Blood Cancer Discovery最新文献

{"title":"Prophylactic IFN-γ blockade drives axi-cel expansion without preventing refractory toxicities: caution against pre-emptive use.","authors":"Viktoria Blumenberg, David J Bozym, Maxx King, Marisa G Ogier, Deshea L Harris, Keshav Sridharan, Jing Li, Patrick C Johnson, Benjamin R Puliafito, Alexandra M Haugh, Jacob D Soumerai, Julie E Haydu, Elliot C Woods, Jeremy S Abramson, Yi-Bin Chen, Mark B Leick, Kathleen Me Gallagher, Marcela V Maus, Matthew J Frigault","doi":"10.1158/2643-3230.BCD-26-0249","DOIUrl":"https://doi.org/10.1158/2643-3230.BCD-26-0249","url":null,"abstract":"<p><p>Cytokine release syndrome (CRS) and immune effector cell-associated neurotoxicity syndrome (ICANS) affect most patients receiving axicabtagene ciloleucel (axi-cel) for relapsed or refractory large B-cell lymphoma (LBCL). Based on pre-clinical data, we hypothesized that prophylactic IFN-γ blockade could prevent toxicity without impairing efficacy. We initiated an open-label phase 2 trial (NCT06550141) evaluating single-dose emapalumab one day before axi-cel. Here, we report the first two patients to caution against the pre-emptive emapalumab use prior axi-cel: Both developed treatment-refractory toxicities including high-grade ICANS and overlapping CRS-IEC-HS requiring multiple immunomodulatory agents. CAR T-cell expansion exceeded levels reported in ZUMA-1 and a standard-of-care axi-cel cohort at our institution. Despite therapeutic emapalumab and suppressed free IFN-γ, IL-2 and sIL-2R were markedly elevated, suggesting CRS was driven independent of IFN-γ. Both patients achieved complete responses, suggesting preserved efficacy. Given the unanticipated severity and refractoriness of toxicities, recruitment with this design was discontinued and the protocol was amended.</p>","PeriodicalId":29944,"journal":{"name":"Blood Cancer Discovery","volume":" ","pages":""},"PeriodicalIF":12.2,"publicationDate":"2026-10-19","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"149224872","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"CD19 CAR T-cell Escape in Large B-cell Lymphoma: Antigen Density Matters after All.","authors":"Eric Perkey, Justin Kline","doi":"10.1158/2643-3230.BCD-26-0260","DOIUrl":"https://doi.org/10.1158/2643-3230.BCD-26-0260","url":null,"abstract":"<p><p>In this issue of Blood Cancer Discovery, Corona, Gillmor, and colleagues show that quantitative CD19 density measured before chimeric antigen receptor (CAR) T-cell infusion stratifies progression-free survival in large B-cell lymphoma, yet low antigen density rarely reflects a genetic lesion at the CD19 locus itself, suggesting that other mechanisms of CD19 downregulation may promote CAR T-cell escape. Moreover, Newsam and colleagues offer one explanation-recurrent del(3p21.31)/RHOA loss that results in decreased CD19 in trans and impairs CAR T-cell efficacy. See related article by Corona, Gillmor, and colleagues, p. XX . See related article by Newsam and colleagues, p. XX .</p>","PeriodicalId":29944,"journal":{"name":"Blood Cancer Discovery","volume":" ","pages":"OF1-OF4"},"PeriodicalIF":12.2,"publicationDate":"2026-10-12","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"149169008","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"A (Post)translational Opportunity in RAS-Dependent Heme Malignancy.","authors":"Lawrence H Boise","doi":"10.1158/2643-3230.BCD-26-0319","DOIUrl":"https://doi.org/10.1158/2643-3230.BCD-26-0319","url":null,"abstract":"<p><p>Zhang and colleagues uncover a mechanism of regulation of RAS stability that is active almost exclusively in hematologic (heme) malignancies. This provides new insights into the consequences of a RAS hotspot mutation found in leukemia and myeloma and points to a new therapeutic opportunity in these diseases. See related article by Zhang et al., p. XX.