Cancer Biology & Therapy最新文献

{"title":"The dual role of leukotrienes in the tumor microenvironment: balancing pro-tumorigenic and anti-tumor immunity.","authors":"Andrew Thake, Maria Caruso, Sebastian Fernandez-Bussy, Keith Sacco","doi":"10.1080/15384047.2026.2692168","DOIUrl":"10.1080/15384047.2026.2692168","url":null,"abstract":"<p><strong>Background: </strong>Leukotrienes are bioactive lipid mediators produced via the 5-lipoxygenase (5-LO) pathway and are essential for inflammatory signaling in the tumor microenvironment (TME), playing roles in angiogenesis, immune modulation and metastatic progression.</p><p><strong>Objective: </strong>This review evaluates the role of leukotriene signaling in cancer progression and highlights biomarker-guided therapeutic strategies targeting these pathways in the TME.</p><p><strong>Methods: </strong>A narrative review of preclinical, clinical, and epidemiological studies was performed, with prespecified inclusion criteria and prioritization of recent evidence.</p><p><strong>Results: </strong>Leukotriene-mediated signaling correlates with biomarkers such as CysLT1 receptor expression, <i>β</i>-catenin activation, and HIF-1α signaling. In preclinical models, pharmacological agents including montelukast, zileuton, and FLAP antagonists suppress tumor growth, and restore apoptotic signaling; current clinical evidence remains largely observational and pharmacoepidemiologic.</p><p><strong>Conclusion: </strong>Targeting this pathway represents a promising avenue in oncology, with potential to enhance precision medicine through biomarker-guided patient stratification. Further clinical validation is warranted to translate these findings into therapeutic benefit.</p>","PeriodicalId":9536,"journal":{"name":"Cancer Biology & Therapy","volume":"27 1","pages":"2692168"},"PeriodicalIF":5.7,"publicationDate":"2026-12-31","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC13313223/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148307013","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Sorting nexin 10 promotes triple-negative breast cancer progression through modulating cholesterol biosynthesis via stabilizing SREBP2.","authors":"Yinping Guo, Jiahui Li, Wenjie Zhang, Min Xia, Gaohua Liu, Xiaolin Zhong, Yan Yi, Yajun Chen, Jing Zhong","doi":"10.1080/15384047.2026.2749334","DOIUrl":"10.1080/15384047.2026.2749334","url":null,"abstract":"<p><strong>Objective: </strong>Triple-negative breast cancer (TNBC) lacks effective therapeutics in clinical practice. Sorting nexin 10 (SNX10) plays essential roles in various cancers, and the role of SNX10 in TNBC remains unknown. This study investigated the role and action mechanism of SNX10 in TNBC.</p><p><strong>Methods: </strong>Using the Kaplan-Meier Plotter database and bc-GenExMiner database to analyze the SNX10 expression and clinical significance. Functional assays, including MTT, colony formation, transwell assays, and xenograft experiments, were used to evaluate the role of SNX10 in TNBC. The GeneChip PrimeView Human Gene Expression Array was used to determine the downstream targets and pathways. Cholesterol levels and the expression of enriched cholesterol synthesis genes were detected by Filipin assay, RT-PCR, and Western Blot. The relationship of SNX10 and cholesterol biosynthesis was confirmed using CO-IP and immunofluorescence staining assays.</p><p><strong>Results: </strong>SNX10 is positively related to poor prognosis of breast cancer and markedly up-regulated in TNBC. Knockdown of SNX10 suppressed cell proliferation, migration, and invasion, and slowed the tumor growth <i>in vivo</i>. Mechanistically, SNX10 positively regulates the content and distribution of cellular cholesterol, as does the expression of enriched cholesterol synthesis genes, and SNX10 interacts with SREBP2 and prolongs its half-life. Blocking with lovastatin, cholesterol, or siSREBP2 reversed these effects caused by altering SNX10 in TNBC cells <i>in vitro</i>.