Journal of Hematology & Oncology最新文献

{"title":"Outcomes of front-line tagraxofusp in patients with blastic plasmacytoid dendritic cell neoplasm (BPDCN) in a real-world scenario","authors":"Jan C. Schroeder,Philipp Faustmann,Snjezana Janjetovic,Anna Ossami Saidy,Hanna K. Zieger,Giuliano Filippini Velazquez,Thomas Melchardt,David Baden,Hristo Boyadzhiev,Tim Sauer,Christoph Schliemann,Jan-Henrik Mikesch,Niklas Gebauer,Susanne von Kroge,Paul J. Bröckelmann,Friederike Hildebrand,Veit Bücklein,Rebecca Wurm-Kuczera,Ulrich Keller,Thomas Pabst,Maher Hanoun,Claudia Lengerke,Evgenii Shumilov,Georg Lenz,Ulrike Bacher,Philipp Berning","doi":"10.1186/s13045-026-01848-w","DOIUrl":"https://doi.org/10.1186/s13045-026-01848-w","url":null,"abstract":"Abstract Tagraxofusp (TAG), a CD123-directed protein-drug conjugate, is approved in front-line and relapsed/refractory blastic plasmacytoid dendritic cell neoplasm (BPDCN). Multicenter real-world outcomes and the contribution of up-front consolidation post-TAG remain less defined. We retrospectively analyzed 32 patients with BPDCN treated with frontline TAG (2019–2024) across 13 tertiary centers, contextualized against a historical cohort treated before TAG availability ( n  = 40). Patients were elderly (median age 71.5 years) with advanced disease, including skin (93.8%), bone marrow (84.4%), and peripheral blood involvement (53.1%). The overall response rate to TAG was 82.1%, with complete responses in 60.7%. Capillary leak syndrome occurred in 53.1% (grade ≥ 3 in 47.1%), with no unexpected safety signals. With a median follow-up of 18.4 months, 2-year overall survival (OS) and progression-free survival were 40.5% and 30.4%. Nearly half of patients proceeded to allogeneic stem cell transplantation post-TAG, associated with improved survival consistent with the primary analysis and landmark-adjusted analyses (HR 0.25 [0.06–1.14]; p  = 0.073). Propensity score–matched comparison with the Non-TAG cohort showed comparable 2-year OS (59.4% vs 60.8%; p  = 0.9). Frontline TAG was not associated with OS in pooled multivariable regression (HR 0.89 [0.37–2.15]; p  = 0.803), while peripheral blood involvement remained associated with reduced OS (HR 2.63, 95% CI 1.1–6.27; p  = 0.03). In this large multicenter real-world cohort, frontline TAG achieved high response rates with manageable toxicity. While unmeasured selection may contribute to the higher transplantation rate after TAG, durable remissions were achieved in patients undergoing post-TAG consolidation, supporting TAG as an induction and bridging strategy to allogeneic stem cell transplantation.","PeriodicalId":16023,"journal":{"name":"Journal of Hematology & Oncology","volume":"36 1","pages":""},"PeriodicalIF":28.5,"publicationDate":"2026-10-07","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"149088432","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":"Mitochondrial genetic variation as a novel predictor of graft-versus-host disease after stem-cell transplantation in myelodysplastic neoplasms","authors":"Shahram Arsang-Jang,Tao Zhang,Maryam Rafati,Yung-Tsi Bolon,Stephen R. Spellman,Zhongyuan Chen,Kristine Jones,Jia Liu,Najla El Jurdi,Xiaowu Gai,Raul Urrutia,Shahinaz M. Gadalla,Paul L. Auer,Wael Saber,Jing Dong","doi":"10.1186/s13045-026-01846-y","DOIUrl":"https://doi.org/10.1186/s13045-026-01846-y","url":null,"abstract":"","PeriodicalId":16023,"journal":{"name":"Journal of Hematology & Oncology","volume":"8 1","pages":""},"PeriodicalIF":28.5,"publicationDate":"2026-10-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"149088549","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":"Targeting cancer-associated fibroblasts: therapeutic strategies, translational challenges, and future perspectives.","authors":"Yanping Jiang, Bo Ding, Han Yin, Yue Hua, Ning Ma, Pengcheng Hu, Jianbin Deng, Fu-Gen Wu, Yang Shen","doi":"10.1186/s13045-026-01845-z","DOIUrl":"10.1186/s13045-026-01845-z","url":null,"abstract":"<p><p>Cancer-associated fibroblasts (CAFs) act as key drivers of cancer progression and therapeutic resistance within the tumor microenvironment, but their diverse and context-dependent functions complicate therapeutic targeting. The limited clinical efficacy of CAF-targeting therapeutics has prompted a critical reassessment of