</p>","PeriodicalId":29944,"journal":{"name":"Blood Cancer Discovery","volume":" ","pages":"OF1-OF3"},"PeriodicalIF":12.2,"publicationDate":"2026-10-02","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"149115539","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"A phase 1, first-in-human study of safimaltib, a MALT1 inhibitor, in B-lymphocytic malignancies.","authors":"Mark Hertzberg, Chan Y Cheah, Stephen Opat, Matko Kalac, Pau Abrisqueta, Vincent Ribrag, Emmanuel Bachy, Loïc Ysebaert, Lugui Qiu, Erel Joffe, Shuhua Yi, Pier Luigi Zinzani, Alessandra Tedeschi, Noriko Nishimura, Charlotte R Lemech, Jacqueline Bussolari, Changchun Deng, Alemu Takele Assefa, Sandy Van Hemelryck, Jan Snoeys, Brendan P Hodkinson, Nele Fourneau, Yu Cao, Srimathi Srinivasan, Yue Guo, Virginie Soete, Isabel Soriano Paradinas, Lorena Fontan, Ulrike Philippar, John F Gerecitano, Franck Morschhauser","doi":"10.1158/2643-3230.BCD-26-0179","DOIUrl":"https://doi.org/10.1158/2643-3230.BCD-26-0179","url":null,"abstract":"<p><p>Following preclinical findings, we evaluated safimaltib (MALT1 protease inhibitor; JNJ-67856633) in relapsed/refractory B-cell non-Hodgkin lymphomas or chronic lymphocytic leukemia in a multi-center, phase-1, dose-escalation/dose-expansion study (NCT03900598). Primary endpoints were recommended phase-2 dose (RP2D) and safety. Among 226 patients, 56.2% had diffuse large B-cell lymphoma (DLBCL); 47.3% received ≥4 prior therapy lines. RP2D was once-daily, 300-mg, oral safimaltib±loading dose. Most common adverse events (AEs) were hyperbilirubinemia (48.2%; off-target related), anemia (36.7%), neutropenia (31.4%), and thrombocytopenia (27.4%). Dose reduction mitigated safimaltib-related AEs. Objective response rate was 28.8% (95% CI: 23.0%-35.1%), including 9 (3.9%) complete responses. All patients with non-germinal-center B-cell-like DLBCL and ≥1 B-cell-receptor pathway activating mutation (n=5) responded to safimaltib. Safimaltib exhibited on-target activity in translational studies, affecting NF-κB-regulated cytokines. Proof-of-principle activity in this first MALT1-targeting study in hematologic malignanices suggest MALT1 may be a feasible target in humans and supports further investigation despite observed off-target effects.</p>","PeriodicalId":29944,"journal":{"name":"Blood Cancer Discovery","volume":" ","pages":""},"PeriodicalIF":12.2,"publicationDate":"2026-09-30","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"149115606","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Very Long Chain Fatty Acid Synthesis is a Targetable Dependency in RAS Pathway Mutant Leukemia.","authors":"Rebecca Gelfer, Maya Bagish, Merve Sahin, Kaitlyn H Ko, Maria Sirenko, Matthew Wereski, Gabriel San Miguel-Matos, Angelica C Romero-Vega, Shoron Mowla, Nathaniel B Long, Michelle Saoi, Clementina Strozek, Su-Fern Tan, Christopher A Famulare, Kevin Chen, B Bishal Paudel, Madhuri Madavaram, Zhuoning Li, Michael R Waarts, Xiaodi Wu, Justin R Cross, Wenbin Xiao, Iannis Aifantis, Tak Wah Mak, Todd E Fox, David J Feith, Elisa de Stanchina, Mara Monetti, Richard P Koche, Sheng F Cai, Ross L Levine","doi":"10.1158/2643-3230.BCD-26-0274","DOIUrl":"10.1158/2643-3230.BCD-26-0274","url":null,"abstract":"<p><p>Oncogenic RAS pathway mutations are associated with therapeutic resistance in acute myeloid leukemia, and identification of therapeutic vulnerabilities has been hindered by a lack of clinically relevant models and tractable ex vivo platforms. We utilize a bone marrow endothelial cell co-culture system to perform CRISPR screens on wild-type hematopoietic cells and isogenic leukemias with and without mutant Nras. We credentialed Elovl1, a very long chain fatty acid elongase, as a dependency in RAS pathway mutant leukemia using genetic and pharmacologic approaches. Metabolic and genetic studies in primary leukemias revealed that the fitness defect from Elovl1 loss reflects a mutant-specific dependency on de novo sphingolipid biosynthesis, specifically sphingomyelin production, as Sgms1 deletion phenocopies Elovl1 loss. Sphingomyelin-mediated generation of lipid rafts, key scaffolds for multiple signaling pathways, is essential to the survival of Nras-mutant AML cells. Our work leverages a new leukemia model to identify a targetable dependency in this treatment-refractory leukemia.