Cancer gene therapy最新文献_第10页

Enhanced epithelial-mesenchymal transition signatures are linked with adverse tumor microenvironment, angiogenesis and worse survival in gastric cancer 上皮-间质转化特征的增强与不良肿瘤微环境、血管生成和胃癌患者生存率下降有关。

IF 6.4 3区医学

Cancer gene therapy Pub Date : 2024-03-26 DOI: 10.1038/s41417-024-00756-w

Masanori Oshi, Arya Mariam Roy, Li Yan, Sachika Kinoshita, Yuko Tamura, Takashi Kosaka, Hirotoshi Akiyama, Chikara Kunisaki, Kazuaki Takabe, Itaru Endo

{"title":"Enhanced epithelial-mesenchymal transition signatures are linked with adverse tumor microenvironment, angiogenesis and worse survival in gastric cancer","authors":"Masanori Oshi, Arya Mariam Roy, Li Yan, Sachika Kinoshita, Yuko Tamura, Takashi Kosaka, Hirotoshi Akiyama, Chikara Kunisaki, Kazuaki Takabe, Itaru Endo","doi":"10.1038/s41417-024-00756-w","DOIUrl":"10.1038/s41417-024-00756-w","url":null,"abstract":"Epithelial-mesenchymal transition (EMT) is a crucial mechanism that facilitates cancer cell metastasis. Despite its importance, the clinical significance of EMT in gastric cancer (GC) patients has yet to be clearly demonstrated. For gauging the extent of EMT in GC, we employed gene set variation analysis to score 807 patient samples from two large cohorts: TCGA and GSE84437. In both cohorts, EMT high GC showed a significant association with worse overall survival (hazard ratio (HR) = 1.74, p = 0.011 and HR = 2.01, p < 0.001, respectively). This association was stronger when considering the EMT signature score compared to the individual expressions of EMT-related genes (CDH1, CDH2, VIM, and FN1). While the EMT signature level did not differ among various cancers, high EMT signature specifically correlated with survival in GC alone. Mucinous and diffuse histological types exhibited higher EMT levels compared to others (p < 0.001), and the EMT signature level was correlated with tumor depth and AJCC stage (all p < 0.001). Interestingly, the EMT score was an independent factor for overall and disease-specific survival (multivariate; p = 0.006 and 0.032, respectively). EMT high GC displayed a lower fraction of Th1 cells and a higher fraction of dendritic cells, M1 macrophages and several stromal cells. EMT high GC exhibited an inverse correlation with cell proliferation-related gene sets. While they significantly enriched multiple pro-cancerous gene sets, such as TGF-β signaling, hypoxia, and angiogenesis. The presence of EMT signature in a bulk tumor was linked to TGF-β signaling, hypoxia, and angiogenesis, and was also associated with poorer survival outcomes in GC patients.","PeriodicalId":9577,"journal":{"name":"Cancer gene therapy","volume":"31 5","pages":"746-754"},"PeriodicalIF":6.4,"publicationDate":"2024-03-26","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"140292895","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}

引用次数: 0

miR-124-3p and miR-194-5p regulation of the PI3K/AKT pathway via ROR2 in medulloblastoma progression miR-124-3p和miR-194-5p通过ROR2调控髓母细胞瘤进展中的PI3K/AKT通路

