Stephen Lloyd Morris,Khaled Elsayad,Michael Storck,Richard T Hoppe,Hans Theodor Eich
Radiotherapy is an established treatment for low-grade primary cutaneous B-cell lymphoma. Recommendations on its use differ internationally, which prompted our group to conduct the present analysis. Twenty-two institutions participated in this international study. Patient eligibility required a diagnosis of limited (T1/T2) primary cutaneous marginal zone or follicle center lymphoma treated with radiotherapy between 1995 and 2023. Data were collected retrospectively until February 2024 in the framework of the International Lymphoma Radiation Oncology Group. Overall, 535 patients were analyzed. Predominant locations were the head (40%) and trunk (36%). Radiotherapy had a median dose of 24 Gy in fractions of 2 Gy. Complete responses were seen in 91% at a median time of 3.6 months following radiotherapy. There was no statistically significant difference between treatments ≤4 Gy or >4 Gy for complete or overall response rates (p=0.077 and p=0.056). However, there was an inferior duration of local control with ≤4 Gy (5-year local control 73% ± 12% vs. 96% ± 2%; p<0.001). Radiation dose was the main prognostic factor in the univariate and multivariate Cox analysis; however, higher doses did not translate into an overall survival benefit. Toxicities rarely exceeded grade 2 but were more frequent in the >4 Gy group. Radiotherapy remains an effective treatment option for indolent skin lymphoma with low toxicities. High response rates are observed with low doses ≤4 Gy. In comparison to conventional doses, these treatments have a shorter duration of local control but a favorable toxicity profile.
放疗是低级别原发性皮肤b细胞淋巴瘤的常用治疗方法。关于其使用的建议在国际上有所不同，这促使我们小组进行了目前的分析。22个机构参与了这项国际研究。患者资格要求在1995年至2023年间接受放疗的有限（T1/T2）原发性皮肤边缘区或滤泡中心淋巴瘤诊断。数据是在国际淋巴瘤放射肿瘤学组织的框架下回顾性收集到2024年2月。总共分析了535例患者。主要部位为头部（40%）和躯干（36%）。放射治疗的中位剂量为24gy，分成2gy的部分。在放疗后3.6个月的中位时间内，91%的患者完全缓解。治疗≤4 Gy和治疗≤4 Gy两组的完全缓解率和总缓解率无统计学差异（p=0.077和p=0.056）。然而，≤4gy组的局部控制时间较短（5年局部控制时间73%±12% vs 96%±2%；p4gy组）。放疗仍然是一种有效的治疗选择，无痛皮肤淋巴瘤低毒性。低剂量≤4 Gy时，观察到高反应率。与常规剂量相比，这些治疗具有较短的局部控制时间，但具有良好的毒性。
{"title":"Radiotherapy for indolent primary cutaneous B-cell lymphoma: an international multicenter ILROG analysis.","authors":"Michael Oertel,Bouthaina S Dabaja,Dennis Görlich,Bjorn R Thomas,Van Sim,Philippa Johnstone,Ayesha Hashmi,Mario Levis,Bradley Ackerson,Christina Hague,Christopher R Weil,John Plastaras,Daniel Edward Roos,Youlia Kirova,Rainer Fietkau,Penny Q Fang,Andrea K Ng,Felix Bock,Yolanda D Tseng,Philipp Linde,Jürgen Dunst,Stephanie A Terezakis,Teresa Easwaran,Jan C Peeken,Andrea Wittig,Hong In Yoon,Randa Tao,Timothy M Illidge,Chris R Kelsey,Umberto Ricardi,Michael S Binkley,Belinda A Campbell,Stephen Lloyd Morris,Khaled Elsayad,Michael Storck,Richard T Hoppe,Hans Theodor Eich","doi":"10.1182/blood.2025032050","DOIUrl":"https://doi.org/10.1182/blood.2025032050","url":null,"abstract":"Radiotherapy is an established treatment for low-grade primary cutaneous B-cell lymphoma. Recommendations on its use differ internationally, which prompted our group to conduct the present analysis. Twenty-two institutions participated in this international study. Patient