</p>","PeriodicalId":29944,"journal":{"name":"Blood Cancer Discovery","volume":" ","pages":""},"PeriodicalIF":12.2,"publicationDate":"2026-09-30","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC13657407/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"149115551","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"In vivo CAR T-cell therapy: determinants of response and durability.","authors":"Mohamed Abou-El-Enein","doi":"10.1158/2643-3230.BCD-26-0116","DOIUrl":"https://doi.org/10.1158/2643-3230.BCD-26-0116","url":null,"abstract":"<p><p>In vivo chimeric antigen receptor (CAR) T-cell therapy generates engineered lymphocytes inside the patient, bypassing leukapheresis, ex vivo manufacturing and, in many programs, lymphodepletion. Studies in relapsed or refractory multiple myeloma report deep responses with measurable residual disease negativity after B-cell maturation antigen-directed treatment. Because the administered product is a delivery system, cells are shaped by the host environment, which may complicate interpretation of efficacy and safety. This Review summarizes clinical data and defines determinants of response that could be optimized for durable translation. It focuses on multiple myeloma, where clinical experience is most mature, while drawing on autoimmune applications.</p>","PeriodicalId":29944,"journal":{"name":"Blood Cancer Discovery","volume":" ","pages":""},"PeriodicalIF":12.2,"publicationDate":"2026-09-23","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"149031548","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"A Phase I/II Trial of Anti-CD22/CD19 CAR-T Cell Therapy, CART2219.1, in Adult and Pediatric Relapsed/Refractory B-ALL.","authors":"Michaela Su-Fern Seng, Zexi Guo, Kai Soon Ng, Shui Yen Soh, Francesca Wei Inng Lim, Liang Piu Koh, William Yk Hwang, Aloysius Yl Ho, Yeh Ching Linn, Esther Hian Li Chan, Michelle L M Poon, Lip Kun Tan, Mickey Bc Koh, Tun Kiat Ko, Jia Yu, King Pan Ng, Teck Guan Soh, Jason Yongsheng Chan, Joe Poh Sheng Yeong, Rimas J Orentas, Wing Leung","doi":"10.1158/2643-3230.BCD-26-0115","DOIUrl":"https://doi.org/10.1158/2643-3230.BCD-26-0115","url":null,"abstract":"<p><p>Durable remissions after anti-CD19 chimeric antigen receptor T cell (CAR-T) therapy in relapsed/refractory B-lineage acute lymphoblastic leukaemia are limited by antigen escape and T-cell dysfunction. The tandem CAR22-19/LTG2737 construct links human-derived anti-CD22 and anti-CD19 scFvs to CD8 hinge/transmembrane, 4-1BB, and CD3ζ domains. In a multicentre phase I/II trial, all patients (n=11; 7 children, 4 adults) achieved complete remission by Day 28 (91% minimal residual disease-negative). At a 34-month median follow-up, median overall survival (OS) and leukaemia-free survival (LFS) were not reached. The 12-month OS was 82% (95%CI: 45%-95%) and LFS was 64% (95%CI: 30%-85%) without consolidative transplantation. Immune-effector cell-associated toxicities included cytokine release syndrome, haematotoxicity, and haemophagocytic lymphohistiocytosis-like syndrome. De novo CD19 escape caused one relapse. Exploratory multi-omic profiling linked durable response to higher CD22 antigen density on blasts; pre-infusion CD4 CAR-T cells expressing IL7Rα, LEF1, BACH2, and TCF7 but lower FOXP3; post-infusion NK-like effector CAR-T expansion; and central-memory CAR-T pool maintenance.