Current gene therapy最新文献

{"title":"Genome Editing Technologies for Cancer Therapy.","authors":"Gautham Chengizkhan, Arumugam Rajavelu, Sridhar Muthusami, Vengatesh Ganapathy, Surajit Pathak, Satish Ramalingam, Lurdes Queimado, Ilangovan Ramachandran, R Ileng Kumaran","doi":"10.2174/0115665232384131251117125106","DOIUrl":"10.2174/0115665232384131251117125106","url":null,"abstract":"<p><p>Cancer remains one of the leading causes of death worldwide, and the limitations of conventional therapies such as surgery, chemotherapy, and radiotherapy underscore the urgent need for innovative therapeutic strategies. While advances in early detection and treatment have improved outcomes in some regions, challenges such as micrometastasis, tumor relapse, and multidrug resistance continue to hinder long-term success. The multifactorial nature of cancer-driven by complex genetic mutations, diverse tumor microenvironments, and adaptive cancer cell behavior- demands more precise and effective solutions. Recent breakthroughs in molecular biology and genetic engineering have led to the emergence of genome editing technologies that offer promising avenues for targeted cancer therapy. This review highlights the evolution and application of key genome editing platforms, including meganucleases, zinc finger nucleases (ZFNs), transcription activator- like effector nucleases (TALENs), and the CRISPR/CAS9 system. Meganucleases were among the earliest tools with site-specific cutting ability, but limited versatility. ZFNs and TALENs offered greater modularity and target specificity through protein-DNA interactions. The CRISPR/CAS9 system revolutionized genome editing with its RNA-guided targeting, allowing for higher efficiency, simplicity, and flexibility in gene modification. These tools have enabled researchers to disrupt oncogenes, repair tumor suppressor genes, and manipulate signalling pathways involved in tumor progression, resistance, and metastasis. Moreover, ongoing advancements in delivery systems and gene repair mechanisms have further enhanced their therapeutic potential. We also discuss their translational potential from bench to bedside and explore future perspectives on how these technologies may revolutionize precision oncology, ultimately contributing to more effective treatment outcomes.</p>","PeriodicalId":10798,"journal":{"name":"Current gene therapy","volume":" ","pages":""},"PeriodicalIF":4.1,"publicationDate":"2026-04-21","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"147764921","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Shaping the Future of Prostate Cancer Care: The Promise and Pitfalls of Gene- and Cell-Based Therapeutics.","authors":"Dherya Guleria, Navjot Kaur Sandhu","doi":"10.2174/0115665232479483260416092641","DOIUrl":"https://doi.org/10.2174/0115665232479483260416092641","url":null,"abstract":"<p><p>Prostate Cancer (PCa) affects the population worldwide on a large scale in men. This paper presents a comprehensive overview of the evolving therapeutic landscape for PCa and highlights the promise and challenges of gene- and cell-based strategies. There are various limitations to conventional modalities, such as radiotherapy, chemotherapy, and surgery; however, the growing impact of molecular precision, immunotherapies, and innovative gene-editing tools, such as the clustered regularly interspaced short palindromic repeat (CRISPR)-associated (Cas) system, minimizes the limitations of these conventional therapies. Comparisons of the current progress in Oncolytic Virus (OV) based therapies, viral and non-viral gene delivery systems, and cell-based immunotherapies including Chimeric Antigen Receptor (CAR) T cells and Dendritic Cell (DC) therapies demonstrate both their therapeutic potentials and key challenges to their effectiveness that include Tumor Heterogeneity (TH), immune evasion, and the immunosuppressive Tumor Microenvironment (TME). The combination approach integrates the control point blockade, radiosensitizing chemotherapeutics, and biomarker-guided interventions to improve treatment outcomes. It also provides a perspective for analyzing the future roles of Artificial Intelligence (AI), multi-omics integration, and collaborative research networks in shaping standards that are more personalized to enhance care for PCa patients.