IF 4.8 3区医学

Cancer gene therapy Pub Date : 2024-03-19 DOI: 10.1038/s41417-024-00762-y

Chen Wang, Runxi Fu, Yunkun Wang, Jia Wei, Ying Yu, Liuhua Hu, Chenran Zhang

{"title":"miR-124-3p and miR-194-5p regulation of the PI3K/AKT pathway via ROR2 in medulloblastoma progression","authors":"Chen Wang, Runxi Fu, Yunkun Wang, Jia Wei, Ying Yu, Liuhua Hu, Chenran Zhang","doi":"10.1038/s41417-024-00762-y","DOIUrl":"10.1038/s41417-024-00762-y","url":null,"abstract":"Medulloblastoma (MB), a prevalent pediatric central nervous system tumor, is influenced by microRNAs (miRNAs) that impact tumor initiation and progression. However, the specific involvement of miRNAs in MB tumorigenesis remains unclear. Using single-cell RNA sequencing, we identified ROR2 expression in normal human fetal cerebellum. Subsequent analyses, including immunofluorescence, quantitative real-time PCR (qRT-PCR), and Western blot, assessed ROR2 expression in MB tissues and cell lines. We investigated miR-124-3p and miR-194-5p and their regulatory role in ROR2 expression through the dual-luciferase reporter, qRT-PCR, and western blot assays. Mechanistic insights were gained through functional assays exploring the impact of miR-124-3p, miR-194-5p, and ROR2 on MB growth in vitro and in vivo. We observed significantly reduced miR-124-3p and miR-194-5p expression and elevated ROR2 expression in MB tissues and cell lines. High ROR2 expression inversely correlated with overall survival in WNT and SHH subgroups of MB patients. Functionally, overexpressing miR-124-3p and miR-194-5p and inhibiting ROR2 suppressed in vitro malignant transformation and in vivo tumorigenicity. Mechanistically, miR-124-3p and miR-194-5p synergistically regulated the ROR2/PI3K/Akt pathway, influencing MB progression. Our findings indicate that miR-124-3p and miR-194-5p function as tumor suppressors, inhibiting MB progression via the ROR2/PI3K/Akt axis, suggesting a key mechanism and therapeutic targets for MB patients.","PeriodicalId":9577,"journal":{"name":"Cancer gene therapy","volume":"31 6","pages":"941-954"},"PeriodicalIF":4.8,"publicationDate":"2024-03-19","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.nature.com/articles/s41417-024-00762-y.pdf","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"140617780","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}

引用次数: 0

Heterogeneity of hepatocellular carcinoma: from mechanisms to clinical implications 肝细胞癌的异质性：从机制到临床意义。

IF 4.8 3区医学

Cancer gene therapy Pub Date : 2024-03-18 DOI: 10.1038/s41417-024-00764-w

Fatema Safri, Romario Nguyen, Shadi Zerehpooshnesfchi, Jacob George, Liang Qiao

引用次数: 0

Hippo pathway in non-small cell lung cancer: mechanisms, potential targets, and biomarkers 非小细胞肺癌中的希波通路：机制、潜在靶点和生物标志物

IF 6.4 3区医学

Cancer gene therapy Pub Date : 2024-03-18 DOI: 10.1038/s41417-024-00761-z

Hongge Liang, Yan Xu, Jing Zhao, Minjiang Chen, Mengzhao Wang

{"title":"Hippo pathway in non-small cell lung cancer: mechanisms, potential targets, and biomarkers","authors":"Hongge Liang, Yan Xu, Jing Zhao, Minjiang Chen, Mengzhao Wang","doi":"10.1038/s41417-024-00761-z","DOIUrl":"10.1038/s41417-024-00761-z","url":null,"abstract":"Lung cancer is the primary contributor to cancer-related deaths globally, and non-small cell lung cancer (NSCLC) constitutes around 85% of all lung cancer cases. Recently, the emergence of targeted therapy and immunotherapy revolutionized the treatment of NSCLC and greatly improved patients’ survival. However, drug resistance is inevitable, and extensive research has demonstrated that the Hippo pathway plays a crucial role in the development of drug resistance in NSCLC. The Hippo pathway is a highly conserved signaling pathway that is essential for various biological processes, including organ development, maintenance of epithelial balance, tissue regeneration, wound healing, and immune regulation. This pathway exerts its effects through two key transcription factors, namely Yes-associated protein (YAP) and transcriptional co-activator PDZ-binding motif (TAZ). They regulate gene expression by interacting with the transcriptional-enhanced associate domain (TEAD) family. In recent years, this pathway has been extensively studied in NSCLC. The review summarizes a comprehensive overview of the involvement of this pathway in NSCLC, and discusses the mechanisms of drug resistance, potential targets, and biomarkers associated with this pathway in NSCLC.","PeriodicalId":9577,"journal":{"name":"Cancer gene therapy","volume":"31 5","pages":"652-666"},"PeriodicalIF":6.4,"publicationDate":"2024-03-18","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.nature.com/articles/s41417-024-00761-z.pdf","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"140155521","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}

引用次数: 0

The pleiotropic nature of NONO, a master regulator of essential biological pathways in cancers 癌症重要生物通路的主调控因子 NONO 的多效性。