</p>","PeriodicalId":29944,"journal":{"name":"Blood Cancer Discovery","volume":" ","pages":""},"PeriodicalIF":12.2,"publicationDate":"2026-09-21","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"149012945","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"RHOA Deletion Downregulates CD19 and Promotes Dysfunctional Immune Microenvironments in CAR-T Resistant Large B-cell Lymphomas.","authors":"Austin D Newsam, Bachisio Ziccheddu, Abdessamad A Youssfi, Venu Venkatarame Gowda Saralamma, Santiago Foos-Russ, Daniel E Tsai, Isaiah Sheffield-Veney, Adithi Jeevan, Paola Manara, Yitzhar E Goretsky, David M Suissa, Marco Vincenzo Russo, Nikolai Fattakhov, David Carmona-Berrio, Natalia Campos Gallego, Caroline A Coughlin, Anya K Sondhi, Evan R Roberts, Jay Y Spiegel, Juan Pablo Alderuccio, Catalina Amador, Daniel Bilbao, David G Coffey, Michael D Jain, Francesco Maura, Frederick L Locke, Jonathan H Schatz","doi":"10.1158/2643-3230.BCD-25-0482","DOIUrl":"10.1158/2643-3230.BCD-25-0482","url":null,"abstract":"<p><p>CD19-directed chimeric antigen receptor (CAR)-T cells are breakthrough therapies for large B-cell lymphomas, but fewer than half of patients achieve durable responses. We previously showed RHOA deletions are enriched in progressing cases, but the role of RHOA deficiency is poorly defined despite frequent occurrence in newly diagnosed disease. Here we show RHOA loss downregulates CD19, promoting cell-intrinsic resistance to CAR-19 in vitro and in vivo. CD19 decline, however, provides an incomplete explanation of resistance and would not explain high frequency of the deletion in newly diagnosed cases. We therefore performed single-cell assessments of immunocompetent RHOA-deficient lymphoma microenvironments, revealing remarkable concordance with features in CAR-19-resistant patients. Despite increased microenvironmental production of interferon gamma (IFNγ), RHOA-deficient tumor cells themselves show impaired response to the cytokine including failed induction of Class I MHC molecules. Overall, we describe for the first time how a single-gene alteration recurrent in CAR-19-resistant lymphoma contributes to treatment failures.</p>","PeriodicalId":29944,"journal":{"name":"Blood Cancer Discovery","volume":" ","pages":""},"PeriodicalIF":12.2,"publicationDate":"2026-09-18","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC13592517/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148991622","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Safety and Clinical Outcomes of a First-in-Human Trial of Point-of-Care Manufactured Trispecific CAR T Cells Targeting CD19, CD20, and CD22.","authors":"Sumithira Vasu, Nathan Denlinger, No-Joon Song, Danielle Elsberry, Qiuhong Zhao, Lianbo Yu, Evandro D Bezerra, Nicole Szuminski, Dina Schneider, Pradyot Dash, Louisa Wirthlin, Narendranath Epperla, Yazeed Sawalha, Jennifer A Woyach, Shamama Nishat, Kerry A Rogers, Seema A Bhat, Hazem E Ghoneim, Gregory K Behbehani, Timothy J Voorhees, Karilyn Larkin, Adam S Kittai, Victoria Churchill, Elizabeth George, Margaret Lamb, Dean A Lee, Wing Keung Chan, Ashley Krull, Rimas J Orentas, Lynn O'Donnell, Zihai Li, Lapo Alinari, Marcos de Lima","doi":"10.1158/2643-3230.BCD-26-0186","DOIUrl":"10.1158/2643-3230.BCD-26-0186","url":null,"abstract":"<p><p>Disease recurrence is the main cause of treatment failure after CD19-directed chimeric antigen receptor (CAR) T cells, often due to CD19 antigen loss, stability, and/or coverage. To overcome single-antigen escape, we evaluated a trispecific CAR targeting CD19, CD20, and CD22 with an OX40 costimulatory domain. Preclinical studies demonstrated potent, antigen-specific cytotoxicity in in vitro and in vivo lymphoma models. We then conducted a first-in-human phase I trial in patients with relapsed/refractory B-cell malignancies. Sixteen patients received infusions at a median vein-to-vein time of 7 days, at doses of 0.5 to 2 × 106 cells/kg. No severe cytokine release syndrome or neurotoxicity occurred. The overall response rate was 50%, including complete responses in 83% of patients with lymphoma. The 1-year overall survival rate was 61%, with durable remissions observed in lymphoma. CAR T expansion did not correlate with dose or response. T-cell exhaustion in apheresis cells correlated with progressive disease. Trispecific CAR T cells are safe and potentially active in lymphoma.