Blood Cancer Journal最新文献

{"title":"A clinico-genomic prognostic model for primary myelodysplastic neoplasm in Asia.","authors":"Harinder Gill,Rita Yim,Paul Lee,Xavier Cheng-Hong Tsai,Vivian W K Li,Garret M K Leung,Melissa Ooi,Tsz-Shing Hui,Radha Raghupathy,Lynn Chin,Lester Au,Qi Zhang,Tony K Y Wu,Carmen Y Y Lee,Wee-Joo Chng,Hwei-Fang Tien,Hsin-An Hou,Yok-Lam Kwong","doi":"10.1038/s41408-025-01339-0","DOIUrl":"https://doi.org/10.1038/s41408-025-01339-0","url":null,"abstract":"A personalized prognostic model that takes into account the unique molecular features of primary myelodysplastic neoplasm (MDS) in Asia patients is lacking. Diagnostic clinicopathologic features, cytogenetic changes, and gene mutations of ethnic Asian patients with primary MDS were analyzed. Variables were evaluated for associations with overall survival (OS), leukemia-free survival (LFS), and time to progression to secondary AML (TTP-sAML). Prognostic scores were built as a weighted sum of prognostic variables for each patient. The cohort comprised 1225 patients, with at least one gene mutation identified in 1177 patients (96%). Genomic factors associated with inferior outcomes included monosomy 7, del(5q), and GNAS and TP53 mutations for OS; trisomy 19, del(5q), monosomy 7, and GNAS, PTPN11 and TP53 mutations for LFS; and i(17q), del(5q), and NPM1, NRAS, GNAS, IDH2, SF3B1 and RUNX1 mutations for TTP-sAML. The Asian Prognostic Scoring System (APSS) was determined, stratifying patients into six prognostic risk categories. The APSS, compared with the International Prognostic Scoring System molecular (IPSS-M), showed superior concordance indices (C-indices) for OS (0.73 versus 0.57), LFS (0.72 versus 0.59), and TTP-sAML (0.75 versus 0.65) for this Asian cohort. In conclusion, the APSS enhanced prognostication of primary MDS in Asia.","PeriodicalId":8989,"journal":{"name":"Blood Cancer Journal","volume":"45 1","pages":"128"},"PeriodicalIF":12.8,"publicationDate":"2025-07-31","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144756077","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":"Activity of CAR-T cells and bispecific antibodies in multiple myeloma with extramedullary involvement","authors":"Maximilian J. Steinhardt, Christoph Schaefers, Lisa B. Leypoldt, Igor-Wolfgang Blau, Marie Harzer, Xiang Zhou, Christine Riedhammer, Abdulaziz Kamili, Ricardo Kosch, Laura S. Topp, Isabel Molwitz, Nils-Ole Gross-Fengels, Yasmin Fede Melzer, Jule Artzenroth, Maximilian Al-Bazaz, Winfried Alsdorf, Max S. Topp, Johannes Duell, Julia Mersi, Johannes Waldschmidt, Carsten Bokemeyer, Hermann Einsele, K. Martin Kortüm, Katja Weisel, Leo Rasche","doi":"10.1038/s41408-025-01330-9","DOIUrl":"https://doi.org/10.1038/s41408-025-01330-9","url":null,"abstract":"<p>Extramedullary multiple myeloma (EMD) is associated with low response rates, short progression-free survival, and poor prognosis. CAR T cells and bispecific antibodies (bsABs) have shown efficacy in relapsed myeloma, but it remains uncertain whether one T cell redirection strategy should be preferred. We retrospectively analyzed 80 patients with EMD not adjacent to the bone treated with ide-cel, cilta-cel, teclistamab, or talquetamab at three academic centers in Germany. All patients were heavily pretreated, and a high-risk cytogenetic profile was prevalent in &gt;41% of patients. All cohorts had a median of 5 to 7 prior lines of therapy. The vast majority of patients receiving cilta-cel, ide-cel, or teclistamab were BCMA-naive ( &gt;88%). Response rates after CAR T cell infusion were significantly higher (100% with cilta-cel, 82% with ide-cel) than with bsABs (29% for talquetamab, 36% for teclistamab). Complete resolution of EMD was more frequent after CAR T cell therapies (50% and 41%) than after bsABs (16% and 14%). With a median follow-up of 12.2 months, median (m)PFS was not reached in patients that had received cilta-cel; mPFS was 7.3 months after ide-cel and significantly longer for both CAR T products compared to talquetamab or teclistamab (mPFS 4.0 and 2.6 months). Effective debulking therapy prolonged remissions after CAR T cell infusion compared to no debulking or no response to debulking. Visceral and soft tissue manifestations responded significantly less frequently than EMD in other locations. With significantly higher response rates, deeper remissions, and longer mPFS, our retrospective data suggest CAR T cells may provide a meaningful benefit in EMD.