IF 4.8 3区医学

Cancer gene therapy Pub Date : 2024-03-16 DOI: 10.1038/s41417-024-00763-x

Domenica Ronchetti, Valentina Traini, Ilaria Silvestris, Giuseppina Fabbiano, Francesco Passamonti, Niccolò Bolli, Elisa Taiana

{"title":"The pleiotropic nature of NONO, a master regulator of essential biological pathways in cancers","authors":"Domenica Ronchetti, Valentina Traini, Ilaria Silvestris, Giuseppina Fabbiano, Francesco Passamonti, Niccolò Bolli, Elisa Taiana","doi":"10.1038/s41417-024-00763-x","DOIUrl":"10.1038/s41417-024-00763-x","url":null,"abstract":"NONO is a member of the Drosophila behavior/human splicing (DBHS) family of proteins. NONO is a multifunctional protein that acts as a “molecular scaffold” to carry out versatile biological activities in many aspects of gene regulation, cell proliferation, apoptosis, migration, DNA damage repair, and maintaining cellular circadian rhythm coupled to the cell cycle. Besides these physiological activities, emerging evidence strongly indicates that NONO-altered expression levels promote tumorigenesis. In addition, NONO can undergo various post-transcriptional or post-translational modifications, including alternative splicing, phosphorylation, methylation, and acetylation, whose impact on cancer remains largely to be elucidated. Overall, altered NONO expression and/or activities are a common feature in cancer. This review provides an integrated scenario of the current understanding of the molecular mechanisms and the biological processes affected by NONO in different tumor contexts, suggesting that a better elucidation of the pleiotropic functions of NONO in physiology and tumorigenesis will make it a potential therapeutic target in cancer. In this respect, due to the complex landscape of NONO activities and interactions, we highlight caveats that must be considered during experimental planning and data interpretation of NONO studies.","PeriodicalId":9577,"journal":{"name":"Cancer gene therapy","volume":"31 7","pages":"984-994"},"PeriodicalIF":4.8,"publicationDate":"2024-03-16","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.nature.com/articles/s41417-024-00763-x.pdf","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"140140027","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}

引用次数: 0

MISEV2023: Shaping the Future of EV Research by Enhancing Rigour, Reproducibility and Transparency MISEV2023：通过提高严谨性、可重复性和透明度塑造电动汽车研究的未来。

IF 6.4 3区医学

Cancer gene therapy Pub Date : 2024-03-14 DOI: 10.1038/s41417-024-00759-7

Mark Samuels, Georgios Giamas

引用次数: 0

Adeno-associated virus-mediated trastuzumab delivery to the central nervous system for human epidermal growth factor receptor 2+ brain metastasis 腺相关病毒介导的曲妥珠单抗向中枢神经系统输送治疗人类表皮生长因子受体 2+ 脑转移瘤的药物

IF 6.4 3区医学

Cancer gene therapy Pub Date : 2024-03-13 DOI: 10.1038/s41417-024-00751-1

Marcela S. Werner, Shweta Aras, Ashleigh R. Morgan, Jillian Roamer, Nesteene J. Param, Kanyin Olagbegi, R. Jason Lamontagne, Jenny A. Greig, James M. Wilson

{"title":"Adeno-associated virus-mediated trastuzumab delivery to the central nervous system for human epidermal growth factor receptor 2+ brain metastasis","authors":"Marcela S. Werner, Shweta Aras, Ashleigh R. Morgan, Jillian Roamer, Nesteene J. Param, Kanyin Olagbegi, R. Jason Lamontagne, Jenny A. Greig, James M. Wilson","doi":"10.1038/s41417-024-00751-1","DOIUrl":"10.1038/s41417-024-00751-1","url":null,"abstract":"Trastuzumab improves overall survival for HER2+ breast cancer, but its short half-life in the cerebrospinal fluid (~2–4 days) and delivery limitations restrict the ability to target HER2+ central nervous system (CNS) disease. We developed an adeno-associated virus (AAV) vector expressing a codon-optimized, ubiquitin C (UbC)-promoter-driven trastuzumab sequence (AAV9.UbC.trastuzumab) for intrathecal administration. Transgene expression was evaluated in adult Rag1 knockout mice and rhesus nonhuman primates (NHPs) after a single intracerebroventricular (ICV) or intra-cisterna magna (ICM) AAV9.UbC.trastuzumab injection, respectively, using real-time PCR, ELISA, Western blot, in situ hybridization, single-nucleus RNA sequencing, and liquid chromatography-mass spectrometry; antitumor efficacy was evaluated in brain xenografts using HER2+ breast cancer cell lines (BT-474, MDA-MB-453). Transgene expression was detected in brain homogenates of Rag1 knockout mice following a single ICV injection of AAV9.UbC.trastuzumab (1 × 1011 vector genome copies [GC]/mouse) and tumor progression was inhibited in xenograft models of breast-to-brain metastasis. In NHPs, ICM delivery of AAV9.UbC.trastuzumab (3 × 1013 GC/animal) was well tolerated (36–37 days in-life) and resulted in transgene expression in CNS tissues and cerebrospinal fluid at levels sufficient to induce complete tumor remission in MDA-MB-453 brain xenografts. With AAV9’s proven clinical safety record, this gene therapy may represent a viable approach for targeting HER2 + CNS malignancies.","PeriodicalId":9577,"journal":{"name":"Cancer gene therapy","volume":"31 5","pages":"766-777"},"PeriodicalIF":6.4,"publicationDate":"2024-03-13","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"140116208","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}