</p><p><strong>Conclusion: </strong>SNX10 promoted TNBC progression through the regulation of cholesterol biosynthesis, which was mediated by interaction with SREBP2 and maintenance of its stability. SNX10 may be an effective therapeutic target for TNBC, and our study provides new insights into therapeutic strategies.</p>","PeriodicalId":9536,"journal":{"name":"Cancer Biology & Therapy","volume":"27 1","pages":"2749334"},"PeriodicalIF":5.7,"publicationDate":"2026-12-31","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC13682392/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"149223361","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Validation of the important role and prognostic value of KIF14 in triple-negative breast cancer.","authors":"Jingjing Yuan, Meilin Zhang, Yaxuan Liu, Yiran Qiu, Mingdi Zhang, Hongliang Chen","doi":"10.1080/15384047.2025.2600705","DOIUrl":"10.1080/15384047.2025.2600705","url":null,"abstract":"<p><strong>Background: </strong>Triple-negative breast cancer (TNBC) is an aggressive subtype with a poor prognosis and limited treatment options. Elevated Kinesin Family Member 14 (KIF14) expression in breast cancer (BC) is correlated with poor prognosis, but its role in TNBC remains unclear.</p><p><strong>Methods: </strong>KIF14 expression was analyzed using TCGA, TIMER, and GEO databases, and its association with prognosis was assessed via Kaplan‒Meier plotter. Functional assays, including CCK-8, wound healing, and Transwell assays, were performed to evaluate KIF14's impact on TNBC cell proliferation, migration, and invasion. GO and KEGG analyses of transcriptome data were used to explore molecular mechanisms. The relationship between KIF14 expression and immune infiltration was assessed in the TIMER database. KIF14 expression in clinical samples was validated using qRT-PCR and immunohistochemistry, and its correlation with clinical features was examined.</p><p><strong>Results: </strong>KIF14 was significantly upregulated in BC (<i>P</i> < 0.05), and elevated KIF14 expression was associated with poor prognosis. KIF14 knockdown reduced cell proliferation, migration, and invasion. Network analysis revealed its involvement in lipid metabolism, NF-κB, PI3K-AKT, and mTOR signaling pathways. Immune infiltration analysis showed a significant association between KIF14 and immune cell types.</p><p><strong>Conclusion: </strong>KIF14 promotes TNBC progression and serves as a potential diagnostic and prognostic biomarker for TNBC.</p>","PeriodicalId":9536,"journal":{"name":"Cancer Biology & Therapy","volume":"26 1","pages":"2600705"},"PeriodicalIF":5.7,"publicationDate":"2025-12-31","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12919895/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145773462","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"YTHDF2 enhances proliferation and metastasis of nasopharyngeal carcinoma by mediating m6A modification in destabilizing FOXO1 mRNA.","authors":"Peng Yu, Wenyang Wei, Xinyun Peng, Jiemei Ye, Yuanli Ji, Bin Zhang, Yonglin Cai","doi":"10.1080/15384047.2025.2582349","DOIUrl":"10.1080/15384047.2025.2582349","url":null,"abstract":"<p><strong>Background: </strong>Aberrant N6-methyladenosine (m6A) modification is linked to cancer development and progression. However, the role of YTH N6-methyladenosine RNA binding protein F2 (YTHDF2), an m6A 'reader protein', in nasopharyngeal carcinoma (NPC) is poorly understood. This study aimed to clarify the role and mechanism of YTHDF2 in NPC development.</p><p><strong>Methods: </strong>Bioinformatics analysis was performed to identify the differential expression, prognostic value, and enriched pathways of YTHDF2 in patients with NPC. Quantitative PCR, western blotting, and immunohistochemistry were used to detect mRNA and protein expression. Biological function of YTHDF2 was investigated using <i>in vitro</i> experiments, including proliferation, wound healing, and invasion assays. RNA immunoprecipitation sequencing (RIP-seq), RIP-qPCR, and Methylated RNA immunoprecipitation sequencing (MeRIP-seq) were employed to determine if YTHDF2 modulates forkhead box O1 (FOXO1) expression through m6A modification.