eligibility required a diagnosis of limited (T1/T2) primary cutaneous marginal zone or follicle center lymphoma treated with radiotherapy between 1995 and 2023. Data were collected retrospectively until February 2024 in the framework of the International Lymphoma Radiation Oncology Group. Overall, 535 patients were analyzed. Predominant locations were the head (40%) and trunk (36%). Radiotherapy had a median dose of 24 Gy in fractions of 2 Gy. Complete responses were seen in 91% at a median time of 3.6 months following radiotherapy. There was no statistically significant difference between treatments ≤4 Gy or >4 Gy for complete or overall response rates (p=0.077 and p=0.056). However, there was an inferior duration of local control with ≤4 Gy (5-year local control 73% ± 12% vs. 96% ± 2%; p<0.001). Radiation dose was the main prognostic factor in the univariate and multivariate Cox analysis; however, higher doses did not translate into an overall survival benefit. Toxicities rarely exceeded grade 2 but were more frequent in the >4 Gy group. Radiotherapy remains an effective treatment option for indolent skin lymphoma with low toxicities. High response rates are observed with low doses ≤4 Gy. In comparison to conventional doses, these treatments have a shorter duration of local control but a favorable toxicity profile.","PeriodicalId":9102,"journal":{"name":"Blood","volume":"52 1","pages":""},"PeriodicalIF":20.3,"publicationDate":"2026-03-13","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"147446930","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}
Erythropoiesis, the process of red blood cell production, is highly dependent on iron uptake via transferrin and its receptor, transferrin receptor 1 (TfR1), but the mechanisms governing the proper recycling of TfR1 in relation to cellular iron demands remain elusive. Here, we identify human TMEM187, a Golgi transmembrane protein of unknown function, as a novel negative regulator of erythropoiesis. Lack of TMEM187 in a cell model initiates erythropoiesis without the normal induction protocol and accelerates iron uptake. Following the induction protocol, TMEM187 ablation leads to premature erythroid maturation, resulting in early phosphatidylserine ectopia and cell membrane fragility, hallmarks of cellular senescence that renders the cells susceptible to macrophage recognition and phagocytosis. In zebrafish embryos, tmem187 deletion leads to enhanced early erythropoiesis, although the phenotype is later compensated, whereas hematopoietic stem-cell expression of human TMEM187 in mice, which lack endogenously a homologous gene, resulted in compromised erythropoiesis and moderate anemia. Mechanistically, we demonstrate that TMEM187 interacts with RAB11 to restrain endosomal recycling, interfering with RAB11-GRAB association that activates RAB11. Consequently, TMEM187 modulates TfR1 recycling to the cell membrane to fine-tune iron uptake efficiency for erythropoiesis. Our findings reveal a novel modulatory pathway in which TMEM187 plays a crucial role in regulating erythroid differentiation, maturation, and senescence, providing a previously unexplored perspective of TMEM187's physiological function.