引用次数: 0

Caffeic acid phenethyl ester suppresses the expression of androgen receptor variant 7 via inhibition of CDK1 and AKT 咖啡酸苯乙酯通过抑制 CDK1 和 AKT 抑制雄激素受体变体 7 的表达。

IF 4.8 3区医学

Cancer gene therapy Pub Date : 2024-03-13 DOI: 10.1038/s41417-024-00753-z

Ying-Yu Kuo, Chieh Huo, Chia-Yang Li, Chih-Pin Chuu

{"title":"Caffeic acid phenethyl ester suppresses the expression of androgen receptor variant 7 via inhibition of CDK1 and AKT","authors":"Ying-Yu Kuo, Chieh Huo, Chia-Yang Li, Chih-Pin Chuu","doi":"10.1038/s41417-024-00753-z","DOIUrl":"10.1038/s41417-024-00753-z","url":null,"abstract":"Androgen receptor (AR) splice variant 7 (AR-V7) is capable to enter nucleus and activate downstream signaling without ligand. AR-V7 assists the tumor growth, cancer metastasis, cancer stemness, and the evolvement of therapy-resistant prostate cancer (PCa). We discovered that caffeic acid phenethyl ester (CAPE) can repress the expression and downstream signaling of AR-V7 in PCa cells. CAPE blocked the gene transcription, nuclear localization, and protein abundance of AR-V7. CAPE inhibited the expression of U2AF65, SF2 and hnRNPF, which were splicing factors for AR-V7 intron. Additionally, CAPE decreased protein stability of AR-V7 and enhanced the proteosome-degradation of AR-V7. We observed that CDK1 and AKT regulated the expression and stability of AR-V7 via phosphorylation of Ser81 and Ser213, respectively. CAPE decreased the expression of CDK1 and AKT. Overexpression of CDK1 restored the abundance of AR-V7 in CAPE-treated PCa cells. Overexpression of AR-V7, AKT or CDK1 rescued the proliferation of PCa cells under CAPE treatment. Intraperitoneal injection of 10 mg/kg CAPE retarded the growth of 22Rv1 xenografts in nude mice and suppressed the protein levels of AR-V7, CDK1 and AKT in 22Rv1 xenografts. Our study provided the rationale of applying CAPE for inhibition of AR-V7 in prostate tumors.","PeriodicalId":9577,"journal":{"name":"Cancer gene therapy","volume":"31 6","pages":"807-815"},"PeriodicalIF":4.8,"publicationDate":"2024-03-13","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"140118849","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}

引用次数: 0

Romidepsin exhibits anti-esophageal squamous cell carcinoma activity through the DDIT4-mTORC1 pathway 罗米地辛通过 DDIT4-mTORC1 通路显示抗食管鳞状细胞癌活性

IF 6.4 3区医学

Cancer gene therapy Pub Date : 2024-03-13 DOI: 10.1038/s41417-024-00760-0

Wei-Feng Xia, Xiao-Li Zheng, Wen-Yi Liu, Yu-Tang Huang, Chun-Jie Wen, Hong-Hao Zhou, Qing-Chen Wu, Lan-Xiang Wu