</p>","PeriodicalId":10798,"journal":{"name":"Current gene therapy","volume":" ","pages":""},"PeriodicalIF":3.3,"publicationDate":"2026-04-17","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"147722012","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"SPTSSA in Head and Neck Squamous Cell Carcinoma: Prognostic Significance and Implications for Gene- and Cell-Based Therapy.","authors":"Zihao Zhang, Wei Zhang, Mingming Tang, Qingwen Chen, Xinjiang Xu, Yingze Wei, Hongyan Qian, Hao Wu, Liang Han","doi":"10.2174/0115665232473951260407050817","DOIUrl":"https://doi.org/10.2174/0115665232473951260407050817","url":null,"abstract":"<p><strong>Objective: </strong>The Tumor Microenvironment (TME) exerts a pivotal regulatory effect on the initiation, progression, and therapeutic response of Head and Neck Squamous Cell Carcinoma (HNSCC). Serine Palmitoyltransferase Small Subunit A (SPTSSA) is a TME-associated gene with well-characterized roles in multiple malignancies, yet its biological function and clinical significance in HNSCC remain largely elusive. This study aimed to systematically investigate the clinical value of SPTSSA in HNSCC and explore its potential as a novel prognostic biomarker and therapeutic target for this disease.</p><p><strong>Methods: </strong>The expression of SPTSSA between Head and Neck Squamous Cell Carcinoma (HNSCC) tissues and non-tumoral tissues was compared using gene expression data. Associations with clinicopathologic features and patient outcomes were also analyzed. In vitro assays in HNSCC cell lines were used to test the effects of SPTSSA on malignant phenotypes. Multiplex immunofluorescence histochemistry was applied to assess SPTSSA protein levels in the TME and their relationship with immune markers and clinical factors. Circulating SPTSSA protein levels were measured in the blood of HNSCC patients to evaluate diagnostic value.</p><p><strong>Results: </strong>SPTSSA expression was significantly higher in HNSCC tissues than in non‑tumoral tissues. Overexpression of SPTSSA enhanced HNSCC cell proliferation in vitro, supporting a pro‑tumorigenic function. Elevated SPTSSA protein levels in patient blood suggested potential diagnostic utility. In tumor tissues, SPTSSA protein expression correlated with CD4+ T cells, CD8+ T cells, and CD56+ natural killer cells, indicating a link with immune remodeling in the TME. High SPTSSA expression and advanced TNM stage independently predicted poor clinical outcomes.</p><p><strong>Discussion: </strong>The study's findings establish SPTSSA as a critical oncogenic driver in HNSCC, with its upregulation closely linked to TME immune remodeling and poor patient prognosis. These results expand the oncogenic landscape of HNSCC and align with SPTSSA's pro-tumorigenic roles in other malignancies. Elevated circulating SPTSSA offers a non-invasive diagnostic tool for early detection, while its correlation with immune cell infiltration positions SPTSSA as a promising molecular target for HNSCC immunotherapy.</p><p><strong>Conclusion: </strong>SPTSSA is an oncogenic gene that drives HNSCC progression and is closely associated with an unfavorable patient prognosis. Its aberrant expression in both tumor tissues and peripheral blood may facilitate risk stratification and early clinical detection of HNSCC. Furthermore, the correlation between SPTSSA and immune cell infiltration in the TME highlights its potential as a promising molecular target for gene- and cell-based immunotherapeutic strategies in HNSCC.</p>","PeriodicalId":10798,"journal":{"name":"Current gene therapy","volume":" ","pages":""},"PeriodicalIF":3.3,"publicationDate":"2026-04-14","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"147765018","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Transcription Factor EB Drives Thrombospondin-1 Expression to Dampen Focal-adhesion Signaling and Limit Post-infarction Cardiac Fibrosis.","authors":"Cong Liu, Qiang Zhang, Dawang Zhou, Bo Li, Jingge Cheng, Yuanzheng Lu","doi":"10.2174/0115665232471521260313132541","DOIUrl":"https://doi.org/10.2174/0115665232471521260313132541","url":null,"abstract":"<p><strong>Background: </strong>Cardiac fibroblasts (CFs) are essential for cardiac morphogenesis and homeostasis. We investigated whether transcription factor EB (TFEB) directly targeted and suppressed the activation of CFs, aiming to elucidate its underlying pathological mechanism from the perspectives of gene and cell therapy.