Molecular Diagnosis & Therapy最新文献

{"title":"Anbalcabtagene Autoleucel: First Approval.","authors":"Arnold Lee","doi":"10.1007/s40291-026-00872-3","DOIUrl":"https://doi.org/10.1007/s40291-026-00872-3","url":null,"abstract":"<p><p>Anbalcabtagene autoleucel (RIMQARTO^®) is a CAR T therapy that includes CAR T cells with dual PD-1 and TIGIT downregulation to mitigate T cell exhaustion. It is being developed by Curocell Inc. for the treatment of diffuse large B-cell lymphoma, acute lymphoblastic leukaemia and autoimmune diseases, which received its first approval in April 2026 in South Korea. This article summarizes the milestones in the development of anbalcabtagene autoleucel leading to this first approval for the treatment of relapsed or refractory diffuse large B-cell lymphoma and primary mediastinal large B-cell lymphoma in adults following ≥ 2 lines of systemic therapy.</p>","PeriodicalId":49797,"journal":{"name":"Molecular Diagnosis & Therapy","volume":" ","pages":""},"PeriodicalIF":5.8,"publicationDate":"2026-09-07","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148907915","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Multidisciplinary and Personalized Molecular Diagnosis to Solving Sudden Death During Sport.","authors":"Andrea Costantino, Oscar Campuzano, Fabio Vaiano, Eleonora Nardi, Alexandra Dimitrova, Andrea Greco, Estefanía Martínez-Barrios, Vincenzo Arena, Hannah Jarvis, Georgia Sarquella-Brugada, Ramon Brugada, Antonio Oliva, Simone Grassi","doi":"10.1007/s40291-026-00867-0","DOIUrl":"10.1007/s40291-026-00867-0","url":null,"abstract":"<p><p>Sudden cardiac death is the leading cause of death among athletes during exercise. These events are devastating for both the family and society, especially when they occur in children and young adults. Some of these unexpected deceases occur in athletes who carry genetic alterations that predispose them to malignant arrhythmias, and exercise is the main trigger for these lethal episodes. These genetic alterations are the origin of inherited arrhythmogenic syndromes, often latent, and the first clinical manifestation can be sudden death itself. It is also important to take into account the toxicology data, since high doses of certain substances, as well as mixtures of them, can also be significant triggers of malignant arrhythmias, especially in genetically predisposed hearts. Genetic studies that can provide a diagnosis can be performed on deceased individuals (molecular autopsy) or on their relatives, who may be carriers of the genetic defect and at risk of malignant arrhythmogenic events. Early identification of individuals at risk allows adoption of preventive measures helping to reduce risk of life-threatening arrhythmogenic episodes. Our study examines the main arrhythmogenic causes of sudden cardiac death in athletes during exercise, highlighting a multidisciplinary interpretation of forensic, clinical, genetic and molecular data to obtain a definite cause for the lethal episode.</p>","PeriodicalId":49797,"journal":{"name":"Molecular Diagnosis & Therapy","volume":" ","pages":"759-770"},"PeriodicalIF":5.8,"publicationDate":"2026-09-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC13499825/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148551267","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Standardized Analytical Verification of ctDNA ESR1 Mutation Testing in Metastatic HR+/HER2- Breast Cancer: A European Multicentre Study Using dPCR and NGS-Based Liquid Biopsy.","authors":"Federico Rojo, Valentina Guarneri, Nicola Fusco, Stefano Indraccolo, Isabelle Vanden Bempt, Elena Guerini Rocco, Ruth Sardinha, Isaac García-Murillas, Riccardo Adorisio, Andrea Boscolo Bragadin, Nerea Carvajal, Francesco Pepe, Sandra Pérez-Buira, Ivan Prieto-Potin, Demi Renders, Gianluca Russo, Claudia Scimone, Claire Swift, Konstantinos Venetis, Sandra Zazo, Umberto Malapelle","doi":"10.1007/s40291-026-00850-9","DOIUrl":"10.1007/s40291-026-00850-9","url":null,"abstract":"<p><strong>Introduction: </strong>Activating ESR1 mutations are a major mechanism of resistance to aromatase inhibitors in hormone receptor-positive, HER2-negative metastatic breast cancer (mBC). International guidelines, including those from ASCO, NCCN, and ESMO, recommend liquid biopsy as the preferred approach for ESR1 mutation