{"title":"TMEM187 is a novel modulator in the regulation of erythropoiesis.","authors":"Yutong Liu,Wenxin Zhang,Jing Cai,Di Zhou,Hongting Zhao,Weichen Dong,Biao Zhao,Yao Lu,Shuangying Hao,Yibing Ding,Nizhen Jiang,Tong Qiao,Kuanyu Li","doi":"10.1182/blood.2025031135","DOIUrl":"https://doi.org/10.1182/blood.2025031135","url":null,"abstract":"Erythropoiesis, the process of red blood cell production, is highly dependent on iron uptake via transferrin and its receptor, transferrin receptor 1 (TfR1), but the mechanisms governing the proper recycling of TfR1 in relation to cellular iron demands remain elusive. Here, we identify human TMEM187, a Golgi transmembrane protein of unknown function, as a novel negative regulator of erythropoiesis. Lack of TMEM187 in a cell model initiates erythropoiesis without the normal induction protocol and accelerates iron uptake. Following the induction protocol, TMEM187 ablation leads to premature erythroid maturation, resulting in early phosphatidylserine ectopia and cell membrane fragility, hallmarks of cellular senescence that renders the cells susceptible to macrophage recognition and phagocytosis. In zebrafish embryos, tmem187 deletion leads to enhanced early erythropoiesis, although the phenotype is later compensated, whereas hematopoietic stem-cell expression of human TMEM187 in mice, which lack endogenously a homologous gene, resulted in compromised erythropoiesis and moderate anemia. Mechanistically, we demonstrate that TMEM187 interacts with RAB11 to restrain endosomal recycling, interfering with RAB11-GRAB association that activates RAB11. Consequently, TMEM187 modulates TfR1 recycling to the cell membrane to fine-tune iron uptake efficiency for erythropoiesis. Our findings reveal a novel modulatory pathway in which TMEM187 plays a crucial role in regulating erythroid differentiation, maturation, and senescence, providing a previously unexplored perspective of TMEM187's physiological function.","PeriodicalId":9102,"journal":{"name":"Blood","volume":"9 1","pages":""},"PeriodicalIF":20.3,"publicationDate":"2026-03-13","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"147446933","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}
Pub Date : 2026-03-13DOI: 10.1182/blood.2025031420
Susan A Maroney,Nicholas D Martinez,Praveen Krishnamoorthy,Paul Ellery,Mark A Rasmussen,Amy E Siebert,Jennifer May,Erin Yttre,Adrianna M Jurek,Randal J Westrick,Donny Hoang,Shikan Zheng,Mark Zogg,John Patrick Sheehan,James Fitzpatrick,Tongjun Gu,Hartmut Weiler,Alan E Mast
Mice lacking Tissue Factor Pathway Inhibitor (Tfpi-/-) succumb to embryonic lethality from excess thrombin production and associated cerebrovascular defects called glomeruloid bodies. A transgene producing hyperactivatable mouse protein C (hMPC) was bred into Tfpi+/- mice to determine if excess activated PC (aPC) would correct the cerebrovascular defects in Tfpi-/- embryos. Tfpi-/-/hMPC+ embryos survived to adulthood. Despite the rescue of embryonic lethality, hMPC reduced glomeruloid body numbers by only 36% and did not prevent fibrin deposition or disruption of the blood-brain barrier within glomeruloid bodies. However, there was decreased hypoxia and cellular death in Tfpi-/-/hMPC+ brains suggesting that cytoprotective effects of hMPC contributed to Tfpi-/- rescue. The glomeruloid bodies were completely resolved in Tfpi-/-/hMPC+ P10 pups revealing a distinct temporal effect of TFPI on embryonic cerebrovascular development. Bulk RNAseq of E15.5 brain tissue identified increased angiogenesis as the overwhelming biological process altered in Tfpi-/- brain. This included changes in genes encoding apelin, adrenomedulin, and UNC5b, which was consistent with abundant endothelial tip cells within glomeruloid bodies. The increased expression of these angiogenic genes was reversed by the hMPC transgene. These findings define TFPI as an essential inhibitor of thrombin generation during embryonic angiogenesis that acts temporally within or around developing cerebral vasculature in a manner that is not compensated for by other anticoagulant proteins. The findings emphasize the importance of blood coagulation proteases and regulation of their activity in diverse biological processes.