</p><p><strong>Results: </strong>YTHDF2 mRNA and protein levels were significantly increased in the NPC tissues and cell lines. Higher expression of YTHDF2 was associated with a poorer prognosis. Overexpressing YTHDF2 enhanced the NPC cell proliferation, migration, and invasion. Conversely, YTHDF2 knockdown inhibited these phenomena. Gene set enrichment analysis revealed that FOXO1-related signaling pathways were enriched in the YTHDF2-activated group. Mechanistically, YTHDF2 overexpression inhibited FOXO1 expression in NPC cells. RIP-seq, RIP-qPCR, and MeRIP-seq assays confirmed that YTHDF2 was bound to FOXO1 mRNA, reducing its stability and accelerated degradation.</p><p><strong>Conclusion: </strong>YTHDF2 potentially functions as an oncogene in NPC by binding to the m6A site of FOXO1, reducing its expression, thereby promoting malignant behavior. It may also be a viable biomarker and therapeutic target for NPC.</p>","PeriodicalId":9536,"journal":{"name":"Cancer Biology & Therapy","volume":"26 1","pages":"2582349"},"PeriodicalIF":4.6,"publicationDate":"2025-12-31","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12698064/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145713422","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Progress in the study of molecular markers in the prognosis assessment and recurrence patterns of glioblastoma.","authors":"Yuqing Hu, Xiaoqin Ge, Qianyun Xie, Ruishuang Ma, Qingsong Tao","doi":"10.1080/15384047.2025.2574179","DOIUrl":"10.1080/15384047.2025.2574179","url":null,"abstract":"<p><p>Glioblastoma multiforme (GBM), the most invasive primary malignant tumor of the central nervous system, is characterized by an extremely poor prognosis and a high recurrence rate. Its significant molecular heterogeneity challenges precise diagnosis and treatment. Recently, with the rapid development of molecular pathology, the combination of histological and molecular typing has become the mainstream method for GBM diagnosis. Here, we review the impact of classic molecular markers on patient prognosis in GBM, as well as the different values of traditional and novel molecular markers in prognosis assessment. We initially discuss the correlation between molecular markers and recurrence, as well as the research progress of molecular markers in emerging technological fields. Moreover, we propose the challenges currently faced by molecular markers in glioblastoma and discuss future research directions in this field.</p>","PeriodicalId":9536,"journal":{"name":"Cancer Biology & Therapy","volume":"26 1","pages":"2574179"},"PeriodicalIF":4.6,"publicationDate":"2025-12-31","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12599557/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145457630","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"<b>ARNTL2 regulated the oncogene c-myc and promoted the progression of esophageal cancer through activating</b> <i><b>ANXA2</b></i> <b>transcription</b>.","authors":"Yanzi Qin, Hongfei Ci, Zhaoyi Wang, Yandie Zhang, Xifeng Xu, Qiang Wu","doi":"10.1080/15384047.2025.2574544","DOIUrl":"10.1080/15384047.2025.2574544","url":null,"abstract":"<p><strong>Objective: </strong>Aryl hydrocarbon receptor nuclear transporter-like 2 (ARNTL2) can bind to clock circadian regulator (CLOCK) to regulate gene expression and is abnormally expressed in various cancers. Nevertheless, its effects on esophageal cancer (ESCC) are unclear. This work can uncover the intriguing mechanism of ARNTL2 in ESCC.</p><p><strong>Methods: </strong>Malignant phenotypes including cell proliferation, invasion, migration, and epithelial mesenchymal transition (EMT), were investigated. We established a BALB/c nude mouse (5-6 weeks) model with ESCC to verify the influence of ARNTL2/ANXA2/C-MYC axis. ESCC tissues (<i>n</i> = 100) and paired adjacent normal tissues (<i>n</i> = 100) from patients with ESCC were collected. The recruitment of ARNTL2 and CLOCK in <i>ANXA2</i> promoter was studied by ChIP and dual-luciferase reporter assay. RIP and RNA pulldown were used to explore the relationship between ANXA2 and <i>C-MYC</i> mRNA.