</p><p><strong>Methods: </strong>Following myocardial infarction (MI) induction, we performed transcriptome sequencing of CFs isolated from R26-LSL-TFEB+/+; Acta2-cre (n = 3) and R26-LSL-TFEB+/+ (n = 3) mice. Differential gene expression and functional enrichment analyses were conducted using R software. The binding between TFEB and Thrombospondin-1 (Thbs1) was validated by ChIP-qPCR assay. CFs were extracted from adult mice in the R26-LSL-TFEB+/+; Acta2-cre and R26-LSL-TFEB+/+ groups. Protein expressions of integrin, CD47, CD36, Thbs1, p-paxillin, vinculin, P-FAK, and α- SMA were detected by Western blot. Cell migration was assessed by the wound healing and Transwell assays.</p><p><strong>Results: </strong>TFEB modulated the expression of a broad spectrum of RNAs associated with the transformation of CFs. Pathway analysis revealed significant enrichment in pathways related to extracellular matrix (ECM) receptor interaction and focal adhesion (FA). Notably, both mRNA and protein levels of Thbs1 were markedly elevated in TFEB-overexpressing CFs. Integrated computational prediction and chromatin immunoprecipitation assays identified that TFEB directly bound to the promoter region of Thbs1. This binding was associated with downstream modulation of its receptor network and a concomitant reduction in FA complex activation at the protein level. These findings positioned Thbs1 as a key transcriptional target through which TFEB regulated ECM-related signaling and cellular adhesion dynamics in CFs.</p><p><strong>Discussion: </strong>The current findings showed that the modulation of Thbs1 and associated FA signaling was a mechanism through which TFEB overexpression exerted its anti-fibrotic effects on CFs. This highlighted the TFEB-Thbs1 axis as a potential novel target for developing therapeutic strategies to mitigate cardiac fibrosis.</p><p><strong>Conclusions: </strong>This study suggested that the protective effect of TFEB against MI injury was associated with the Thbs1/FA signaling pathway, providing a novel potential therapeutic target for cardiac fibrosis.</p>","PeriodicalId":10798,"journal":{"name":"Current gene therapy","volume":" ","pages":""},"PeriodicalIF":3.3,"publicationDate":"2026-04-03","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"147618503","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Selecting Candidates for Genetic Therapy: A Patient-Centered Framework.","authors":"Marc Henein, Yannis Trakadis","doi":"10.2174/0115665232471894260326103649","DOIUrl":"https://doi.org/10.2174/0115665232471894260326103649","url":null,"abstract":"<p><p>The rapid expansion of genetic therapies for the treatment of monogenic disorders represents one of the most transformative developments in contemporary medicine. Given the novelty, significant risks, and high costs of these treatments, there is a need for a systematic approach to patient selection. We propose a patient-centered framework for identifying candidates for genetic therapy based on five key clinical questions and demonstrate its application through illustrative examples.</p>","PeriodicalId":10798,"journal":{"name":"Current gene therapy","volume":" ","pages":""},"PeriodicalIF":3.3,"publicationDate":"2026-04-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"147948038","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Decoding Programmed Cell Death Genes: Innovations in Cancer Diagnosis and Treatment.","authors":"Aman Kumar, Balak Das Kurmi","doi":"10.2174/0115665232448221260312032539","DOIUrl":"https://doi.org/10.2174/0115665232448221260312032539","url":null,"abstract":"<p><p>Programmed cell death (PCD) profoundly influences cancer initiation, progression, and therapeutic response through interconnected pathways such as apoptosis, autophagy, ferroptosis, necroptosis, and pyroptosis. This perspective summarizes recent mechanistic insights, highlights pathway crosstalk, and underscores the diagnostic and therapeutic relevance of PCD-associated genes. Advances in biomarker discovery, targeted small molecules, and the immunomodulatory effects of PCD offer promising avenues for precision oncology. Emphasis is placed on ferroptosis as a rising therapeutic vulnerability and on addressing key challenges, including inflammatory toxicity, pathway switching, and biomarker standardization. Harnessing PCD with improved specificity may enable more effective and durable cancer treatments.