Translational Oncology最新文献

{"title":"Exploring the therapeutic role of thiabendazole in lung adenocarcinoma via network pharmacology and single-cell analysis.","authors":"Wanghong Qi, Guoqiu Xu, Lang Tang, Chunlin Ye, Xi Liu","doi":"10.1016/j.tranon.2025.102548","DOIUrl":"https://doi.org/10.1016/j.tranon.2025.102548","url":null,"abstract":"<p><strong>Background: </strong>Lung adenocarcinoma (LUAD) is the leading cause of cancer-related deaths globally, with over 2.2 million new cases in 2020. Despite advances in targeted therapies, challenges such as drug resistance and severe side effects persist. Thiabendazole, an antiparasitic drug, has shown potential anticancer effects in LUAD.</p><p><strong>Methods: </strong>This study used network pharmacology, integrating single-cell RNA sequencing (scRNA-seq) data (GSE136103), GEO transcriptome datasets (GSE10072, GSE19188, GSE19804, GSE30219, GSE40791), and bioinformatics tools to explore Thiabendazole's mechanisms in LUAD. Potential targets were predicted through PubChem and SwissTargetPrediction. scRNA-seq data were analyzed using Seurat, and key genes and pathways were identified via Weighted Gene Co-expression Network Analysis (WGCNA) and multi-omics integration. Diagnostic genes were further screened using LASSO regression, Support Vector Machine (SVM), and random forest (RF) models.</p><p><strong>Results: </strong>Single-cell analysis revealed macrophages as key targets of Thiabendazole. Transcriptomic analysis identified 2034 downregulated and 2388 upregulated genes. WGCNA found a core gene module (MEred) strongly correlated with Thiabendazole (r = 0.75, p = 2e-07). Four diagnostic genes-ACE, ALDOA, MME, and PMP22-showed high accuracy (0.982). Thiabendazole also modulated immune cell infiltration, particularly affecting macrophage activity. Molecular docking confirmed stable binding to ACE, ALDOA, and MME.</p><p><strong>Conclusion: </strong>Thiabendazole demonstrates promising anticancer potential in LUAD, influencing key genes and immune pathways. It may serve as an effective therapeutic agent targeting both cancer cells and the tumor microenvironment.</p>","PeriodicalId":23244,"journal":{"name":"Translational Oncology","volume":"62 ","pages":"102548"},"PeriodicalIF":4.1,"publicationDate":"2025-10-22","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145356009","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Propofol inhibits glioma growth by blocking the formation of the NF-κB/LGI4 feedback loop to activate TP53 self-transcription.","authors":"Zhi Wang, Li-Na Zhang, Ting Wu, Xu Pan, Le Li","doi":"10.1016/j.tranon.2025.102578","DOIUrl":"https://doi.org/10.1016/j.tranon.2025.102578","url":null,"abstract":"<p><p>Accumulating evidence has clarified the anti-cancer function of propofol (PPF) in glioma. However, the underlying regulatory mechanism still remains not fully understood. Our current study screens out a novel gene-leucine-rich glioma-inactivated 4 (LGI4), as a target molecule of PPF, and shows that 10 μg/ml of PPF (a clinically relevant concentration commonly used in multiple previous studies) suppresses the NF-κB signaling pathway to inhibit LGI4 transcription in glioma cells. Clinically, the expression of LGI4 is upregulated in glioma tissues, and its high expression correlates with unfavorable prognosis. Functionally and mechanically, LGI4 promotes tumor growth through blocking TP53 self-transcription by binding to p53 and hindering its nuclear import. Significantly, LGI4 is not only transcriptionally activated by the NF-κB signaling pathway but also feedback activates NF-κB signaling by inhibiting the interaction of IKIP with the IKKα/IKKβ/NEMO complex. Importantly, PPF treatment can break this positive feedback loop. Collectively, our findings uncover that PPF upregulates p53 expression by disrupting the NF-κB/LGI4 feedback loop, thereby inhibiting glioma growth, highlighting it is a potential therapeutic target for future glioma treatment.</p>","PeriodicalId":23244,"journal":{"name":"Translational Oncology","volume":"62 ","pages":"102578"},"PeriodicalIF":4.1,"publicationDate":"2025-10-22","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145355937","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Knockdown of LRP11-AS1 inhibits papillary thyroid tumor growth by modulating miR-615-3p/AKT2 axis.","authors":"Peng Li, Zhongguang Wu, Lanlan Li, Yudan Chen, Chi Zhang, Weidong Zheng","doi":"10.1016/j.tranon.2025.102574","DOIUrl":"https://doi.org/10.1016/j.tranon.2025.102574","url":null,"abstract":"<p><p>Patients with papillary thyroid cancer (PTC) who experience local recurrence and distant metastases have a poor clinical prognosis and low survival rate. In this study, the expression of LRP11-AS1 was evaluated in both tissue samples from patients with papillary thyroid cancer