Blood最新文献

{"title":"Real-world outcomes of patients with aggressive B-cell lymphoma treated with epcoritamab or glofitamab.","authors":"Taylor R Brooks,Emily C Zabor,Yohanna Bedelu,Xi Yang,Yasmin H Karimi,Adrienne N Nedved,Yucai Wang,Nikita K Dave,Daniel J Landsburg,Kelsey Baron,Boyu Hu,Daniel Trotier,Priyanka A Pophali,Jordan Miller,Natalie S Grover,Catherine Reinert,Ajay Major,Tenley Schwarz,Krish Patel,Kiarash Salafian,Emily C Ayers,Suchitra Sundaram,Joshua D Brody,Marshall McKenna,Yun Kyoung Ryu Tiger,Megan Sears-Smith,Nilanjan Ghosh,Chelsea Peterson,Cyrus Khan,Sean P Bliven,Mayur Narkhede,Alyssa Gibson,Justin Kline,Javier Munoz,Rodolfo Garza Morales,Carrie Ho,Stephen D Smith,Alex Niu,Francisco J Hernandez-Ilizaliturri,Fadzai Chinyengetere,Sandeep S Dave,Nayef Abdel-Razeq,Muhamad Alhaj Moustafa,Paolo Caimi,Brian T Hill","doi":"10.1182/blood.2025029117","DOIUrl":"https://doi.org/10.1182/blood.2025029117","url":null,"abstract":"Epcoritamab and glofitamab are CD20-directed bispecific antibodies approved in the US for relapsed or refractory (R/R) diffuse large B-cell lymphoma (DLBCL). Limited data exist for patients treated outside of trials. Patients with R/R DLBCL receiving commercial epcoritamab or glofitamab between January 1, 2023 and October 15, 2024 were collected from 21 US institutions. Among 245 patients, 156 received epcoritamab and 89 received glofitamab, 113 were refractory to front-line therapy, 40 had MYC and BCL2 and/or BCL6 rearrangements, 147 received prior chimeric antigen receptor T-cell therapy, and 174 patients would have been ineligible for registrational trials. The overall response rate (ORR) for epcoritamab and glofitamab was 51% (23% complete response, [CR]) and 53% (30% CR), respectively. Median progression-free survival (mPFS) was 2.6 months (95% confidence interval [CI] 2.0 to 3.8 months), and median overall survival (mOS) was 7.8 months (95% CI 6.2 to 11.0 months). The 6-month PFS was 36% (95% CI 30% to 44%) and the 6-month OS was 60% (95% CI 54% to 67%). Both trial ineligibility and undetectable CD20 pre-bispecific portended shorter PFS and OS. Of 17 individuals with paired biopsies, 15 (88.2%) lost CD20 expression after bispecifics with a median time to progression of 3.7 months. This analysis including R/R DLBCL patients shows the ORR to CD3/CD20 BsAbs was comparable to pivotal trials, although PFS and OS were lower. Baseline undetectable levels of CD20 was associated with poor outcomes. These results demonstrate the activity of BsAbs in R/R DLBCL and underscore the importance of target antigen expression.","PeriodicalId":9102,"journal":{"name":"Blood","volume":"130 1","pages":""},"PeriodicalIF":20.3,"publicationDate":"2025-07-15","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144640083","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 cause of type 1 von Willebrand disease: impaired exocytosis of Weibel-Palade bodies due to biallelic MADD variants.","authors":"Sophie Hordijk,Stijn A Groten,Petra E Bürgisser,Sebastiaan N J Laan,Georg-Christoph Korenke,Diane Beysen,Frank W G Leebeek,Paul A Skehel,Maartje van den Biggelaar,Tom Carter,Ruben Bierings","doi":"10.1182/blood.2024027935","DOIUrl":"https://doi.org/10.1182/blood.2024027935","url":null,"abstract":"The regulated secretion of von Willebrand factor (VWF) from Weibel-Palade bodies (WPB) in endothelial cells is fundamental to hemostasis. This process relies on recruiting Rab GTPases and their effectors to the WPB membrane, with the guanine nucleotide exchange factor (GEF) MAP-kinase activating death domain (MADD) playing a central role. Biallelic variants in MADD lead to a pleiotropic neurological and developmental disorder that can include bleeding abnormalities. This study investigates the impact of pathogenic MADD variants on VWF secretion using patient-derived endothelial cells. We isolated endothelial colony forming cells (ECFCs) from three pediatric patients with biallelic MADD variants and unaffected heterozygous family members. All patients exhibited low VWF plasma levels (22-30 IU/dL). Proteomic analysis of patient-derived ECFCs revealed an absence of MADD peptides, reduced VWF, and downregulation of proteins involved in the exocytotic