Leukemia最新文献

{"title":"Measurable residual disease is not a universally reliable surrogate for progression-free survival in clinical trials of new chronic lymphocytic leukemia therapies.","authors":"Yun Wang, Chunhua Li, Robert Peter Gale, Qi Liang, Neil E Kay, Qianqian Huang, Yiling Song, Weida Wang, Yang Liang","doi":"10.1038/s41375-026-02970-x","DOIUrl":"https://doi.org/10.1038/s41375-026-02970-x","url":null,"abstract":"<p><p>Several recent trials of new chronic lymphocytic leukemia (CLL) therapies used results of measurable residual disease (MRD)-testing as a primary endpoint assuming it is an accurate surrogate for progression-free survival (PFS) which is, itself, a surrogate endpoint for survival. But whether MRD-testing results accurately correlates with PFS following Bruton tyrosine kinase-inhibitor (BTK-i) therapy with or without venetoclax or for fixed duration therapy regimens is controversial. We searched PubMed, Web of Science, Embase, and Cochrane Library up to February 8, 2025, identifying 43 trials involving 9628 subjects to assess MRD's accuracy in predicting PFS. At the individual-level subjects with detectable MRD (dMRD) had a significantly higher risk of progression or death than those with undetectable MRD (uMRD; Hazard Ratio [HR] = 3.67; 95% Credibility Interval [CrI] 3.34, 4.03; P < 0.01). In contrast, MRD-testing results and PFS were weak at the trial-level (Spearman rho [R] = -0.33; Determination Coefficients [R² ] = 0.06), especially for BTKi- therapy (R = -0.05, R² = 0.03) and venetoclax-based therapies (R = -0.28, R² = 0.02). Correlations were stronger for therapies involving drugs such as chemoimmunotherapy and/or monoclonal antibodies, where MRD tests of bone marrow (R = -0.94; R² = 0.86) were more accurately predicted PFS than blood. In sensitivity analyses stratified by treatment approach we found a correlation of treatment-effect in fixed-duration therapy approaching the pre-specified validity threshold (R = -0.80 [-0.93, -0.53]; R² = 0.43, P < 0.01). Our data indicate the accuracy of MRD-testing results to surrogate PFS is context-dependent, influenced by treatment approach, therapy type, and the sampling source, and should be interpreted cautiously when informing clinical or regulatory decisions.</p>","PeriodicalId":18109,"journal":{"name":"Leukemia","volume":" ","pages":""},"PeriodicalIF":13.4,"publicationDate":"2026-04-30","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"147816612","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":"Multi-omics analysis of pediatric minimally differentiated acute myeloid leukemia reveals RUNX1-driven stemness and chemoresistance.","authors":"Tatsuya Kamitori, Satoshi Saida, Kazuki Mitani, Shinichi Tsujimoto, Hiroaki Goto, Hirofumi Shibata, Ryo Akazawa, Kiyotaka Isobe, Hiroo Ueno, Nobuyuki Kakiuchi, Akiko M Saito, Mitsuteru Hiwatari, Ko Kudo, Shinsuke Hirabayashi, Kohei Fukuoka, Katsuyoshi Koh, Takashi Taga, Hirohito Kubota, Itaru Kato, Katsutsugu Umeda, Souichi Adachi, Tomoko Kawai, Daisuke Tomizawa, Junji Ikeda, Norio Shiba, Yasuhide Hayashi, Seishi Ogawa, Junko Takita","doi":"10.1038/s41375-026-02967-6","DOIUrl":"https://doi.org/10.1038/s41375-026-02967-6","url":null,"abstract":"<p><p>Minimally differentiated acute myeloid leukemia (AML-M0) is a rare and therapeutically challenging subgroup of AML characterized by immature hematopoietic stem cell-like features. To uncover the molecular basis, we conducted a comprehensive multi-omics analysis of 23 pediatric AML-M0 cases and compared them with 1483 leukemia samples. AML-M0 formed a characteristic group that exhibited global DNA hypermethylation and transcriptional suppression, particularly downregulation of genes related to oxidative phosphorylation and ribosome assembly compared to non-M0 AML. Genomic profiling revealed frequent loss-of-function alterations in RUNX1 (26%) and ETV6 (22%), along with activating mutations in signaling pathways (83%), such as RAS, FLT3, and JAK. Notably, RUNX1 alterations were significantly associated with a poor prognosis. Functional analyses using a CRISPR/Cas9-mediated RUNX1 knockout in a pediatric AML-M0 cell line showed stem cell-like transcriptional features and reduced expression of genes related to oxidative phosphorylation and ribosomal pathways. RUNX1 disruption was also associated with reduced in vitro sensitivity to multiple drugs, including cytarabine and anthracyclines. Our study provides the most comprehensive molecular characterization of pediatric AML-M0 to date and identifies RUNX1 alterations as important biological and clinical determinants. These insights highlight the potential strategies for precision therapy, including hypomethylating agents, signaling inhibitors, and metabolic targeting, to improve outcomes.</p>","PeriodicalId":18109,"journal":{"name":"Leukemia","volume":" ","pages":""},"PeriodicalIF":13.4,"publicationDate":"2026-04-29","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"147775457","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":"Chronic myelomonocytic leukemia beyond the marrow: biology, patterns, and management of extramedullary disease.","authors":"Manal Ahmidouch,Priya Deshpande,Christian Salib,Patrick Brunner,Patricia Heller,Dalia Abdel Azim,Somedeb Ball,Douglas Tremblay","doi":"10.1038/s41375-026-02966-7","DOIUrl":"https://doi.org/10.1038/s41375-026-02966-7","url":null,"abstract":"Chronic myelomonocytic leukemia (CMML) is an MDS/MPN overlap neoplasm defined by monocytosis, clonal hematopoiesis, and marrow dysplasia, with outcomes ranging from indolent cytopenic disease to aggressive proliferative phenotypes with early AML transformation. Extramedullary disease (EMD) refers to clonal myelomonocytic infiltration outside the bone marrow and is an underrecognized, consequential manifestation that can dominate presentation, drive morbidity, and identify adverse disease biology. While hepatosplenic involvement, often reflecting extramedullary hematopoiesis, is common, biopsy proven non-hepatosplenic EMD occurs in a subset of patients, 10-15 percent, and most frequently involves skin, lymph nodes, serosal fluids, and soft tissue, with visceral sites including lung, kidney, and central nervous system. Importantly, EMD is enriched in proliferative and higher grade CMML and is associated with inferior outcomes, including shorter overall survival and increased AML transformation, with poor prognosis after EMD onset. Biologically, EMD appears linked to mutation-driven proliferative signaling, enrichment of RAS MAPK pathway alterations, co-occurring with adverse epigenetic lesions such as ASXL1, together with cytokine-mediated inflammation and dysregulated trafficking and retention programs that facilitate tissue homing and persistence. Because EMD frequently mimics infection, autoimmune and inflammatory syndromes common in CMML, or second malignancy, diagnosis requires an integrated strategy incorporating cross sectional imaging, PET-CT to localize and prioritize biopsy targets, and tissue confirmation with immunophenotyping including CD68, CD163, and lysozyme and selective molecular profiling to establish clonality. Management is primarily systemic, with hypomethylating agents as the backbone, cytoreduction for proliferative disease, local radiotherapy for symptomatic lesions, and early consideration of allogeneic transplantation in eligible high risk or refractory cases. This review synthesizes current evidence on the epidemiology, biology, diagnostic approach, prognostic implications, and treatment of EMD in CMML and highlights the need for standardized definitions and prospective, genomics-informed studies to improve detection and outcomes.","PeriodicalId":18109,"journal":{"name":"Leukemia","volume":"26 1","pages":""},"PeriodicalIF":11.4,"publicationDate":"2026-04-27","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"147753151","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":"Development