</p><p><strong>Results: </strong>Compared to adjacent normal tissues, ESCC tissues developed the significant increase <i>ARNTL2</i>, <i>ANXA2,</i> and <i>C-MYC</i>. ARNTL2, which interacts with CLOCK, was recruited in <i>ANXA2</i> promoter and elevated ANXA2. ARNTL2 silence reduced cell proliferation, migration and invasion and inhibited EMT, which was reversed by ANXA2 overexpression. ANXA2 can bind to the 3'UTR of <i>C-MYC</i> transcript; further assays confirmed that ANXA2 increased the protein abundance of C-MYC. ANXA2 knockdown resulted in a decrease in malignant phenotypes, whereas C-MYC overexpression reversed these changes. ARNTL2 silence inhibited the formation, growth and EMT of subcutaneous tumors and suppressed C-MYC; ANXA2 overexpression reversed these alterations.</p><p><strong>Conclusion: </strong>ARNTL2 activated the transcription of <i>ANXA2</i>, which interacts with <i>C-MYC</i> transcript, promoting the development of malignant behaviors of ESCC cells.</p>","PeriodicalId":9536,"journal":{"name":"Cancer Biology & Therapy","volume":"26 1","pages":"2574544"},"PeriodicalIF":4.6,"publicationDate":"2025-12-31","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12629337/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145534449","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Yes-associated protein 1 in cancer: bridging mechanical transduction and epigenetic regulation.","authors":"Tingting Liu, Shuo Yu, Lu Zhang, Wenwen Ji, Guangdong Wang, Na Wang, Mengcong Li, Tinghua Hu, Zhihong Shi","doi":"10.1080/15384047.2025.2562726","DOIUrl":"10.1080/15384047.2025.2562726","url":null,"abstract":"<p><p>Yes-associated protein 1 (YAP1) and its paralog TAZ serve as central mechanotransductive transcription coactivators that integrate mechanical cues from the extracellular matrix, such as stiffness and fluid shear stress, with epigenetic modifications to drive oncogenic processes. They regulate diverse biological functions, including proliferation, metastasis, immune evasion, autophagy, ferroptosis, and metabolism. This review highlights how YAP1/TAZ signaling is modulated by mechanosensitive pathways (Integrin/FAK, Rho GTPases) and epigenetic mechanisms (m6A methylation, DNA methylation), contributing to therapy resistance and disease progression. Targeting the mechano-epigenetic axis of YAP1/TAZ offers promising therapeutic strategies for cancer treatment.</p>","PeriodicalId":9536,"journal":{"name":"Cancer Biology & Therapy","volume":"26 1","pages":"2562726"},"PeriodicalIF":4.6,"publicationDate":"2025-12-31","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12456216/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145112070","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Patient-derived organoids (PDOs) as a promising platform for personalized treatment of colorectal cancer: current applications and future challenges.","authors":"Yan Liu, Yao Zhang, Ran Zhang, Chengzhao Zhang, Xinlu Liu","doi":"10.1080/15384047.2025.2567802","DOIUrl":"10.1080/15384047.2025.2567802","url":null,"abstract":"<p><p>Colorectal cancer is a heterogeneous and molecularly complex cancer that often leads to poor prognosis. The standard treatment includes surgical resection and adjuvant therapies such as chemotherapy, radiotherapy, targeted therapy, and immunotherapy. However, owing to the individual heterogeneity of patients, the effectiveness of these treatments is difficult to achieve consistently and efficiently. Patient-derived organoids (PDOs), by mimicking key genes, physical, and mechanical cues from the tumor microenvironment, simulates tumor heterogeneity, tissue structure, and molecular characteristics, as well as the cellular interactions within the tumor microenvironment. Additionally, it provides a more physiological and relevant environment for anticancer drug screening and predicting patient responses to personalized approaches, bridging the gap between simplified 2D models and animal models. Here, we review the roles of PDOs in customizing CRC treatment, discussing its roles in predicting drug sensitivity, drug screening, studying drug resistance mechanisms, simulating cell-to-cell interactions, and exploring immunotherapy targets to develop personalized therapies.