缺乏组织因子通路抑制剂（Tfpi-/-）的小鼠会因凝血酶过量产生和相关的称为肾小球体的脑血管缺陷而导致胚胎死亡。将产生高活化小鼠蛋白C （hyperactivatable mouse protein C, hMPC）的转基因基因植入Tfpi+/-小鼠体内，观察过量活化PC （hyperactivatable mouse protein C, aPC）是否能纠正Tfpi-/-胚胎的脑血管缺陷。Tfpi-/-/hMPC+胚胎存活至成年。尽管挽救了胚胎致死性，hMPC仅减少了36%的肾小球体数量，并不能阻止肾小球体内的纤维蛋白沉积或血脑屏障的破坏。然而，在Tfpi-/-/hMPC+脑中，缺氧和细胞死亡减少，表明hMPC的细胞保护作用有助于Tfpi-/-的拯救。在Tfpi-/-/hMPC+ P10幼崽中，肾小球小体完全溶解，表明Tfpi对胚胎脑血管发育具有明显的时间效应。E15.5脑组织的大量RNAseq表明，血管生成增加是Tfpi-/-脑中压倒性的生物过程改变。这包括编码apelin、肾上腺髓质素和UNC5b的基因的变化，这与肾小球体内丰富的内皮尖端细胞一致。这些血管生成基因的表达增加被hMPC转基因逆转。这些发现将TFPI定义为胚胎血管生成过程中凝血酶生成的重要抑制剂，它在发育中的脑血管系统内或周围暂时起作用，而其他抗凝蛋白无法补偿这种作用。这些发现强调了凝血蛋白酶及其在多种生物过程中活性调控的重要性。
{"title":"Defective cerebrovascular development in mice lacking TFPI is restored by activated protein C.","authors":"Susan A Maroney,Nicholas D Martinez,Praveen Krishnamoorthy,Paul Ellery,Mark A Rasmussen,Amy E Siebert,Jennifer May,Erin Yttre,Adrianna M Jurek,Randal J Westrick,Donny Hoang,Shikan Zheng,Mark Zogg,John Patrick Sheehan,James Fitzpatrick,Tongjun Gu,Hartmut Weiler,Alan E Mast","doi":"10.1182/blood.2025031420","DOIUrl":"https://doi.org/10.1182/blood.2025031420","url":null,"abstract":"Mice lacking Tissue Factor Pathway Inhibitor (Tfpi-/-) succumb to embryonic lethality from excess thrombin production and associated cerebrovascular defects called glomeruloid bodies. A transgene producing hyperactivatable mouse protein C (hMPC) was bred into Tfpi+/- mice to determine if excess activated PC (aPC) would correct the cerebrovascular defects in Tfpi-/- embryos. Tfpi-/-/hMPC+ embryos survived to adulthood. Despite the rescue of embryonic lethality, hMPC reduced glomeruloid body numbers by only 36% and did not prevent fibrin deposition or disruption of the blood-brain barrier within glomeruloid bodies. However, there was decreased hypoxia and cellular death in Tfpi-/-/hMPC+ brains suggesting that cytoprotective effects of hMPC contributed to Tfpi-/- rescue. The glomeruloid bodies were completely resolved in Tfpi-/-/hMPC+ P10 pups revealing a distinct temporal effect of TFPI on embryonic cerebrovascular development. Bulk RNAseq of E15.5 brain tissue identified increased angiogenesis as the overwhelming biological process altered in Tfpi-/- brain. This included changes in genes encoding apelin, adrenomedulin, and UNC5b, which was consistent with abundant endothelial tip cells within glomeruloid bodies. The increased expression of these angiogenic genes was reversed by the hMPC transgene. These findings define TFPI as an essential inhibitor of thrombin generation during embryonic angiogenesis that acts temporally within or around developing cerebral vasculature in a manner that is not compensated for by other anticoagulant proteins. The findings emphasize the importance of blood coagulation proteases and regulation of their activity in diverse biological processes.","PeriodicalId":9102,"journal":{"name":"Blood","volume":"9 1","pages":""},"PeriodicalIF":20.3,"publicationDate":"2026-03-13","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"147446962","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}
Pub Date : 2026-03-13DOI: 10.1182/blood.2025031047
Johanna M Horns,Thomas Beder,Axel Künstner,Malwine Jeanette Barz,Sonja Bendig,Cecilia Bozzetti,Guranda Chitadze,Nikos Darzentas,Katharina Iben,Michaela Kotrova,José-Ignacio Martín-Subero,Mayukh Mondal,Martin Neumann,Raul Fernandez Perez,Aeint-Steffen Ströh,Wiebke Weßels,Lennart Lenk,Lars Velten,Boris Böll,Krischan Braitsch,Veit L Bücklein,Johannes Duell,Christoph Faul,Walter Fiedler,Maher Hanoun,Snjezana Janjetovic,Felix Klingler,Stefan Knop,Christoph Röllig,Stefan Schwartz,Bernd M Spriewald,Björn Steffen,Klaus Wethmar,Hauke Busch,Nicola Gökbuget,Claudia D Baldus,Lorenz Bastian,Monika Brüggemann