and validation of the predictive aplastic score system (PASS): a simplified tool to diagnose acquired aplastic anemia in adults","authors":"Gabriel Aleixo, HeeJin Cheon, Jiayin Zheng, Stephanie Soewito, Jimmy Lee, Eléonore Kaphan, Neha Kalakuntla, Wei-Ying Jen, Sumasri Kotha, Alex Rupsee, Mia Djulbegovic, Jairo A. Matthews, Tapan M. Kadia, Timothy S. Olson, Régis Peffault de Latour, Flore Sicre De Fontbrune, Taha Bat, Courtney D. DiNardo, Daria V. Babushok","doi":"10.1038/s41375-026-02924-3","DOIUrl":"https://doi.org/10.1038/s41375-026-02924-3","url":null,"abstract":"Acquired aplastic anemia (AA) can present similarly to inherited bone marrow failure syndromes (IBMFS) but treatment differs. AA diagnosis relies on excluding IBMFS; however, genetic testing is not always available, may delay care or be inconclusive. We developed the Predictive Aplastic Score System (PASS), a clinical tool using readily available data to distinguish AA from IBMFS in adults. The training cohort included 212 adults (162 AA, 50 IBMFS). Compared to IBMFS, AA patients were older and more likely to have acute-onset, severe cytopenias. Using logistic regression with LASSO, we selected seven clinical variables for model inclusion: severity, acuity, age, IBMFS red flags, AA-associated conditions, AA-associated somatic changes, and telomere lengths. The model achieved AUC of 0.990 (95% CI: 0.982–0.999), with 100% positive predictive value (PPV) for AA for scores ≥30. 86.8% of patients with scores <0 had IBMFS. We validated PASS in 716 patients from four external cohorts with AUC of 0.977 (95% CI: 0.968–0.987). Threshold analysis confirmed 100% PPV for scores ≥30, rapidly diagnosing 80% of AA cases. PASS is a practical and accurate clinical tool that can rapidly distinguish AA from IBMFS for most adult patients. To promote clinical adoption, we developed an open-access web calculator (https://pennmedicine.shinyapps.io/passcalc/).","PeriodicalId":18109,"journal":{"name":"Leukemia","volume":"32 1","pages":""},"PeriodicalIF":11.4,"publicationDate":"2026-04-27","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"147751792","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 small proportion of CD8 T cells expand robustly when stimulated with BCMAxCD3 bispecific T-cell engagers in vitro","authors":"Kumi Shibata, Kazuhito Tsutsumi, Hiraku Murakami, Emiko Mizuta, Shunya Ikeda, Yosuke Kogue, Mizuki Kano, Kazuhiro Sanda, Yuto Maehara, Hiroki Akamine, Ryuhei Kawamoto, Mayuko Noguchi, Makiko Suga, Shuhei Kida, Yuta Yamaguchi, Yo Mizutani, Hisashi Kato, Yasutaka Ueda, Jiro Fujita, Shinsuke Kusakabe, Hidenori Kasahara, Akihisa Hino, Daisuke Motooka, Daisuke Okuzaki, Tomoaki Ueda, Kentaro Fukushima, Michiko Ichii, Naoki Hosen","doi":"10.1038/s41375-026-02969-4","DOIUrl":"https://doi.org/10.1038/s41375-026-02969-4","url":null,"abstract":"","PeriodicalId":18109,"journal":{"name":"Leukemia","volume":"56 1","pages":""},"PeriodicalIF":11.4,"publicationDate":"2026-04-27","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"147751772","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":"Blinatumomab in pediatric acute lymphoblastic leukemia: current and future use.","authors":"Nawachai Lertvivatpong,Hiroto Inaba","doi":"10.1038/s41375-026-02962-x","DOIUrl":"https://doi.org/10.1038/s41375-026-02962-x","url":null,"abstract":"Treatment outcomes for pediatric acute lymphoblastic leukemia (ALL) have improved considerably, with overall survival rates in high-income countries now exceeding 90% as a result of the introduction of risk-adapted chemotherapy and improved supportive care. Further improvement in the outcome of ALL requires new approaches, such as immunotherapy. Blinatumomab, a bispecific antibody to CD3 and CD19, is approved by the U.S. Food and Drug Administration for use in the consolidation phase of multi-agent chemotherapy for B-ALL in adults