{"title":"Romidepsin exhibits anti-esophageal squamous cell carcinoma activity through the DDIT4-mTORC1 pathway","authors":"Wei-Feng Xia, Xiao-Li Zheng, Wen-Yi Liu, Yu-Tang Huang, Chun-Jie Wen, Hong-Hao Zhou, Qing-Chen Wu, Lan-Xiang Wu","doi":"10.1038/s41417-024-00760-0","DOIUrl":"10.1038/s41417-024-00760-0","url":null,"abstract":"Esophageal squamous cell carcinoma (ESCC) is one of the most common human malignancies worldwide and is associated with high morbidity and mortality. Current treatment options are limited, highlighting the need for development of novel effective agents. Here, a high-throughput drug screening (HTS) was performed using ESCC cell lines in both two- and three-dimensional culture systems to screen compounds that have anti-ESCC activity. Our screen identified romidepsin, a histone deactylase inhibitor, as a potential anti-ESCC agent. Romidepsin treatment decreased cell viability, induced apoptosis and cell cycle arrest in ESCC cell lines, and these findings were confirmed in ESCC cell line-derived xenografted (CDX) mouse models. Mechanically, romidepsin induced transcriptional upregulation of DNA damage-inducible transcript 4 (DDIT4) gene by histone hyperacetylation at its promoter region, leading to the inhibition of mammalian target of rapamycin complex 1 (mTORC1) pathway. Furthermore, romidepsin exhibited better efficacy and safety compared to the conventional therapeutic drugs in ESCC patient-derived xenografted (PDX) mouse models. These data indicate that romidepsin may be a novel option for anti-ESCC therapy.","PeriodicalId":9577,"journal":{"name":"Cancer gene therapy","volume":"31 5","pages":"778-789"},"PeriodicalIF":6.4,"publicationDate":"2024-03-13","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"140115856","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}

引用次数: 0

The integrate profiling of single-cell and spatial transcriptome RNA-seq reveals tumor heterogeneity, therapeutic targets, and prognostic subtypes in ccRCC 单细胞和空间转录组 RNA-seq 的整合分析揭示了 ccRCC 的肿瘤异质性、治疗靶点和预后亚型。

IF 4.8 3区医学

Cancer gene therapy Pub Date : 2024-03-13 DOI: 10.1038/s41417-024-00755-x

Yanlong Zhang, Xuefeng Huang, Minghang Yu, Menghan Zhang, Li Zhao, Yong Yan, Liyun Zhang, Xi Wang

{"title":"The integrate profiling of single-cell and spatial transcriptome RNA-seq reveals tumor heterogeneity, therapeutic targets, and prognostic subtypes in ccRCC","authors":"Yanlong Zhang, Xuefeng Huang, Minghang Yu, Menghan Zhang, Li Zhao, Yong Yan, Liyun Zhang, Xi Wang","doi":"10.1038/s41417-024-00755-x","DOIUrl":"10.1038/s41417-024-00755-x","url":null,"abstract":"Clear-cell renal cell carcinoma (ccRCC) is the most common type of RCC; however, the intratumoral heterogeneity in ccRCC remains unclear. We first identified markers and biological features of each cell cluster using bioinformatics analysis based on single-cell and spatial transcriptome RNA-sequencing data. We found that gene copy number loss on chromosome 3p and amplification on chromosome 5q were common features in ccRCC cells. Meanwhile, NNMT and HILPDA, which are associated with the response to hypoxia and metabolism, are potential therapeutic targets for ccRCC. In addition, CD8+ exhausted T cells (LAG3+ HAVCR2+), CD8+ proliferated T cells (STMN+), and M2-like macrophages (CD68+ CD163+ APOC1+), which are closely associated with immunosuppression, played vital roles in ccRCC occurrence and development. These results were further verified by whole exome sequencing, cell line and xenograft experiments, and immunofluorescence staining. Finally, we divide patients with ccRCC into three subtypes using unsupervised cluster analysis. and generated a classifier to reproduce these subtypes using the eXtreme Gradient Boosting algorithm. Our classifier can help clinicians evaluate prognosis and design personalized treatment strategies for ccRCC. In summary, our work provides a new perspective for understanding tumor heterogeneity and will aid in the design of antitumor therapeutic strategies for ccRCC.","PeriodicalId":9577,"journal":{"name":"Cancer gene therapy","volume":"31 6","pages":"917-932"},"PeriodicalIF":4.8,"publicationDate":"2024-03-13","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"140118850","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}

引用次数: 0