testing at progression on endocrine therapy, with digital PCR (dPCR) and next-generation sequencing (NGS) as the preferred analytical platforms. Although elacestrant was approved by the U.S. Food and Drug Administration together with Guardant360® Dx as its companion diagnostic, European regulatory frameworks allow the use of validated in-house assays for ESR1 testing, which are increasingly being implemented across clinical laboratories. To support the clinical implementation of ESR1 testing and improve analytical standardization in routine practice, we performed a European multicentre analytical verification study using dPCR- and NGS-based liquid biopsy workflows.</p><p><strong>Methods: </strong>Six referral institutions participated in this study. All laboratories verified dPCR workflows and four also verified NGS-based assays using standardized reference materials containing clinically relevant ESR1 mutations. Limit of detection (LoD) and limit of blank (LoB) were determined in each laboratory according to locally validated workflows following CLSI-based verification procedures. Analytical sensitivity and specificity were assessed across platforms, focusing on the two most frequently tested ESR1 hotspot mutations, p.Y537S and p.D538G. Total DNA input ranged from 10 to 30 ng per reaction for dPCR assays, while NGS input followed platform-specific requirements.</p><p><strong>Results: </strong>LoD values ranged from 0.01% to 0.07% variant allele frequency (VAF) for dPCR assays and from 0.01% to 0.1% for NGS-based workflows, depending on platform characteristics and DNA input. Limit of blank values were low across laboratories, with minimal background signal detected in plasma samples from healthy donors. Comparable analytical performance was observed across different platforms when assays were performed under validated laboratory conditions.</p><p><strong>Discussion: </strong>These results demonstrate that both dPCR and NGS-based liquid biopsy workflows can be successfully implemented for ESR1 mutation testing in routine clinical practice using locally validated assays. This multicentre verification study provides practical guidance on assay verification, DNA input requirements, and key analytical parameters required to ensure reliable ESR1 mutation detection across different European laboratories. Robust analytical verification of ESR1 testing may improve diagnostic reliability and support personalized treatment strategies for patients with hormone receptor-positive, HER2-negative metastatic breast cancer.</p>","PeriodicalId":49797,"journal":{"name":"Molecular Diagnosis & Therapy","volume":" ","pages":"807-820"},"PeriodicalIF":5.8,"publicationDate":"2026-09-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC13499828/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148266654","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Decoding and Overcoming Temozolomide Resistance Through CRISPR/Cas Technologies.","authors":"Bárbara S Marques, Maria Mendes, José Luís Alves, Alberto Pais, Carla Vitorino","doi":"10.1007/s40291-026-00864-3","DOIUrl":"10.1007/s40291-026-00864-3","url":null,"abstract":"<p><p>Intrinsic and acquired resistance to temozolomide (TMZ), the standard chemotherapeutic agent for glioblastoma (GBM), is highly common and results in poor clinical outcomes. This review highlights the emerging dual role of Clustered Regularly Interspaced Short Palindromic Repeats (CRISPR)-associated protein (Cas) technologies in addressing this challenge. First, it examines genome-wide CRISPR screens that revealed DNA damage repair networks, stress adaptations, stemness maintenance, and tumor heterogeneity as key drivers of resistance to TMZ. Second, it examines CRISPR/Cas-based strategies, including targeted gene disruption and epigenetic silencing of O⁶-methylguanine-DNA methyltransferase (MGMT), to restore TMZ sensitivity. Finally, it explores CRISPR/Cas-engineered brain tumor models. Alongside these approaches, CRISPR/Cas technologies highlight the value of decoding the multifactorial basis of TMZ resistance and guiding rational therapeutic strategies. Continued refinement of CRISPR/Cas tools may ultimately contribute to more effective treatments for GBM.