</p>","PeriodicalId":8989,"journal":{"name":"Blood Cancer Journal","volume":"25 1","pages":""},"PeriodicalIF":12.8,"publicationDate":"2025-07-30","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144737174","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 SOX11:SMARCA4 complex is a driver of oncogenic transcriptional programs in mantle cell lymphoma","authors":"Anna De Bolòs, Maria Carreras-Caballé, Marta Sureda-Gómez, Marta-Leonor Rodríguez, Stella Charalampopoulou, Robert Albero, Alba Maiques-Diaz, Heribert Playa-Albinyana, Guillem Clot, Cristina López, Dolors Colomer, José I Martin-Subero, Elías Campo, David Reverter, Josep Villanueva, Virginia Amador","doi":"10.1038/s41408-025-01333-6","DOIUrl":"https://doi.org/10.1038/s41408-025-01333-6","url":null,"abstract":"<p>Mantle cell lymphoma (MCL) is considered one of the most aggressive B-cell lymphoid neoplasms. The transcription factor SOX11 is aberrantly expressed in conventional aggressive MCL, while it is not or weakly expressed in the leukemic non-nodal MCL subtype with a predominantly indolent clinical evolution. SOX11 is a key driver of MCL through the regulation of several oncogenic mechanisms, suggesting that it may be interacting with different protein complexes to exert its multiple actions. Using proteomic strategies, we characterized the SOX11-interactome and validated its physical interaction with SMARCA4, the catalytic subunit of the SWI/SNF chromatin-remodeling complex. <i>SMARCA4</i> expression is directly regulated by SOX11, and its upregulation significantly associates with worse outcomes of patients. Integration of global DNA-binding and transcriptomic profiles revealed that SOX11 and SMARCA4 share binding sites enriched in open chromatin and active promoters and regulate common key oncogenic pathways crucial for MCL progression and aggressiveness. The SMARCA4-specific PROTAC-degrader AU-15330 significantly reduced SOX11 binding to specific regulatory regions and diminished the activation of BCR-, NIK-, and BCL2-signaling pathways. Moreover, SMARCA4 degradation significantly reduced proliferation and induced apoptosis of SOX11-positive MCL cells, highlighting AU-15330 as a promising therapeutic approach for patients who may relapse from current target therapies in MCL.</p><figure></figure>","PeriodicalId":8989,"journal":{"name":"Blood Cancer Journal","volume":"717 1","pages":""},"PeriodicalIF":12.8,"publicationDate":"2025-07-30","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144737179","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":"Reconstructing CML guidelines for first line treatment from two different points of view","authors":"Carlo Gambacorti-Passerini, Giulia Bassi, Stefano Bonfanti, Francesca Duca, Rocco Giovanni Piazza, Elisabetta Lattuada, Alberto Rapella, Elsa Masedu","doi":"10.1038/s41408-025-01331-8","DOIUrl":"https://doi.org/10.1038/s41408-025-01331-8","url":null,"abstract":"","PeriodicalId":8989,"journal":{"name":"Blood Cancer Journal","volume":"52 1","pages":""},"PeriodicalIF":12.8,"publicationDate":"2025-07-24","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144694028","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":"Venetoclax plus arsenic and all-trans retinoic acid in patients with relapsed/refractory acute promyelocytic leukemia","authors":"Bingqian Jiang, Hongyan Tong, Min Yang, Huafeng Wang, Shanshan Suo, Chenying Li, Liping Mao, Xingnong Ye, Haitao Meng, Wenjuan Yu, Jie Jin, Yinjun