Lenalidomide, a maintenance treatment in multiple myeloma first-line therapy, increases the risk of secondary malignancies, including B-cell precursor acute lymphoblastic leukemia (B‑ALL). We present a comprehensive molecular characterization of 57 patients with lenalidomide-associated B-ALL (LenB-ALL), revealing three mutational subgroups: (1) TP53mt (30%), (2) IDH2mt (p.R140Q) (23%) and (3) other, including NRAS/KRASmt. Remarkably, IDH2 R140Q mutations were highly enriched in LenB-ALL compared to primary B-ALL (p<0.001). Furthermore, IKZF1 intragenic deletions - often subclonal and likely RAG-mediated - were observed in 54% (7/13) of IDH2mt LenB-ALL cases. IDH2 mutations were not restricted to the leukemic clone: they persisted during MRD-negative remission and were identified in lymphoid as well as myeloid cell populations using fluorescence-activated cell sorting and single-cell RNA sequencing. This indicates a preleukemic origin of the IDH2 mutation within the context of clonal hematopoiesis. Transcriptomic and DNA methylation analyses revealed a distinct gene expression profile and a DNA hypermethylation phenotype in IDH2mt LenB-ALL, including IDH2mt-specific as well as lenalidomide-associated features. We propose that lenalidomide promotes expansion of IDH2-mutated clonal hematopoiesis and, via IKAROS downregulation, induces a maturation arrest at the B-cell precursor stage. Subsequent genetic or epigenetic alterations render leukemogenesis independent of ongoing lenalidomide exposure. Altogether, these data define IDH2mt B-ALL as a distinct molecular subtype that is markedly overrepresented after lenalidomide treatment and highlight clonal hematopoiesis as a key contributing factor in the development of LenB-ALL.
{"title":"IDH2 Clonal Hematopoiesis and IKAROS Loss Cooperate in a B-ALL Subtype after Lenalidomide Therapy for Multiple Myeloma.","authors":"Johanna M Horns,Thomas Beder,Axel Künstner,Malwine Jeanette Barz,Sonja Bendig,Cecilia Bozzetti,Guranda Chitadze,Nikos Darzentas,Katharina Iben,Michaela Kotrova,José-Ignacio Martín-Subero,Mayukh Mondal,Martin Neumann,Raul Fernandez Perez,Aeint-Steffen Ströh,Wiebke Weßels,Lennart Lenk,Lars Velten,Boris Böll,Krischan Braitsch,Veit L Bücklein,Johannes Duell,Christoph Faul,Walter Fiedler,Maher Hanoun,Snjezana Janjetovic,Felix Klingler,Stefan Knop,Christoph Röllig,Stefan Schwartz,Bernd M Spriewald,Björn Steffen,Klaus Wethmar,Hauke Busch,Nicola Gökbuget,Claudia D Baldus,Lorenz Bastian,Monika Brüggemann","doi":"10.1182/blood.2025031047","DOIUrl":"https://doi.org/10.1182/blood.2025031047","url":null,"abstract":"Lenalidomide, a maintenance treatment in multiple myeloma first-line therapy, increases the risk of secondary malignancies, including B-cell precursor acute lymphoblastic leukemia (B‑ALL). We present a comprehensive molecular characterization of 57 patients with lenalidomide-associated B-ALL (LenB-ALL), revealing three mutational subgroups: (1) TP53mt (30%), (2) IDH2mt (p.R140Q) (23%) and (3) other, including NRAS/KRASmt. Remarkably, IDH2 R140Q mutations were highly enriched in LenB-ALL compared to primary B-ALL (p<0.001). Furthermore, IKZF1 intragenic deletions - often subclonal and likely RAG-mediated - were observed in 54% (7/13) of IDH2mt LenB-ALL cases. IDH2 mutations were not restricted to the leukemic clone: they persisted during MRD-negative remission and were identified in lymphoid as well as myeloid cell populations using fluorescence-activated cell sorting and single-cell RNA sequencing. This indicates a preleukemic origin of the IDH2 mutation within the context of clonal hematopoiesis. Transcriptomic and DNA methylation analyses