</p>","PeriodicalId":9536,"journal":{"name":"Cancer Biology & Therapy","volume":"26 1","pages":"2567802"},"PeriodicalIF":4.6,"publicationDate":"2025-12-31","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12530486/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145285742","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Correction.","authors":"","doi":"10.1080/15384047.2025.2585668","DOIUrl":"10.1080/15384047.2025.2585668","url":null,"abstract":"","PeriodicalId":9536,"journal":{"name":"Cancer Biology & Therapy","volume":"26 1","pages":"2585668"},"PeriodicalIF":5.7,"publicationDate":"2025-12-31","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12677740/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145451077","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"High-throughput screening identifies the activity of histone deacetylase inhibitors in patient-derived models of soft tissue sarcoma.","authors":"Molly R Danks, Piotr J Manasterski, Henry Beetham, John C Dawson, Richard J R Elliott, Jayne Culley, Rashi Krishna, Morwenna Muir, John P Thomson, Ailsa J Oswald, Ailith Ewing, William G J Kerrison, Paul H Huang, Ioanna Nixon, Neil O Carragher, Valerie G Brunton","doi":"10.1080/15384047.2025.2589666","DOIUrl":"10.1080/15384047.2025.2589666","url":null,"abstract":"<p><strong>Background: </strong>Undifferentiated pleomorphic sarcoma (UPS) is a rare and aggressive soft tissue sarcoma with limited treatment options and a poor prognosis. As a complex karyotype tumor, UPS lacks recurrent targetable mutations, and response rates to standard first-line doxorubicin therapy are low. Phenotypic drug screening offers an alternative approach to identify new therapeutic targets without requiring prior knowledge of molecular mechanisms.</p><p><strong>Methods: </strong>A library of FDA-approved compounds and a custom histone deacetylase (HDAC) inhibitor library were screened using well-annotated patient-derived cell lines. Hit compounds were further characterized using apoptosis assays and <i>in vivo</i> xenograft studies. Biomarkers of activity were evaluated using gene expression and western blot analyses. Synergy with doxorubicin was evaluated in combination assays.</p><p><strong>Results: </strong>HDAC inhibitors emerged as a promising therapeutic class, demonstrating low IC₅₀ values across cell lines (14.8-26.89 nM), with quisinostat taken forward for further evaluation. Gene expression changes in <i>EPAS1, FOXO1, AMOT,</i> and <i>FOSL1</i> were observed as potential biomarkers of activity. Combination assays revealed synergy between quisinostat and doxorubicin (average ZIP score: 1.02-15.65; ZIP_max: 3.98-33.71), increasing apoptotic cell death <i>in vitro</i>. <i>In vivo</i>, quisinostat alone and in combination with doxorubicin significantly reduced the tumor volume (vehicle 160.0 ± 63.2 mm³, doxorubicin 78.0 ± 35.2 mm³, quisinostat 84.3 ± 13.1 mm³, and combination 49.2 ± 10.2 mm³). Quisinostat also showed potent activity in leiomyosarcoma (LMS) cell lines (5.82-31.32 nM), which represent an additional complex karyotype soft tissue sarcoma.</p><p><strong>Conclusions: </strong>Quisinostat demonstrated strong preclinical activity and synergy with standard-of-care doxorubicin in models of UPS and LMS.</p>","PeriodicalId":9536,"journal":{"name":"Cancer Biology & Therapy","volume":"26 1","pages":"2589666"},"PeriodicalIF":4.6,"publicationDate":"2025-12-31","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12667636/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145630361","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}