</p>","PeriodicalId":10798,"journal":{"name":"Current gene therapy","volume":" ","pages":""},"PeriodicalIF":3.3,"publicationDate":"2026-03-30","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"147590498","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"CFTR mRNA-Based Gene Therapy for Cystic Fibrosis: A Mutation-Agnostic Strategy to Restore Ion Transport Function.","authors":"Jayendra Kumar, Mehetre Dattatraya Martand, Arpan Kumar Tripathi, Prabhat Agarwal, Hitesh Kumar, Shamim Shamim, Shadab Ali","doi":"10.2174/0115665232413980251103133741","DOIUrl":"https://doi.org/10.2174/0115665232413980251103133741","url":null,"abstract":"<p><p>Cystic fibrosis is a severe autosomal recessive disorder caused by mutations in the CFTR gene, leading to dysfunctional chloride ion transport across epithelial cells. This results in the accumulation of thick, sticky mucus, primarily affecting the lungs, pancreas, and gastrointestinal tract, leading to chronic respiratory infections and progressive lung damage. Although CFTR modulators have significantly improved outcomes for some patients, their efficacy is limited to specific mutations, leaving many without adequate treatment. CFTR-mRNA-based gene therapy serves as an advantageous therapeutic method for all mutations, independent of the treatment target. Through synthetic CFTR mRNA delivery to epithelial cells using this method, the cells can synthesize the functional CFTR protein required for proper ion transport and mucus hydration. mRNA therapy avoids nuclear entry and genomic integration, reducing the risk of insertional mutagenesis and long-term genetic alterations. Lipid nanoparticles, together with other non-viral delivery carriers, demonstrate significant potential to protect mRNA structures and enhance their ability to enter cells while promoting protein production. Research conducted using animal models has revealed that mRNA therapy leads to the successful restoration of CFTR function, accompanied by improved airway hydration outcomes. Ongoing challenges exist for this therapy, as mRNA encounters instability issues while triggering immune reactions and requires constant dose delivery. Multiple scientific research fields are collaborating on mRNA engineering advancements, along with the development of delivery technologies and combination therapy strategies, to overcome existing obstacles. The study examines current therapeutic approaches while assessing delivery pathways and pharmaceutical advancements, as well as expected research directions regarding CFTR-mRNA therapy, which demonstrates potential to treat all Cystic fibrosis patients through a single, comprehensive treatment.</p>","PeriodicalId":10798,"journal":{"name":"Current gene therapy","volume":" ","pages":""},"PeriodicalIF":3.3,"publicationDate":"2026-03-25","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"147615753","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Challenges in the Stability, Safety, and Efficacy of Antisense Oligonucleotide Therapeutics.","authors":"Mohini Santosh Jamadade, Rashmi Bhushan, Sakshi Ramesh Mahadik, Arka Karmakar, Naresh Dhanavath, Lalit Kumar, Krishna Murti, Nitesh Kumar","doi":"10.2174/0115665232388456251203140240","DOIUrl":"https://doi.org/10.2174/0115665232388456251203140240","url":null,"abstract":"<p><p>Antisense oligonucleotides represent a promising class of therapeutic agents due to their high specificity in modulating gene expression. These short, single-stranded synthetic sequences (typically 13-25 nucleotides) function by binding to complementary RNA targets, thereby influencing RNA processing or translation, primarily through RNase H-mediated degradation. Over the past decade, significant advances in chemical modifications and delivery strategies have led to a notable increase in the number of ASO-based therapies that have reached the market. Despite this progress, several challenges persist, including poor stability in biological fluids, limited cellular uptake, and safety concerns related to off-target effects and immunogenicity. This review provides a comprehensive overview of the mechanisms of action of ASOs, their pharmacological applications, current market status, and clinical progress. Special attention is given to evaluating in vitro and in vivo ASO stability using nanotechnology-based delivery approaches to improve pharmacokinetics/ pharmacodynamics and structural modifications to enhance therapeutic potential. Additionally, we discuss the associated adverse effects and propose strategies to mitigate them.