revealed a distinct gene expression profile and a DNA hypermethylation phenotype in IDH2mt LenB-ALL, including IDH2mt-specific as well as lenalidomide-associated features. We propose that lenalidomide promotes expansion of IDH2-mutated clonal hematopoiesis and, via IKAROS downregulation, induces a maturation arrest at the B-cell precursor stage. Subsequent genetic or epigenetic alterations render leukemogenesis independent of ongoing lenalidomide exposure. Altogether, these data define IDH2mt B-ALL as a distinct molecular subtype that is markedly overrepresented after lenalidomide treatment and highlight clonal hematopoiesis as a key contributing factor in the development of LenB-ALL.","PeriodicalId":9102,"journal":{"name":"Blood","volume":"43 1","pages":""},"PeriodicalIF":20.3,"publicationDate":"2026-03-13","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"147446928","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}
Pub Date : 2026-03-12DOI: 10.1182/blood.2025032458
Simón Méndez-Ferrer, Angela G Fleischman
{"title":"A niche for every stem cell in myeloproliferative neoplasms.","authors":"Simón Méndez-Ferrer, Angela G Fleischman","doi":"10.1182/blood.2025032458","DOIUrl":"https://doi.org/10.1182/blood.2025032458","url":null,"abstract":"","PeriodicalId":9102,"journal":{"name":"Blood","volume":"147 11","pages":"1143-1144"},"PeriodicalIF":23.1,"publicationDate":"2026-03-12","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"147430450","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}
Pub Date : 2026-03-12DOI: 10.1182/blood.2025031931
Samuel Y Ng
{"title":"Splitting from a lump: harmonizing ALCL classification.","authors":"Samuel Y Ng","doi":"10.1182/blood.2025031931","DOIUrl":"https://doi.org/10.1182/blood.2025031931","url":null,"abstract":"","PeriodicalId":9102,"journal":{"name":"Blood","volume":"147 11","pages":"1142-1143"},"PeriodicalIF":23.1,"publicationDate":"2026-03-12","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"147430562","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}
Pub Date : 2026-03-12DOI: 10.1182/blood.2025030986
David M Bodine
{"title":"A mechanism for a VEXing problem.","authors":"David M Bodine","doi":"10.1182/blood.2025030986","DOIUrl":"https://doi.org/10.1182/blood.2025030986","url":null,"abstract":"","PeriodicalId":9102,"journal":{"name":"Blood","volume":"147 11","pages":"1138-1139"},"PeriodicalIF":23.1,"publicationDate":"2026-03-12","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"147430515","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}
Pub Date : 2026-03-12DOI: 10.1182/blood.2025032334
Viktoria Blumenberg, Marcela V Maus
{"title":"When CAR T cells become the disease.","authors":"Viktoria Blumenberg, Marcela V Maus","doi":"10.1182/blood.2025032334","DOIUrl":"https://doi.org/10.1182/blood.2025032334","url":null,"abstract":"","PeriodicalId":9102,"journal":{"name":"Blood","volume":"147 11","pages":"1139-1141"},"PeriodicalIF":23.1,"publicationDate":"2026-03-12","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"147430613","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}
Pub Date : 2026-03-12DOI: 10.1182/blood.2025032403
Mattias Carlsten
{"title":"Maneuvering ofCS toward precision medicine for AML?","authors":"Mattias Carlsten","doi":"10.1182/blood.2025032403","DOIUrl":"https://doi.org/10.1182/blood.2025032403","url":null,"abstract":"","PeriodicalId":9102,"journal":{"name":"Blood","volume":"147 11","pages":"1144-1145"},"PeriodicalIF":23.1,"publicationDate":"2026-03-12","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"147430634","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}
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