machinery, including Rab3D and the Rab3/27 effector Slp4-a. Functional assays demonstrated diminished Rab27A and Rab3D activity and their failure to localize to WPBs in patient cells. Biochemical and live-imaging studies showed that histamine-induced VWF and VWFpp secretion were significantly reduced in patient cells due to delayed and reduced degranulation of WPBs. Our findings demonstrate the critical role of MADD in maintaining the secretion competence of WPBs and the magnitude of VWF secretion by regulating the recruitment of the endothelial exocytotic machinery. This study highlights the in vivo significance of WPB exocytosis in maintaining plasma VWF levels and establishes MADD as the first causal gene for quantitative von Willebrand Disease (VWD) in patients without pathogenic VWF variants.","PeriodicalId":9102,"journal":{"name":"Blood","volume":"6 1","pages":""},"PeriodicalIF":20.3,"publicationDate":"2025-07-15","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144645881","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":"Clinical presentation, management, and outcome of TIAN in CNS lymphoma treated with CD19-CAR T-cell Therapy.","authors":"Leon D Kaulen,Maria Martinez-Lage,Jeremy S Abramson,Philipp Karschnia,Sofia Doubrovinskaia,Ganesh M Shankar,Bryan D Choi,Christopher Michael Ramundo,Felix Ehret,Jeffrey A Barnes,Areej El-Jawahri,Ephraim Hochberg,P Connor Johnson,Jacob D Soumerai,Scott R Plotkin,Tracy T Batchelor,Wolfgang Wick,Marcela V Maus,Yi-Bin Chen,Matthew J Frigault,Jorg Dietrich","doi":"10.1182/blood.2025028964","DOIUrl":"https://doi.org/10.1182/blood.2025028964","url":null,"abstract":"Tumor inflammation-associated neurotoxicity (TIAN) was recently proposed as a unique complication of immunotherapy in brain tumor patients. Here, we report a first comprehensive characterization of TIAN in CNS lymphoma (CNSL) patients treated with CD19-directed chimeric antigen receptor T-cells (CD19-CAR). TIAN occurred in 10/56 (17.9%) CNSL with clinical onset at a median 3.5 days (range: 1-9) after CD19-CAR infusion. It was less frequently associated with cytokine release syndrome (60% vs 100%, p = 0.009) than immune effector cell-associated neurotoxicity syndrome (ICANS). Although symptoms were usually transient and fully reversible, TIAN was associated with a fatal outcome in one patient. Larger CNS tumor volume at baseline allowed the identification of patients at risk for TIAN (AUC: 0.847, p = 0.002). Maximizing Youden J statistics, a discriminatory tumor volume threshold >3.4cm3 was determined, which carried 87.5% sensitivity and 80.5% specificity. TIAN correlated with higher overall response rates to CD19-CAR (90% vs 52%, p = 0.036) and improved progression-free survival (Hazard ratio: 0.22; 95%-Confidence interval: 0.07-0.61, p = 0.006) on multivariate Cox proportional hazard regression. Post-mortem histopathological evaluation of a TIAN lesion revealed a dense macrophage population with central necrosis and peripheral reactive gliosis, accompanied by loss of white matter and intracytoplasmic myelin in foamy macrophages. Collectively, our work supports TIAN as a localized on-tumor, on-target neurotoxicity syndrome, closely related to pre-existing CNSL lesions and distinct from ICANS. CNS tumor volume at baseline may allow to identify patients at risk and may guide management.","PeriodicalId":9102,"journal":{"name":"Blood","volume":"94 1","pages":""},"PeriodicalIF":20.3,"publicationDate":"2025-07-15","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144640103","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":"The Treatment of Marginal Zone Lymphoma.","authors":"Juan Pablo Alderuccio, Ariela Noy","doi":"10.1182/blood.2024028269","DOIUrl":"https://doi.org/10.1182/blood.2024028269","url":null,"abstract":"<p><p>The treatment landscape of B-cell non-Hodgkin lymphomas is rapidly evolving. However, few advances have occurred in marginal zone lymphoma (MZL) with a single FDA-approved agent impacting the treatment landscape. Multiple factors are associated with this slower pace of progress, with a lower MZL incidence representing a significant factor. Pivotal randomized indolent lymphoma clinical trials analyzed MZL subsets without