</p><p><strong>Significance: </strong>This first-in-human trial demonstrates that point-of-care manufactured trispecific CD19/20/22 CAR T cells with OX40 costimulation can be rapidly produced, safely administered, and induce durable remissions in relapsed B-cell lymphoma. Findings highlight multispecific targeting to mitigate antigen escape and identify T-cell exhaustion as a key biomarker guiding future CAR T optimization. See related commentary by Merz and Luttwak, p. 652.</p>","PeriodicalId":29944,"journal":{"name":"Blood Cancer Discovery","volume":" ","pages":"711-725"},"PeriodicalIF":12.2,"publicationDate":"2026-09-03","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148438126","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Genomic Features Do Not Account for Differences in Multiple Myeloma Risk by Ancestry.","authors":"Kylee H Maclachlan, Marios Papadimitriou, Patrick Blaney, Linda B Baughn, Tala Shekarkhand, Alexandra M Poos, Bachisio Ziccheddu, Hongwei Tang, Huihuang Yan, Benjamin Diamond, Yanming Zhang, Robert Cimera, Ahmet Dogan, Dylan Gagler, Eileen Boyle, Malin Hultcrantz, Sham Mailankody, Hani Hassoun, Urvi A Shah, Carlyn Tan, Elizabeth E Brown, Lara Winterkorn, Timothy Chu, Zoe Steinsnyder, Zalman Vaksman, Faith E Davies, Neha Korde, Ola Landgren, Marc S Raab, Alexander M Lesokhin, Nicolas Robine, Niels Weinhold, Saad Z Usmani, Francesco Maura, Gareth J Morgan","doi":"10.1158/2643-3230.BCD-25-0259","DOIUrl":"10.1158/2643-3230.BCD-25-0259","url":null,"abstract":"<p><p>Studies have reported conflicting findings regarding the contribution of germline variants or somatic genomic drivers to racial disparities in multiple myeloma. To comprehensively investigate somatic drivers in relation to inherited genetics in multiple myeloma, we combined newly sequenced whole-genome sequencing data with publicly available datasets (total n = 1,286). Overall, we did not identify germline or somatic genomic differences that explain the different risk of developing multiple myeloma between patients with genetic similarity to African (AFR) or European (EUR) reference populations. A difference in the detectability and timing of APOBEC-associated and germinal center mutational activity was observed. Integrating epidemiologic data and mutational signature-based temporal estimates, we challenge the assumption that individuals in the AFR group develop multiple myeloma at a younger age. Finally, we demonstrate that, with equal access to efficacious therapies, patients in the AFR and EUR groups have equivalent clinical outcomes.</p><p><strong>Significance: </strong>Multiple myeloma is reported to occur at higher rates in individuals who self-identify as non-Hispanic Black. In this large dataset, genomic drivers occur at the same rate among ancestry groups, except for APOBEC mutagenesis. With equivalent therapy, clinical outcomes did not differ for patients grouped by genetic ancestry similarity.</p>","PeriodicalId":29944,"journal":{"name":"Blood Cancer Discovery","volume":" ","pages":"742-758"},"PeriodicalIF":12.2,"publicationDate":"2026-09-03","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC13338918/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148240356","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}