</p>","PeriodicalId":49797,"journal":{"name":"Molecular Diagnosis & Therapy","volume":" ","pages":"739-757"},"PeriodicalIF":5.8,"publicationDate":"2026-09-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC13499772/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148450150","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Tividenofusp Alfa: First Approval.","authors":"Matt Shirley","doi":"10.1007/s40291-026-00859-0","DOIUrl":"10.1007/s40291-026-00859-0","url":null,"abstract":"<p><p>Tividenofusp alfa (tividenofusp alfa-eknm; AVLAYAH^™) is an intravenous brain-penetrant enzyme replacement therapy being developed by Denali Therapeutics for the treatment of mucopolysaccharidosis type II (MPS II). Also known as Hunter syndrome, MPS II is a rare X-linked recessive lysosomal storage disease caused by a deficiency of the lysosomal enzyme iduronate-2-sulfatase resulting in accumulation of glycosaminoglycans, heparan sulphate and dermatan sulphate. Consisting of the iduronate-2-sulfatase enzyme fused to a transferrin receptor-binding Fc domain, tividenofusp alfa has been designed to enable distribution of exogenous iduronate-2-sulfatase into both the central nervous system and peripheral tissues. Based on a reduction in cerebrospinal fluid heparan sulphate levels in patients with MPS II treated with tividenofusp alfa in a phase I/II trial, in March 2026 tividenofusp alfa was approved in the USA, under accelerated approval, for the treatment of neurologic manifestations of MPS II when initiated in presymptomatic or symptomatic paediatric patients weighing ≥ 5 kg prior to advanced neurologic impairment. Continued approval for tividenofusp alfa may be contingent upon verification of clinical benefit in a confirmatory trial. Tividenofusp alfa has also been granted Priority Medicine designation by the European Medicines Agency. This article summarises the milestones in the development of tividenofusp alfa leading to this first approval for MPS II.</p>","PeriodicalId":49797,"journal":{"name":"Molecular Diagnosis & Therapy","volume":" ","pages":"839-844"},"PeriodicalIF":5.8,"publicationDate":"2026-09-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148273417","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"LINE-1 Deregulation in Ovarian Cancer: Implications for Diagnosis, Prognosis, and Therapeutic Targeting.","authors":"Nicoletta Bonci, Valentina Schiavoni, Jesmina Rexha, Alice Romagnoli, Roberto Campagna, Giovanni Tossetta","doi":"10.1007/s40291-026-00861-6","DOIUrl":"10.1007/s40291-026-00861-6","url":null,"abstract":"<p><p>Ovarian cancer is a highly heterogeneous malignancy and remains a major cause of cancer-related mortality, mainly due to late diagnosis and frequent development of therapy resistance. Current diagnostic markers show limited sensitivity for early-stage disease, highlighting the need for novel biomarkers and improved understanding of tumor biology. Epigenetic deregulation is a hallmark of ovarian cancer, characterized by global DNA hypomethylation and focal hypermethylation of tumor suppressor genes. Among hypomethylated genomic regions, long interspersed nuclear elements-1 (LINE-1) represent a large fraction of the human genome and a widely used surrogate marker of global epigenetic instability. LINE-1 elements are normally epigenetically silenced. In ovarian cancer, loss of LINE-1 methylation leads to transcriptional reactivation, expression of ORF1p and ORF2p, and increased retrotransposition activity. These events contribute to genomic instability, DNA damage, insertional mutagenesis, tumor heterogeneity, and clonal evolution. LINE-1 deregulation is also associated with defects in DNA repair pathways, including homologous recombination deficiency, and may influence tumor progression and response to therapy. In addition, aberrant LINE-1 activity has been linked to activation of innate immune and interferon-related signaling pathways, supporting its biological relevance in cancer. Several studies indicate that LINE-1 hypomethylation is associated with aggressive tumor features and adverse clinical outcomes in ovarian cancer. Importantly, repetitive elements, including LINE-1, can be detected in circulating cell-free DNA (cfDNA), providing a technical basis for their evaluation as minimally invasive biomarkers. This review summarizes current knowledge on LINE-1 biology, epigenetic regulation, and functional consequences in ovarian cancer. In addition, we discuss the realistic potential of LINE-1 as a circulating epigenetic biomarker and therapeutic target.