the appropriate power to capture differences between treatment arms. Furthermore, the current Lugano Classification may not fully capture the presentation or treatment responses of some subtypes, preventing access to clinical trials and limiting an efficacy assessment across the disease spectrum. Thus, current MZL treatment is largely informed by single-arm studies with relatively empiric treatment sequencing among available agents. While frontline strategies in early- and advanced-stage MZL can achieve prolonged disease control, few options exist in the relapsed/refractory setting capable of achieving similar results. Emerging data demonstrate the encouraging efficacy of CD3xCD20 bispecific antibodies and antibody-drug conjugates in achieving deep responses, as well as the potential of circulating tumor DNA in risk stratification and molecular response monitoring. Compounding all these considerations, it is essential to recognize MZL as a heterogeneous group of diseases characterized by unique biology, clinical presentation, treatment response, toxicity, and survival. Nonetheless, a common characteristic across MZL subtypes is their general indolent disease course, emphasizing the need to incorporate patient-centered assessment in clinical trials to better inform the decision-making process.</p>","PeriodicalId":9102,"journal":{"name":"Blood","volume":" ","pages":""},"PeriodicalIF":21.0,"publicationDate":"2025-07-15","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144641802","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":"Visualizing amyloidosis: The role of radionuclide imaging in systemic amyloidosis.","authors":"Nirija Ranjit Anderson,Sharmila Dorbala,Peter Mollee","doi":"10.1182/blood.2024026386","DOIUrl":"https://doi.org/10.1182/blood.2024026386","url":null,"abstract":"Hematologists have a significant role in the diagnosis and management of light chain (AL) amyloidosis and are also frequently involved in diagnosing transthyretin (ATTR) and other rarer types of amyloidosis. Recent advances in diagnostic techniques and therapies are dramatically improving patient prognosis. Radionuclide imaging methods are emerging as a highly specific and non-invasive way to diagnose, quantify and monitor organ involvement representing a major advance in amyloidosis management.","PeriodicalId":9102,"journal":{"name":"Blood","volume":"74 1","pages":""},"PeriodicalIF":20.3,"publicationDate":"2025-07-15","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144640011","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 New Prognostic Index (CLIPI) for Advanced Cutaneous Lymphoma Enables Precise Patient Risk Stratification.","authors":"Julia J Scarisbrick,Pietro Quaglino,Sean J Whittaker,Martine Bagot,Emmanuella Guenova,Evangelia Papadavid,H Miles Prince,Jose Antonio Sanches,Denis Miyashiro,Octavio Servitje,Christiane Querfeld,Oleg E Akilov,Arvind Arumainathan,Luke Bennett,Maxime Battistella,Kim Benstead,Emilio Francesco Berti,Marie Beylot-Barry,Anne-Marie Busschots,Richard Andrew Cowan,Reinhard Dummer,Giles Dunnill,Maria Teresa Estrach,Felicity Evison,Abraham Ellahi Bashir,Larisa J Geskin,Alejandro Gru,Joan Guitart,Melba C Herrera,Emmilia Hodak,Steven M Horwitz,Constanze Jonak,Claus-Detlev Klemke,Robert Knobler,Pamela McKay,Marta Marschalkó,Cesare Massone,Rubeta Matin,Christina Mitteldorf,Roberto Andres Novoa,Pablo L Ortiz-Romero,Nicola Pimpinelli,Ramon M Pujol,Annmari Ranki,Liisa Vankeva,Kerri E Rieger,Rudolf Stadler,Franz Trautinger,Johanna Latzka,Maarten H Vermeer,Rachel Wachsmuth,Sophie Weatherhead,Ulrike Wehkamp,Marion Wobser,Youn H Kim","doi":"10.1182/blood.2025029628","DOIUrl":"https://doi.org/10.1182/blood.2025029628","url":null,"abstract":"Advanced mycosis fungoides (MF) and Sézary syndrome (SS) have a poor prognosis with overall survival <5 years. Studies have found the current clinical staging (IA-IVB) inadequate for risk stratification. Developing a prognostic index in MF/SS will identify patients with poor outcomes and may allow better management decisions and improved survival.PROCLIPI (Prospective Cutaneous Lymphoma International Prognostic Index) Study was launched in 2015 at 46 international expert MF/SS Centers, prospectively