and children (aged ≥1 month). Randomized studies in pediatric patients with B-ALL in the relapsed/refractory and frontline settings have shown that blinatumomab, when added to chemotherapy or used to replace intensive chemotherapy, results in better outcomes and fewer adverse effects than are observed with conventional chemotherapy alone. Resistance to blinatumomab is associated with high ALL burden, CD19 loss/downregulation, and T-cell dysfunction, and its efficacy against extramedullary disease, especially in the central nervous system, is limited. In addition, the serum half-life of blinatumomab is short, necessitating continuous intravenous infusion, and it can cause distinct adverse effects such as cytokine release syndrome, immune effector cell-associated neurotoxicity syndrome, and hypogammaglobulinemia. Therefore, medical staff require training in administering blinatumomab and monitoring its adverse effects. The development of subcutaneous administration of blinatumomab will make its delivery easier. Whether it is feasible to reduce or eliminate conventional chemotherapy by combining blinatumomab, other forms of immunotherapy, and molecular targeting therapy to improve outcomes while reducing adverse effects requires further evaluation in the frontline setting. Furthermore, longitudinal monitoring is necessary to evaluate the as-yet-unknown long-term adverse effects. Lastly, the experience obtained with blinatumomab in high-income countries should be expanded to low-/middle-income countries, where most of the global population reside and where the outcomes of ALL are suboptimal.","PeriodicalId":18109,"journal":{"name":"Leukemia","volume":"61 1","pages":""},"PeriodicalIF":11.4,"publicationDate":"2026-04-27","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"147753152","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":"Prevalence and characterization of germline RAS pathway variants in children with chronic myeloid leukemia.","authors":"Tabita Ghete,Laura Gaschler,Manuela Krumbholz,Stephanie Sembill,Yvonne Lisa Behrens,Axel Karow,Matthias Wölfl,Franziska Auer,Julia Hauer,Maria Giulia Carta,Fulvia Ferrazzi,Stephan Hutter,Anselm H C Horn,Heinrich Sticht,Paul-Gerhardt Schlegel,Markus Metzler","doi":"10.1038/s41375-026-02952-z","DOIUrl":"https://doi.org/10.1038/s41375-026-02952-z","url":null,"abstract":"","PeriodicalId":18109,"journal":{"name":"Leukemia","volume":"23 1","pages":""},"PeriodicalIF":11.4,"publicationDate":"2026-04-24","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"147738977","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":"Hemophagocytic lymphohistiocytosis in HIV-related lymphomas: a multicentre retrospective cohort study","authors":"Pascal Migaud, Alessia Dalla Pria, Daniela Drauz, Niroshan Dayalan, Claudia AM Fulgenzi, Kai Hosmann, Alberto Giovanni Leone, Markus Müller, Hartmut Stocker, Adam Temple, Marcus Hentrich, Mark Bower","doi":"10.1038/s41375-026-02929-y","DOIUrl":"https://doi.org/10.1038/s41375-026-02929-y","url":null,"abstract":"","PeriodicalId":18109,"journal":{"name":"Leukemia","volume":"144 1","pages":""},"PeriodicalIF":11.4,"publicationDate":"2026-04-23","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"147734026","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":"ASC4OPT: asciminib treatment optimization study in patients with chronic myeloid leukemia in chronic phase previously treated with two or more tyrosine kinase inhibitors","authors":"Andreas Hochhaus, Philipp le Coutre, Dragana Milojkovic, Dennis Dong Hwan Kim, Soo Min Lim, Carolina Pavlovsky, Thanh Nguyen, Franck Emmanuel Nicolini, Beatriz Moiraghi, Sebastian Grosicki, Chi Dung Phu, Gabriel Etienne, Fernando Marco de Lucas, Rosa Maria Ayala Diaz, Massimo Breccia, Charles Chuah, Roberto Abi Rached, Himanshu Pokhriyal, Aswin IC, Peter Schuld, Virginia Pilipovic, Franz Alisch, Carla Maria