</p>","PeriodicalId":49797,"journal":{"name":"Molecular Diagnosis & Therapy","volume":" ","pages":"721-738"},"PeriodicalIF":5.8,"publicationDate":"2026-09-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148228442","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Marnetegragene Autotemcel: First Approval.","authors":"Simon Fung","doi":"10.1007/s40291-026-00863-4","DOIUrl":"10.1007/s40291-026-00863-4","url":null,"abstract":"<p><p>Marnetegragene autotemcel (KRESLADI™), an autologous stem cell-based gene therapy that adds functional copies of the ITGB2 gene to haematopoietic stem cells, was developed by Rocket Pharmaceuticals for the treatment of leukocyte adhesion deficiency-I (LAD-I). In March 2026, marnetegragene autotemcel received its first approval in the USA for the treatment of paediatric patients with severe LAD-I due to biallelic variants in ITGB2 without an available human leukocyte antigen (HLA)-matched sibling donor for allogeneic haematopoietic stem cell transplant. This article summarises the milestones in the development of marnetegragene autotemcel leading to this first approval for treatment of paediatric patients with severe LAD-I.</p>","PeriodicalId":49797,"journal":{"name":"Molecular Diagnosis & Therapy","volume":" ","pages":"833-837"},"PeriodicalIF":5.8,"publicationDate":"2026-09-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148450135","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Development of a Point-of-Care Recombinase Polymerase Amplification Assay for Detection of Neisseria gonorrhoeae and Ceftriaxone-Resistance Associated penA Allele 60.001.","authors":"Xia Sun, Ying Fu, Yi Liu, Qiongyao Liu, Luxia Chen, Jiang Zhu, Xu'ai Lin, Hao Cheng, Stijn van der Veen","doi":"10.1007/s40291-026-00868-z","DOIUrl":"10.1007/s40291-026-00868-z","url":null,"abstract":"<p><strong>Background: </strong>Neisseria gonorrhoeae is a global public health threat, exacerbated by the rapid dissemination of ceftriaxone-resistant strains harboring penA allele 60.001. Current diagnostics are limited by long turnaround times, reliance on thermal cycling equipment, and poor suitability for resource-limited settings.</p><p><strong>Methods: </strong>We developed an isothermal recombinase polymerase amplification assay coupled with a lateral flow strip (RPA-LFS) for separate identification of N. gonorrhoeae and the ceftriaxone resistance-associated SNP C932T (A311V) in penA 60.001 and limited closely related alleles. Species detection employed an RPA-Nfo probe targeting the conserved porA pseudogene. Resistance detection employed an allele-specific amplification refractory mutation system RPA (ARMS-RPA) strategy, incorporating artificial mismatches to specifically discriminate the C932T SNP. Assay performance was evaluated using genomic DNA of a panel of gonococcal and non-gonococcal strains and validated directly on unprocessed clinical urine samples.</p><p><strong>Results: </strong>The porA RPA-LFS assay demonstrated a detection limit of 30 fg of genomic DNA with no cross-reactivity against closely related Neisseria species or other bacterial pathogens. The mismatch penA 60.001 RPA-LFS assay achieved a detection limit of 300 fg and exhibited absolute analytical specificity, with no amplification observed from wild-type or other mosaic penA alleles. Validation using 50 clinical urine samples yielded 100% concordance (95% CI: 92.9-100%) with gonorrhoea identification by reference nucleic acid amplification tests, with 100% sensitivity (95% CI: 87.1-100%) and 100% specificity (95% CI: 85.7-100%), and 100% concordance (95% CI: 85.7-100%) with resistance allele detection, with 100% sensitivity (95% CI: 67.6-100%) and 100% specificity (95% CI: 79.6-100%).</p><p><strong>Conclusions: </strong>This integrated RPA-LFS platform provides rapid detection of gonococcal infections and ceftriaxone resistance without requiring a thermal cycler, delivering visual results within 20 minutes. The assay represents a promising point-of-care solution for timely diagnosis, targeted antibiotic therapy, and resistance surveillance in resource-limited settings, though further validation on diverse specimen types and integration of an internal amplification control are needed.