collecting pre-defined datasets in newly diagnosed MF/SS patients to determine a cutaneous lymphoma IPI (CLIPI).552 advanced stage MF/SS patients were recruited. The 5-year overall survival (OS) was IIB=50.0%, IIIA=64.8%, IIIB=43.9%, IVA1=50.8%, IVA2=25.9%, IVB=36.9%. Factors at diagnosis associated with a significantly worse survival were N3 status; p<0.001, age>60yrs; p<0.001, raised serum lactate dehydrogenase; p=0.005 and large-cell transformation in skin; p=0.006. Modelling these 4 independent risk-factors into a CLIPI found there was a statistically significant worse OS in high-versus low-risk p<0.001, high-versus intermediate-risk p=0.002 as well as intermediate-versus low-risk p=0.010. 5 Year OS were 63.3%, 44.7% and 18.3% in the low-, intermediate- and high-risk PROCLIPI cohort respectively.In advanced stage MF/SS there was a low 5-year survival rate and increasing stage was not associated with worsening survival. The use of CLIPI to stratify patients into low, intermediate, and high-risk prognostic groups has the potential to improve patient outcomes by helping guide optimal treatment selection. CPMS ID 17662 (PROCLIPI), RRK4970, ClinicalTrials.Gov ID: NCT02848274.","PeriodicalId":9102,"journal":{"name":"Blood","volume":"104 1","pages":""},"PeriodicalIF":20.3,"publicationDate":"2025-07-15","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144640085","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":"Factor IXa and Factor X Influence Factor VIIIa Stability and Inactivation Mechanisms In Vitro and In Vivo.","authors":"Johnathan J Morris,Nicole A Parsons,Amelia R Wilhelm,Robert J Davidson,Lauren K Olenick,Connor T Watson,Andrew R Vanden Heuvel,Lindsey A George","doi":"10.1182/blood.2024027705","DOIUrl":"https://doi.org/10.1182/blood.2024027705","url":null,"abstract":"Deficiency of (f)actor VIII causes hemophilia A and excess FVIII function increases venous thromboembolic risk. The phenotypic consequences of aberrant FVIII function underscore the importance of understanding mechanisms that downregulate (a)ctivated FVIII to inform disease pathology and therapeutic drug design. Spontaneous A2-domain dissociation and activated protein C (APC) proteolysis are established mechanisms of FVIIIa inactivation. However, we know very little about how FVIIIa binding interactions with FIXa and FX impact FVIIIa inactivation in vivo. Here we investigate this using recombinant FVIIIa variants to probe A2-domain dissociation (FVIIIa-D519V,E665V) and APC cleavage (FVIIIa-R336Q,R562Q) or both (FVIIIa-R336Q,R562Q/D519V,E665V) in biochemical assays and in HA mouse injury models. We found that FIXa binding to FVIIIa stabilized the A2 domain and increased the contribution of APC to FVIIIa inactivation. Additional studies using individual APC cleavage site variants (FVIIIa-R336Q and FVIIIa-R562Q) demonstrated that FIXa and FX can protect FVIIIa from APC cleavage at Arg562 and Arg336, respectively, in a manner that is incomplete in vivo. Data also demonstrate that APC inactivation of FVIIIa exceeds FVIII suggesting differential APC recognition of FVIIIa relative to FVIII. Hemostatic studies of FVIII variants with altered inactivation demonstrated that both A2-domain dissociation and APC cleavage contribute to in vivo FVIIIa regulation. Specifically, stabilizing the A2-domain, inhibiting APC cleavage, or both improved potency 2.4, 4.8, and >10-fold, respectively, over wild type FVIII in a mouse hemostatic assay. Data support that both mechanisms of FVIIIa inactivation and FIXa interactions could be leveraged to enhance FVIII function for therapeutic benefit.","PeriodicalId":9102,"journal":{"name":"Blood","volume":"8 1","pages":""},"PeriodicalIF":20.3,"publicationDate":"2025-07-15","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144640086","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":"How I Treat Pediatric Pulmonary Embolism.","authors":"Ayesha Zia,Neil A Goldenberg,Madhvi Rajpurkar","doi":"10.1182/blood.2024026599","DOIUrl":"https://doi.org/10.1182/blood.2024026599","url":null,"abstract":"Venous thromboembolism (VTE) affects approximately 1 in 200 hospitalized children. The diagnosis of pulmonary embolism (PE), the most severe clinical