CAF biology, therapeutic development, and emerging CAF-directed strategies. Unlike prior reviews that predominantly focused on CAF heterogeneity or isolated therapeutic modalities, this review systematically compares pharmacological and biologic CAF-targeting therapeutics, multifunctional nanomedicines, and biologically inspired and living platforms in terms of their underlying mechanisms of action and translational bottlenecks. Drawing on clinical evidence from CAF-targeting therapeutics, we identify several interconnected barriers to successful translation, including CAF heterogeneity and plasticity, patient-selection and biomarker limitations, preclinical-clinical mismatch and combination-treatment dependency, insufficient tumor penetration and systemic toxicity, and signaling redundancy and pathway compensation. Importantly, lessons from unsuccessful clinical trials are used to critically reassess whether current CAF-targeting nanomedicines and platforms adequately address these barriers. In parallel, we evaluate platform-specific translational challenges, particularly those related to biosafety and manufacturing feasibility. These analyses highlight the persistent gaps between the evolving understanding of CAF functional states, existing design rationales for nanomedicine and platforms, and real-world clinical practice. Future directions should therefore prioritize the identification of functionally defined CAF states, the optimization of clinically relevant models of advanced disease, and the development of therapeutic platforms tailored to clearly defined clinical needs. Finally, we propose an iterative translational roadmap and a hypothesis-generating sequential cancer cell/CAF dual-targeting framework to guide the development of clinically translatable CAF-directed therapies.</p>","PeriodicalId":16023,"journal":{"name":"Journal of Hematology & Oncology","volume":"19 1","pages":""},"PeriodicalIF":47.8,"publicationDate":"2026-09-29","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC13625475/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"149080966","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":1,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Cellular senescence and regulated cell death in cancer: mechanisms, cross-regulatory networks and therapeutic implications.","authors":"Linna Du, Yueyue Zhang, Ruohan Liang, Bin Song, Jun Zhou, Xianwu Xia, Chibo Liu, Kongming Wu, Xuan Cao","doi":"10.1186/s13045-026-01847-x","DOIUrl":"10.1186/s13045-026-01847-x","url":null,"abstract":"<p><p>Cellular senescence and regulated cell death represent two fundamental but intricately connected biological programs that govern tumor cell fate. Cellular senescence can suppress tumor growth by inducing stable cell-cycle arrest and promoting immune clearance, but persistent senescent cells may also drive tumor progression through the senescence-associated secretory phenotype (SASP). Concurrently, multiple modalities of regulated cell death-including apoptosis, ferroptosis, cuproptosis, necroptosis, pyroptosis, parthanatos, and autophagy-dependent cell death-have emerged as critical determinants of therapeutic response. The crosstalk between senescence and cell death is orchestrated by key molecular hubs including p53, mitochondria, autophagy machinery, and epigenetic regulators. In this review, we summarize the hallmarks and classification of cellular senescence in cancer, outline major cell death modalities, discuss the cross-regulatory networks linking senescence and death, and highlight emerging therapeutic strategies that target these interconnected processes for cancer treatment.