</p>","PeriodicalId":10798,"journal":{"name":"Current gene therapy","volume":" ","pages":""},"PeriodicalIF":3.3,"publicationDate":"2026-03-19","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"147493620","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Cas9 Delivery: Focused Ultrasound and Nanotechnology Approaches.","authors":"Vatan Chaudhary, Atul Pratap Singh, Himanchal Sharma, Dhananjay Taumar, Anshu Gujjar, Iram Rajpoot","doi":"10.2174/0115665232391997251205093227","DOIUrl":"https://doi.org/10.2174/0115665232391997251205093227","url":null,"abstract":"<p><strong>Introduction: </strong>CRISPR-Cas9 enables precise genome editing but faces delivery challenges, including poor cellular uptake, off-target effects, and immune activation. Focused ultrasound (FUS) and nanotechnology-based carriers offer synergistic, non-invasive solutions, enhancing delivery efficiency, tissue penetration, and targeting.</p><p><strong>Methods: </strong>A systematic search (January 2010-March 2025) of PubMed, Web of Science, Scopus, Embase, and Google Scholar databases, preprint servers, and clinical trial registries identified studies employing FUS, nanoparticles (NPs), or combined approaches for CRISPR-Cas9 delivery. Eligible studies reported outcomes on efficiency, specificity, safety, or therapeutic effect in cell lines, animal models, or humans. Data extraction and quality assessment were performed by two independent reviewers. Narrative synthesis and meta-analysis were conducted where appropriate.</p><p><strong>Results: </strong>Forty-eight studies (21 in vitro, 19 in vivo, 8 clinical) met the inclusion criteria. NPmediated delivery achieved ~75% editing efficiency and enhanced stability versus viral or naked methods. FUS increased tissue penetration by threefold and reduced systemic toxicity. Combined FUS-NP systems improved blood-brain barrier penetration and maintained low off-target rates (>80% of studies) with minimal immune responses.</p><p><strong>Discussion: </strong>Hybrid FUS-NP delivery platforms address key barriers in CRISPR-Cas9 therapy, particularly for neurological, oncological, and genetic disorders. Nonetheless, heterogeneity in NP composition, ultrasound settings, and target genes limits direct comparability, and long-term clinical safety remains underexplored.</p><p><strong>Conclusion: </strong>FUS-assisted nanotechnology provides a promising non-viral strategy for precise, safe, and targeted CRISPR-Cas9 delivery. Standardization of technical parameters and regulatory frameworks are essential for successful clinical translation.</p>","PeriodicalId":10798,"journal":{"name":"Current gene therapy","volume":" ","pages":""},"PeriodicalIF":3.3,"publicationDate":"2026-03-19","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"147493590","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Gene Therapy for Hemophilia: Innovations, Milestones, and Future Prospects.","authors":"Dinesh Kumar, Vrinda Gupta, Rajni Tanwar, Nicky Kumar Jaiswal, Sonia Gupta","doi":"10.2174/0115665232391816251126073522","DOIUrl":"https://doi.org/10.2174/0115665232391816251126073522","url":null,"abstract":"<p><p>Haemophilia, a genetic bleeding disorder predominantly affecting males, arises from deficiencies or dysfunctions in clotting factors VIII or IX. Conventional treatments, such as frequent intravenous infusions of clotting factor concentrates, pose challenges in terms of cost, accessibility, and patient adherence. Gene therapy offers a transformative solution by correcting genetic mutations, enabling the body to produce clotting factors endogenously. Indian scientists have recently pioneered advances in this field, employing adeno-associated viral vectors for efficient and safe gene delivery. This approach addresses limitations of traditional therapies, including the development of inhibitors and the need for repetitive infusions. With the integration of cutting-edge genome editing technologies, such as CRISPR/Cas9, hemophilia treatment is poised for long-term efficacy and improved quality of life. Despite these promising developments, challenges remain, including affordability, ethical considerations, and equitable access. This paper highlights the latest breakthroughs, clinical advancements, and future directions in gene therapy for hemophilia, emphasizing India's significant contributions to global research. The findings underscore the potential of gene therapy to shift hemophilia management from routine care to curative strategies, redefining therapeutic possibilities for this chronic condition.</p>","PeriodicalId":10798,"journal":{"name":"Current gene therapy","volume":" ","pages":""},"PeriodicalIF":3.3,"publicationDate":"2026-03-16","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"147493660","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}