presentation of VTE, has increased dramatically by ~200% over the past two decades, disproportionately affecting adolescents, and is associated with adverse long-term post-PE sequelae. Nevertheless, the management of pediatric PE remains highly variable. This review focuses on significant advances in pediatric PE with a focus on published studies within the past decade. Using a representative case, we: (1) summarize existing risk prediction tools for acute pediatric PE and a shift in clinical practice in the management of acute PE with the implementation of pediatric PE Response Teams and multidisciplinary decision-making for severe pediatric PE; (2) describe recently completed clinical trials of anticoagulation in children and adolescents and ongoing work to elucidate the appropriate duration of therapy for children and adolescents with PE; (3) review advances in understanding post-PE syndrome and the need for continued refinement of evaluation tools and management approaches. Many unanswered questions remain despite the significant advances in pediatric thrombosis over the past decade.","PeriodicalId":9102,"journal":{"name":"Blood","volume":"7 1","pages":""},"PeriodicalIF":20.3,"publicationDate":"2025-07-11","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144603965","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":"Profiling the spatial architecture of multiple myeloma in human bone marrow trephine biopsy specimens with spatial transcriptomics.","authors":"Raymond K H Yip,Jeremy Er,Lei Qin,Quoc Hoang Nguyen,Allan Motyer,Joel S Rimes,Amanda Light,Ruvimbo D Mishi,Ling Ling,Casey J A Anttila,Ellen Tsui,Daniela Amann-Zalcenstein,Mark R Dowling,Kelly L Rogers,Rory Bowden,Yunshun Chen,Simon J Harrison,Edwin D Hawkins","doi":"10.1182/blood.2025028896","DOIUrl":"https://doi.org/10.1182/blood.2025028896","url":null,"abstract":"The bone marrow microenvironment is intimately linked to the biology that underpins the development and progression of multiple myeloma. However, the complex cellular and molecular features that form bone marrow niches are poorly defined. Here, we used subcellular spatial transcriptomics to profile the expression of 5,001 genes in human bone marrow in the context of multiple myeloma. Using this approach, we explored the plasma cell and stroma ecosystem in bone marrow trephines from 21 individuals, including 7 with pre-malignant disease and 10 with newly diagnosed multiple myeloma. Using spatial transcriptomics in conjunction with an optimised trephine biobanking methodology, we could resolve major components of the human bone marrow microenvironment and reliably characterise distinct plasma cell populations in samples from healthy, pre-malignant disease and active myeloma. When plasma cells were visualised in the context of location, we detected spatially restricted subpopulations of plasma cells in five of ten newly diagnosed myeloma trephines. Surprisingly, the composition of haematopoietic and stromal microenvironments varied significantly between newly diagnosed myeloma trephines. Furthermore, these differences in microenvironments were also observed within trephines that had spatially restricted plasma cell subpopulations. Thus, these data are not consistent with the hypothesis that a universal bone marrow microenvironment supports the expansion of malignant plasma cells in myeloma. Instead, we propose that myeloma subpopulations form distinct microenvironments and can vary between both patients and spatial location.","PeriodicalId":9102,"journal":{"name":"Blood","volume":"138 1","pages":""},"PeriodicalIF":20.3,"publicationDate":"2025-07-11","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144603912","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":"Reshaping the TME to enhance checkpoint blockade in ENKTL.","authors":"Annika Dechow,Till Braun","doi":"10.1182/blood.2025028917","DOIUrl":"https://doi.org/10.1182/blood.2025028917","url":null,"abstract":"","PeriodicalId":9102,"journal":{"name":"Blood","volume":"68 1","pages":"129-131"},"PeriodicalIF":20.3,"publicationDate":"2025-07-10","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144594037","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}