</p>","PeriodicalId":16023,"journal":{"name":"Journal of Hematology & Oncology","volume":"19 1","pages":""},"PeriodicalIF":47.8,"publicationDate":"2026-09-29","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC13625508/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"149080949","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":1,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Next-generation antibody-based therapeutics in cancer: antibody-drug conjugates bispecific antibodies across hematologic malignancies and solid tumors.","authors":"Jiacheng Lou, Yizhu Lyu","doi":"10.1186/s13045-026-01843-1","DOIUrl":"10.1186/s13045-026-01843-1","url":null,"abstract":"<p><p>The therapeutic paradigm in oncology is undergoing a profound transformation driven by antibody-drug conjugates (ADCs) and bispecific antibodies (bsAbs). This review comprehensively summarizes recent clinical advances of these platforms across both hematologic malignancies and solid tumors. ADCs such as trastuzumab deruxtecan have expanded the concept of targetable HER2 expression, demonstrating meaningful intracranial activity and redefining standards of care in HER2-low breast cancer and beyond. The landscape continues to broaden with novel ADC targets (TROP2, CLDN18.2, B7-H3, HER3) and bispecific ADC constructs. Concurrently, T‑cell-engaging bsAbs-CD20×CD3 in B‑cell lymphomas, BCMA×CD3 and GPRC5D×CD3 in multiple myeloma, and CD19×CD3 in acute lymphoblastic leukemia-have achieved deep and durable responses in heavily pretreated populations. In solid tumors, EGFR‑MET and DLL3‑targeted bsAbs have delivered clinically validated efficacy in historically refractory settings, including regulatory approval of tarlatamab. Despite these successes, critical challenges persist, including the management of unique toxicity profiles, the emergence of resistance via antigen escape and T‑cell exhaustion, and the absence of validated predictive biomarkers. Optimal sequencing of these agents with one another and with chimeric antigen receptor T‑cell therapy remains largely empirical. Next‑generation strategies-bispecific ADCs, probody‑drug conjugates, and immune‑stimulating antibody conjugates-combined with immunotherapy partnerships hold promise for overcoming resistance and improving therapeutic indices. By distilling pivotal clinical data and highlighting unresolved questions, this review provides a roadmap for translating antibody‑based innovations into precision oncology.</p>","PeriodicalId":16023,"journal":{"name":"Journal of Hematology & Oncology","volume":"19 1","pages":""},"PeriodicalIF":47.8,"publicationDate":"2026-09-09","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC13555957/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148912487","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":1,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Cytokine fusion proteins for solid tumor therapy: mechanistic insights and clinical advances","authors":"Yufang Wang,Jing Zheng,Zhen Li,Jingjing Qu,Yuqing Ren,Ziwan Cai,Yuekang Li,Wenjia Sun,Nan Jiang,Cuihong Cai,Kexin Ruan,Jiahe Shi,Zheya Zhang,Jianya Zhou","doi":"10.1186/s13045-026-01842-2","DOIUrl":"https://doi.org/10.1186/s13045-026-01842-2","url":null,"abstract":"","PeriodicalId":16023,"journal":{"name":"Journal of Hematology & Oncology","volume":"53 1","pages":""},"PeriodicalIF":28.5,"publicationDate":"2026-09-05","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148893676","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":"Glutathione reductase deficiency potentiates the immunogenicity of ferroptosis and cuproptosis via amplified reactive oxygen species accumulation and cGAS-STING pathway activation.","authors":"Xiaoyi Deng, Zaidong Deng, Bin Zhu, Ruiqi Hu, Jing Ma, Changheng Li, Pu Zhang, Lei Li, Hui Yang, Yu Liu, Yanxun V Yu, Youngnam N Jin","doi":"10.1186/s13045-026-01840-4","DOIUrl":"10.1186/s13045-026-01840-4","url":null,"abstract":"<p><strong>Background: </strong>Cancer remains a major therapeutic challenge due to drug resistance and metastasis, processes driven by oxidative stress and redox imbalance. Targeting this vulnerability through ferroptosis (iron-dependent lipid peroxidation) and cuproptosis (copper-driven mitochondrial dysfunction), two ROS-mediated cell death pathways, offers a promising therapeutic strategy. However, clinical translation is hindered by incomplete understanding of their redox regulation and limited immunogenicity.</p><p><strong>Methods: </strong>A genome-wide CRISPR knockout screen was performed to identify key regulators of ferroptosis. Genetic depletion or pharmacological inhibition of candidate genes was evaluated across multiple cancer cell lines for sensitivity to ferroptosis inducer RSL3 and the cuproptosis inducer elesclomol (Es). Antitumor efficacy was assessed in xenograft, orthotopic, metastatic, and syngeneic mouse models, alone or combined with immune checkpoint inhibitors. Mechanistic studies also examined ROS production, mitochondrial stress, mitochondrial DNA release, cGAS-STING activation, and immune responses within the tumor microenvironment.