Lou","doi":"10.1038/s41408-025-01336-3","DOIUrl":"https://doi.org/10.1038/s41408-025-01336-3","url":null,"abstract":"","PeriodicalId":8989,"journal":{"name":"Blood Cancer Journal","volume":"52 1","pages":""},"PeriodicalIF":12.8,"publicationDate":"2025-07-21","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144677537","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":"Prognostic gene expression and microRNA profiling signatures and genetic alterations in primary testicular diffuse large B-cell lymphoma","authors":"Wenyu Shi, Zijun Y. Xu-Monette, Youchao Jia, Alexandar Tzankov, Heounjeong Go, Ling Li, Maurilio Ponzoni, Yafei Wang, Qiongli Zhai, Anamarija M. Perry, Shi Wang, Xiaoxiao Wang, April Chiu, Mina L. Xu, Carlo Visco, Karen Dybkaer, Henry Withers, Mark Long, Alyssa F. Yuan, Yi Miao, Everardo Macias, Dehong Wu, Wen Shuai, Bangchen Wang, Jianyong Li, Govind Bhagat, Youli Zu, Zenggang Pan, William Choi, Santiago Montes-Moreno, Weina Chen, J. Han van Krieken, Michael B. Møller, Xinfang Yu, Benjamin M. Parsons, Shanxiang Zhang, Eric D. Hsi, Aliyah R. Sohani, Jeremy S. Abramson, Andrés J. M. Ferreri, Bing Xu, Yong Li, Ken H. Young","doi":"10.1038/s41408-025-01323-8","DOIUrl":"https://doi.org/10.1038/s41408-025-01323-8","url":null,"abstract":"<p>Primary testicular (PT) diffuse large B-cell lymphoma (DLBCL) is a rare and aggressive lymphoma with distinct clinical and molecular characteristics. To identify prognostic biomarkers in PT-DLBCL, in this study we analyzed DNA and RNA samples of PT-DLBCL tumors from 206 patients using next-generation sequencing platforms and assays. Genetic alteration analysis found that multiple chromosomal copy number variations (CNVs), <i>TP53</i> transcript mutations with high variant allele frequency, and MCD subtype had significantly adverse prognostic effects, whereas elevated microsatellite instability had a significantly favorable prognostic effect in PT-DLBCL. Targeted RNA-seq analysis identified a PTL gene expression signature by comparing PT-DLBCL with systemic DLBCL and revealed the heterogeneity within PT-DLBCL by unsupervised clustering, which classified PT-DLBCLs into a testicular lymphoma tumor (TLT) subtype and a microenvironment (ME) subtype. The TLT subtype featured upregulation of genes functioning in DNA damage response, DNA repair, chromatin remodeling, the cell cycle, and the nucleus, and was associated with significantly poorer patient survival and higher frequencies of <i>MYD88</i> mutations, multiple CNVs, MCD subtype, bulk tumors, and elderly patients in the PT-DLBCL cohort. In contrast, the ME subtype distinctively featured upregulation of various signaling pathway genes involving the tumor microenvironment and downregulation of <i>BTK</i> and B-cell receptor signaling genes, and was associated with significantly better clinical outcome than the TLT subtype of PT-DLBCL independently of CNVs, MCD and <i>MYD88</i> mutation and than systemic DLBCL. Moreover, genomic microRNA profiling analysis identified a PTL microRNA signature significantly differentially expressed between PT-DLBCL and systemic DLBCL patients and within the PT-DLBCL cohort, and PT-DLBCL patients with higher expression of 16 PTL microRNAs (14 are testicular tissue-specific) had significantly better survival. In summary, this study revealed the molecular heterogeneity in genetic abnormalities and expression profiles of coding genes and microRNAs within the PT-DLBCL entity, and identified significant prognostic biomarkers and PTL signatures.