</p>","PeriodicalId":49797,"journal":{"name":"Molecular Diagnosis & Therapy","volume":" ","pages":"795-805"},"PeriodicalIF":5.8,"publicationDate":"2026-09-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148585825","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Advances in Gene and Cellular Therapy in Friedreich Ataxia.","authors":"Michael P Lazaropoulos, David R Lynch","doi":"10.1007/s40291-026-00854-5","DOIUrl":"10.1007/s40291-026-00854-5","url":null,"abstract":"<p><p>Friedreich ataxia is a rare, autosomal recessive neurogenerative disorder caused by mutations to the frataxin (FXN) gene resulting in loss of functional FXN protein. Applications of cutting-edge genetic and cellular therapies expand therapeutic options for patients with rare, genetic diseases including Friedreich ataxia. Multiple investigational techniques and strategies seek to permanently alter the disease course in patients with Friedreich ataxia, although no product has established definitive benefit. This review catalogs both the history and ongoing efforts of genetic and cellular therapies applied to Friedreich ataxia and its disease models, including therapeutic efficacy and adverse effects. We list the key limitations and cautions of such therapies, chiefly those of potential FXN overexpression toxicity, critical therapeutic windows, and adverse effects of these therapies applicable to any disease target. As gene and cellular therapy continue to diversify in design and strategy, Friedreich ataxia patients will likely have multiple therapeutic options in the future from both investigational therapies described here and future ones yet to be optimized.</p>","PeriodicalId":49797,"journal":{"name":"Molecular Diagnosis & Therapy","volume":" ","pages":"771-782"},"PeriodicalIF":5.8,"publicationDate":"2026-09-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC13499882/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148354553","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Individualized Longitudinal ctDNA Monitoring in Melanoma Using Multiplexed USE-PCR.","authors":"Annalara G Fischer, Hunter A Miller, Melissa B Hall, Kavitha Yadannapudi, Lucien Jacky, John Alvarado, Aaron Aguiar, Nathaniel Clark, Paul Belitz, Jeremy Myslinski, Paul Flook, Jerrod J Schwartz, Mark W Linder","doi":"10.1007/s40291-026-00862-5","DOIUrl":"10.1007/s40291-026-00862-5","url":null,"abstract":"<p><strong>Background and objective: </strong>Circulating tumor DNA enables longitudinal monitoring in cancer, but current sequencing-based assays are limited by cost, turnaround time, performance in difficult genomic regions, and infrequent sampling. Universal Signal Encoding PCR (USE-PCR) is a highly multiplexed digital PCR chemistry that enables measurement of up to 32 tumor-informed targets per reaction. Here, we evaluated USE-PCR for dense longitudinal circulating tumor DNA monitoring in patients with metastatic melanoma undergoing immunotherapy.</p><p><strong>Methods: </strong>Tumor and plasma sequencing identified subject-specific variants from nine subjects with melanoma, including variants in GC-rich and historically challenging loci such as the TERT promoter. Subject-specific USE-PCR panels were designed using an automated cloud workflow and applied to plasma cell-free DNA and matched peripheral blood mononuclear cell sample DNA, with up to 21 timepoints per subject, collected over a 2-year window. Variant allele fractions were quantified on a commercial digital PCR platform and interpreted with a peripheral blood mononuclear cell genomic DNA background.</p><p><strong>Conclusions: </strong>USE-PCR resolved variant-specific circulating tumor DNA trajectories across longitudinal plasma samples. Dense sampling revealed rapid and low-level circulating tumor DNA shifts, including subclonal variants below the 0.2% variant allele fraction that may not be captured through less frequent surveillance intervals. Panels supported the incorporation of new variants without compromising analytical performance.</p>","PeriodicalId":49797,"journal":{"name":"Molecular Diagnosis & Therapy","volume":" ","pages":"783-794"},"PeriodicalIF":5.8,"publicationDate":"2026-09-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148377709","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}