</p><p><strong>Results: </strong>Glutathione reductase (GSR), a central enzyme maintaining reduced glutathione (GSH) homeostasis, was identified as the top suppressor of ferroptosis. GSR knockout or pharmacological inhibition markedly sensitized diverse cancer cell lines to RSL3-induced ferroptosis, while GSR overexpression conferred resistance. Strikingly, GSR depletion also enhanced sensitivity to cuproptosis triggered by the copper ionophore Es. In multiple in vivo tumor models, GSR inhibition synergizes with RSL3 or Es to suppress tumor growth, inhibit lung metastasis, and prolong survival. Mechanistically, GSR deficiency amplified ROS production, induced mitochondrial stress, and triggered the cytosolic mitochondrial DNA release under ferroptotic or cuproptotic stress, activating the cGAS-STING pathway in vitro and in vivo. This increased inflammatory cytokine production, promoted immunogenic cell death, and enhanced the release of damage-associated molecular patterns (DAMPs), including HMGB1. Together, GSR inhibition combined with a ferroptosis or cuproptosis inducer transformed the tumor microenvironment into a highly immune stimulatory state, thereby enhancing the efficacy of immune checkpoint blockade through increased dendritic cell activation and T-cell infiltration and activation.</p><p><strong>Conclusions: </strong>GSR represents a key molecular node connecting and modulating ferroptosis and cuproptosis through redox regulation. Targeting GSR amplifies ROS-mediated immunogenic cell death, triggers cGAS-STING activation in cancer cells, and enhances the efficacy of cancer immunotherapy, providing a promising redox-based therapeutic strategy.</p>","PeriodicalId":16023,"journal":{"name":"Journal of Hematology & Oncology","volume":"19 1","pages":""},"PeriodicalIF":47.8,"publicationDate":"2026-09-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC13531920/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148874471","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":1,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"High-definition spatial transcriptomics visualizes the cellular and molecular architecture underlying perineural invasion in localized prostate cancer.","authors":"Paul Vinu Salachan, Line Raaby, Jacob Fredsøe, Benedicte Ulhøi, Michael Borre, Karina D Sørensen","doi":"10.1186/s13045-026-01841-3","DOIUrl":"10.1186/s13045-026-01841-3","url":null,"abstract":"<p><p>Distinguishing indolent from aggressive tumors remains a key challenge in the clinical management of prostate cancer (PC), highlighting the need for better tools for accurate risk stratification. A defining feature of aggressive PC is its propensity for perineural invasion (PNI), a pathological finding that is associated with poor prognosis. Despite its clinical significance, very little is known about the spatial and molecular determinants of PNI in PC. To address this, we used high-definition spatial transcriptomics (Visium HD) to profile the PNI-associated tumor microenvironment (TME) of a representative PC patient at near single-cell resolution. Spatial mapping of the expressed genes and inferred cell types revealed transcriptionally divergent malignant cell states spatially linked to PNI within this patient. Nerve-invasive PC cells were organized within a distinct spatially localized niche that exhibited altered TME characteristics, including increased proportions of macrophages, CD4 T-cells, and endothelial cells, suggesting coordinated changes in the tumor- and immune microenvironments. The PNI-associated niche in this patient further displayed enrichment of pathways involved in immune regulation and extracellular matrix remodeling, consistent with PNI-associated niche remodeling. APP-CD74 was identified as a potential signaling axis associated with tumor-nerve, nerve-macrophage, and nerve-endothelial cell interactions, suggesting PNI in this patient may be associated with distinct microenvironmental signaling programs. We further revealed a PNI-associated PC signature that held biomarker potential at the early-localized and advanced-metastatic disease stages. Although based on a single patient, these results contribute to our understanding of the spatial and molecular features of PNI in PC and may help guide personalized treatment choices for PC patients in the future.