</p><figure></figure>","PeriodicalId":8989,"journal":{"name":"Blood Cancer Journal","volume":"5 1","pages":""},"PeriodicalIF":12.8,"publicationDate":"2025-07-17","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144652216","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":"Whole body MRI by MY-RADS for imaging response assessment in multiple myeloma","authors":"Christina Messiou, Nuria Porta, Dow-Mu Koh, Angela Riddell, Katherine Downey, James Croft, Leonora Conneely, Georgina Hopkinson, Alina Dragan, Tommy Brown, Simon Stern, Betty Cheung, Charalampia Kyriakou, Pawel Kaczmarek, Kevin Boyd, Charlotte Pawlyn, Jessica Winfield, Martin F. Kaiser","doi":"10.1038/s41408-025-01327-4","DOIUrl":"https://doi.org/10.1038/s41408-025-01327-4","url":null,"abstract":"<p>Minimal residual disease (MRD) testing has underpinned the evaluation and expansion of therapeutic options for patients with multiple myeloma (MM). Imaging is essential for evaluating residual disease status, overcoming sampling errors inherent with other MRD modalities. The accuracy of whole-body MRI (WB-MRI) has led to its incorporation into MM diagnostic imaging guidelines. We report here on the prospective iTIMM trial (image-guided theranostics in MM; NCT02403102), designed to evaluate imaging residual disease using contemporary, functional WB-MRI as per MY-RADS protocol. In iTIMM, 70 MM patients planned to undergo autologous stem cell transplantation ASCT in newly diagnosed MM or at first relapse, underwent WB-MRI before start of induction and at day 100 post-ASCT. Patients with residual disease post-ASCT (RAC2 or higher) had shorter progression-free survival (median 24 months, 95% confidence interval (CI): 19–41 vs. 42 months, 95% CI: 37–not evaluable (NE), log-rank <i>p</i> = 0.013; hazard ratio (HR) 2.09 (95% CI: 1.15–3.78) and overall survival (median 47 months, 95% CI: 30.9–NE vs. NE (95% CI: NE–NE), <i>p</i> = 0.002, HR = 5.45 (95% CI: 1.67–17.87) than those without (RAC1). Imaging response also refined the prognostic association of bone marrow MRD and serological response. Our results support WB-MRI implementation for evaluation of residual disease alongside conventional laboratory-based assessments.</p>","PeriodicalId":8989,"journal":{"name":"Blood Cancer Journal","volume":"46 1","pages":""},"PeriodicalIF":12.8,"publicationDate":"2025-07-17","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144645588","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":"Age-dependent phenotypic and molecular evolution of pediatric MDS arising from GATA2 deficiency","authors":"Lili Kotmayer, Emilia J. Kozyra, Guolian Kang, Brigitte Strahm, Ayami Yoshimi, Sushree S. Sahoo, Victor B. Pastor, Enrico Attardi, Rebecca Voss, Luca Vinci, Max Kaiser, Michael N. Dworzak, Barbara De Moerloose, Martina Sukova, Jan Starý, Henrik Hasle, Kirsi Jahnukainen, Sophia Polychronopoulou, Krisztián Kállay, Owen P. Smith, Andrea Malone, Shlomit Barzilai Birenboim, Riccardo Masetti, Jochen Buechner, Marek Ussowicz, Paula Kjöllerström, Ivana Bodova, Marko Kavcic, Albert Català, Dominik Turkiewicz, Markus Schmugge, Valerie de Haas, Victoria I. Okhomina, Cristian Sotomayor, Paula Catalán, Claudia Wehr, Ulrich Salzer, Ulrich Germing, Norbert Gattermann, Csaba Bödör, Nathan Gray, Sara Lewis, Akiko Shimamura, Alessandra Giorgetti, Miriam Erlacher, Charlotte M. Niemeyer, Marcin W. Wlodarski","doi":"10.1038/s41408-025-01309-6","DOIUrl":"https://doi.org/10.1038/s41408-025-01309-6","url":null,"abstract":"<p>GATA2 deficiency is an autosomal dominant transcriptopathy disorder with high risk for myelodysplastic syndrome (MDS). To elucidate genotype-phenotype associations and identify new genetic risk factors for MDS, we analyzed 218 individuals with germline heterozygous <i>GATA2</i> variants. We observed striking age-dependent incidence patterns in GATA2-related MDS (GATA2-MDS), with MDS being absent in infants, rare before age 6 years, and steeply increasing in older children. Among 108 distinct <i>GATA2</i> variants (67 novel), null mutations conferred a 1.7-fold increased risk for MDS, had earlier MDS onset compared to other variants (12.2 vs. 14.6 years, <i>p</i> = 0.009) and were associated with lymphedema and deafness. In contrast, intron 4 variants exhibited reduced penetrance and lower risk for MDS development. Analysis of the somatic landscape revealed unique patterns of clonal hematopoiesis. <i>SETBP1</i> mutations occurred exclusively in patients with monosomy 7 and their frequency decreased with age. Conversely, the frequency of <i>STAG2</i> mutations and trisomy 8 increased with age and appeared protective against early development of advanced MDS. Overall, the majority (73.9%) of mutation-positive cases harbored monosomy 7, suggesting it serves as a major driver in malignant progression. Our findings provide evidence for age-appropriate surveillance, and a foundation for genotype-driven risk stratification in GATA2 deficiency.