Boquimpani","doi":"10.1038/s41375-026-02965-8","DOIUrl":"https://doi.org/10.1038/s41375-026-02965-8","url":null,"abstract":"The ASC4OPT non-comparative phase 3b study (NCT04948333) evaluates asciminib once daily (QD) or twice daily (BID) in chronic myeloid leukemia in chronic phase (CML-CP) treated with ≥2 tyrosine kinase inhibitors (TKIs). This study enrolled 169 patients not in major molecular response (MMR), with unsatisfactory response (intolerant, warning or failure) as defined by European LeukemiaNet (ELN) 2020 criteria. Patients intolerant to their most recent TKI and in MMR at baseline (n = 30) were also enrolled. The primary endpoint was the MMR rate at Week 48 for patients not in MMR at baseline. Results showed an overall MMR rate of 39.4% at Week 48 (40 mg BID, 43.4%; 80 mg QD, 35.4%) and 43.6% at Week 96 (40 mg BID, 45.8%; 80 mg QD, 41.5%) in patients not in MMR at baseline. Among 40 patients who had their asciminib dose escalated to 200 mg QD, 17.5% were in MMR at Week 96. Most patients in MMR at baseline remained in MMR at 48 and 96 weeks (93.3% and 86.7%, respectively). Safety for both dosing regimens was consistent with that of previous studies. Findings support asciminib as a potential standard of care for patients with CML-CP who have not responded optimally to prior TKI therapy.","PeriodicalId":18109,"journal":{"name":"Leukemia","volume":"24 1","pages":""},"PeriodicalIF":11.4,"publicationDate":"2026-04-23","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"147734043","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 spectrum of immunoglobulin heavy chain enhancer hijacking in chronic lymphocytic leukemia","authors":"Cosima Drewes, Cristina López, Nnamdi Okeke, Billy Jebaraj, Christoph Wiegreffe, Isabelle Kraus, Sina Hillebrecht, Amani Awada, Susanne Bens, Emil Chteinberg, Barbara Eichhorst, Sarah Datismann, Martin J. S. Dyer, Anja Fischer, Kirsten Fischer, Selina Glaser, Michael Hallek, Helene Kretzmer, Anja Mottok, Dominick Pfaff, Karoline Schnitzler, Jan P. Meier-Kolthoff, Matthias Schlesner, Christof Schneider, Stefan Britsch, Ole Ammerpohl, Stephan Stilgenbauer, Eugen Tausch, Reiner Siebert","doi":"10.1038/s41375-026-02902-9","DOIUrl":"https://doi.org/10.1038/s41375-026-02902-9","url":null,"abstract":"Activation of oncogenes by hijacking immunoglobulin gene loci (IG) enhancers via chromosomal translocation is a common pathogenetic mechanism in B-cell malignancies, affecting 5–10% of chronic lymphocytic leukemia (CLL). The oncogenic partners in many of these cases remain unidentified. Therefore, we conducted a comprehensive analysis of 144 CLL samples with IGH-translocation excluding IGH::BCL2, IGH::CCND1, IGH::BCL3 and IGH::MYC. By combining fluorescence in situ hybridization (FISH) with whole-genome, targeted sequencing, and RNA expression profiling, we identified 25 IG-translocation partners; 12 were previously unreported. Of 142 cases, 107 (75%) displayed an unmutated IGHV. Genetic profiling showed a heterogenous distribution of chromosomal aberrations and recurrently mutated genes across the groups. Of 41 informative cases, 32 (78%) exhibited breakpoints driven by aberrant class-switch recombination (CSR), with prominent involvement of IGHM (9/41) and IGHG3 (9/41). Three cases with unmutated IGHV carried a juxtaposition of the IGH locus 5’ to the intact NKX2.6 gene in chromosome 8p21.2 due to illegitimate VDJ recombination, associated with significant ectopic upregulation of NKX2.6 transcriptional expression (FDR < 0.001, logFC: 15). Similarly, METRNL, located at the telomere of chromosome 17q25, was identified as a translocation partner gene in four cases. Our findings expand the spectrum of the oncogenic translocation partners targeting IGH in CLL.","PeriodicalId":18109,"journal":{"name":"Leukemia","volume":"65 1","pages":""},"PeriodicalIF":11.4,"publicationDate":"2026-04-23","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"147734025","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}