</p>","PeriodicalId":16023,"journal":{"name":"Journal of Hematology & Oncology","volume":"19 1","pages":""},"PeriodicalIF":47.8,"publicationDate":"2026-09-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC13531779/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148873136","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":1,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Mucosal immunity: mechanism and application in cancer immunotherapy.","authors":"Maosen Xu, Ruolan Xia, Yuquan Wei, Xingchen Peng, Xiawei Wei","doi":"10.1186/s13045-026-01829-z","DOIUrl":"10.1186/s13045-026-01829-z","url":null,"abstract":"<p><p>Recent advances in immunotherapy have significantly revolutionized cancer treatment landscape and prompted extensive research into novel vaccine-based anti-tumor therapy. As the primary defense against external infections, the mucosal immune response plays a pivotal role in maintaining normal physiological functions and preventing pathogen invasion. Mucosal tissues are among the most common sites of tumor initiation, and therefore harnessing mucosal immune to fight against malignant cells represents a feasible option for optimizing and improving current antitumor therapies. Over the past few decades, numerous efforts have been devoted to designing ideal and effective mucosal vaccine. Some clinical trials using mucosal vaccine for cancer therapy have been also launched continually. In this review, we introduce the mechanisms of mucosal immunity, with a focus on the respiratory, gastrointestinal, and urogenital tracts. We also summarize recent research and clinical trials on the application of mucosal vaccines in anti-tumor therapy, aiming to provide new perspectives and directions for future studies.</p>","PeriodicalId":16023,"journal":{"name":"Journal of Hematology & Oncology","volume":"19 1","pages":""},"PeriodicalIF":47.8,"publicationDate":"2026-09-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC13531972/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148873075","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":1,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Current and future therapies for triple-negative breast cancer.","authors":"Zi-Xun Wang, Xi-Yu Liu, Yu-Xiao Wu, Yu-Ling Xiao, Li-Ping Ge, Song-Yang Wu, Yi-Zhou Jiang, Zhi-Ming Shao","doi":"10.1186/s13045-026-01839-x","DOIUrl":"10.1186/s13045-026-01839-x","url":null,"abstract":"<p><p>Triple-negative breast cancer remains an aggressive and biologically heterogeneous breast cancer subtype. Although the therapeutic landscape has expanded, durable disease control remains clinically challenging in many settings. Existing reviews often organize TNBC therapy by drug class or molecular subtype, which can obscure how treatment response is shaped by interacting biological layers. Here, we review current and emerging therapeutic strategies through a three-layer framework: tumor-cell-intrinsic vulnerabilities, the local immune and stromal microenvironment, and host-level systemic modifiers. We summarize established approaches, including chemotherapy, immune checkpoint blockade, antibody-drug conjugates and PARP inhibition in biomarker-defined settings, and distinguish them from maturing or exploratory strategies such as pathway-directed therapy, epigenetic modulation, anti-vascular combinations, regulated cell-death induction, cellular therapy, vaccines, microbiome-related interventions, liquid biopsy, AI-supported multiomics and adaptive trial designs. This framework integrates evidence level, disease stage, biomarker reliability and patient tolerance into treatment selection for TNBC precision therapy.</p>","PeriodicalId":16023,"journal":{"name":"Journal of Hematology & Oncology","volume":"19 1","pages":""},"PeriodicalIF":47.8,"publicationDate":"2026-08-26","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC13520289/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148829323","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":1,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}