</p>","PeriodicalId":8989,"journal":{"name":"Blood Cancer Journal","volume":"12 1","pages":""},"PeriodicalIF":12.8,"publicationDate":"2025-07-15","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144629884","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":"Integrated genomics with refined cell-of-origin subtyping distinguishes subtype-specific mechanisms of treatment resistance and relapse in diffuse large B-cell lymphoma","authors":"Janek S. Walker, Kerstin Wenzl, Joseph P. Novak, Matthew E. Stokes, Melissa A. Hopper, Abigail R. Dropik, Miranda S. Siminski, Allison M. Bock, Vivekananda Sarangi, Maria Ortiz, Nicholas Stong, C. Chris Huang, Matthew J. Maurer, Brian K. Link, Stephen M. Ansell, Thomas M. Habermann, Thomas E. Witzig, Rebecca L. King, Grzegorz Nowakowski, James R. Cerhan, Anita K. Gandhi, Anne J. Novak","doi":"10.1038/s41408-025-01326-5","DOIUrl":"https://doi.org/10.1038/s41408-025-01326-5","url":null,"abstract":"<p>Up to 40% of diffuse large B-cell lymphoma (DLBCL) patients do not experience a durable response to frontline immunochemotherapy, and prospective identification of high-risk cases that may benefit from personalized therapeutic management remains an unmet need. Molecular phenotyping techniques have established a landscape of genomic variants in diagnostic DLBCL; however, these have not yet been applied in large-scale studies of relapsed/refractory DLBCL, resulting in incomplete characterization of mechanisms driving tumor progression and treatment resistance. Here, we performed an integrated multiomic analysis on 228 relapsed/refractory DLBCL samples, including 24 with serial biopsies. Refined cell-of-origin subtyping identified patients harboring GCB and DZsig+ relapsed/refractory tumors in cases with primary refractory disease with remarkably poor outcomes, and comparative analysis of genomic features between relapsed and diagnostic samples identified subtype-specific mechanisms of therapeutic resistance driven by frequent alteration to <i>MYC</i>, <i>BCL2</i>, <i>BCL6</i>, and <i>TP53</i> among additional strong lymphoma driver genes. Tumor evolution dynamics suggest innate mechanisms of chemoresistance are present in many DLBCL tumors at diagnosis, and that relapsed/refractory tumors are primarily comprised of a homogenous clonal expansion with reduced tumor microenvironment activity. Adaptation of personalized therapeutic strategies targeting DLBCL subtype-specific resistance mechanisms should be considered to benefit these high-risk populations.</p><figure></figure>","PeriodicalId":8989,"journal":{"name":"Blood Cancer Journal","volume":"37 1","pages":""},"PeriodicalIF":12.8,"publicationDate":"2025-07-12","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144612872","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":"Fine particulate matter exposure is linked to worse myeloma outcomes in a diverse urban cohort","authors":"Michael Wysota, Kith Pradhan, Sarah Jacobs, Joel Rosiene, Charles Hall, George Downward, Yocheved Halberstam, Nishi Shah, Dean Hosgood, Aditi Shastri","doi":"10.1038/s41408-025-01301-0","DOIUrl":"https://doi.org/10.1038/s41408-025-01301-0","url":null,"abstract":"","PeriodicalId":8989,"journal":{"name":"Blood Cancer Journal","volume":"31 1","pages":""},"PeriodicalIF":12.8,"publicationDate":"2025-07-07","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144568323","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}