and in PTC cell lines. We observed significant overexpression of LRP11-AS1 in both PTC tissues and PTC cell lines and inhibitory effects of LRP11-AS1 knockdown on the growth and migration of PTC cells. Mechanistically, knockdown of LRP11-AS1 led to upregulation of miR-615-3p, overexpression of miR-615-3p decreased the expression of both LRP11-AS1 and AKT2. The dual-luciferase reporter assay confirmed the inhibitory effect of miR-615-3p on the expression of LRP11-AS1 and AKT2. Knockdown of LRP11-AS1 inhibited in vivo growth of PTC tumor in nude mice model. LRP11-AS1 exhibited potential oncogenic effects in PTC by regulating the miR-615-3p/AKT2 axis, suggesting that LRP11-AS1 could serve as a potential diagnostic biomarker and therapeutic target in PTC.</p>","PeriodicalId":23244,"journal":{"name":"Translational Oncology","volume":"62 ","pages":"102574"},"PeriodicalIF":4.1,"publicationDate":"2025-10-22","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145355940","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"TRIM26 as a dual regulator of ferroptosis and chemoresistance in gastric cancer through HSF1 ubiquitination and exosomal miR-24-3p signaling.","authors":"Nouf S Al-Abbas","doi":"10.1016/j.tranon.2025.102489","DOIUrl":"10.1016/j.tranon.2025.102489","url":null,"abstract":"<p><p>Gastric cancer (GC) remains a major global health concern due to its frequent late-stage diagnosis, persistent chemoresistance, and high metastatic potential, all of which contribute to poor clinical outcomes. TRIM26, an E3 ubiquitin ligase with emerging tumor-suppressive functions, has been implicated in various malignancies; however, its precise role in GC has not been fully elucidated. This study elucidates in ferroptosis and chemoresistance while uncovering stromal-tumor crosstalk mechanisms underlying its suppression. Using public databases and clinical GC specimens and established cell lines (MGC-803, HGC27, MKN45), we observed significant downregulation of TRIM26 expression in tumor tissues compared to adjacent normal counterparts (p < 0.001), which correlated with advanced clinical stage and unfavorable prognosis. Functional assays including CCK-8, wound healing, colony formation, and Transwell migration, demonstrated that TRIM26 knockdown significantly enhanced GC cell proliferation, migration, and invasion, whereas TRIM26 overexpression reversed these malignant phenotypes. Mechanistically, TRIM26 induced ferroptosis via HSF1 ubiquitination and degradation, leading to reduced glutathione (GSH) levels and elevated levels of reactive oxygen species (ROS) and malondialdehyde (MDA). Additionally, we identified cancer-associated fibroblast (CAF)-derived exosomal miR-24-3p as a key upstream regulator that directly targets the 3' untranslated region (3' UTR) of TRIM26, thereby suppressing its expression, as confirmed by luciferase reporter assays. In cisplatin-resistant GC models (MGC803/DDP and AGS/DDP), prolonged cisplatin exposure resulted in a pronounced reduction in TRIM26 expression, corresponding with a 5.6-fold increase in IC₅₀ and a heightened metastatic profile. TRIM26 silencing further potentiated chemoresistance and invasive behavior, which coincided with epithelial-mesenchymal transition (EMT), as evidenced by decreased E-cadherin and increased N-cadherin and Vimentin expression. In contrast, TRIM26 restoration re-sensitized resistant GC cells to cisplatin and mitigated their metastatic capacity. Collectively, these findings reveal TRIM26 as a pivotal suppressor of GC progression, acting through the regulation of ferroptosis and EMT while being modulated by stromal exosomal miR-24-3p Therapeutic strategies aimed at restoring TRIM26 expression or disrupting the miR-24-3p/TRIM26/HSF1 axis may offer promising avenues for overcoming chemoresistance and limiting metastasis in GC.</p>","PeriodicalId":23244,"journal":{"name":"Translational Oncology","volume":"60 ","pages":"102489"},"PeriodicalIF":4.1,"publicationDate":"2025-10-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12355122/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144812443","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"NR4A3high mast cells promote ovarian cancer metastasis by reprogramming tumor-associated macrophages via JAK2/STAT6 signaling.","authors":"Xiaofeng Bian, Yirong Chen, Caixia Zhang, Shijia Huang, Xueting Fu, Bowen Yang, Siyan Lu, Wei Zhao, Yan Pan, Shuli Zhao","doi":"10.1016/j.tranon.2025.102494","DOIUrl":"10.1016/j.tranon.2025.102494","url":null,"abstract":"<p><p>Tumor-associated mast cells in the tumor microenvironment play a critical and complex role in the progression of tumor malignancy. However, the key molecules that control mast cell activation and target the biological function of ovarian cancer (OC) cells are still not fully understood. In this study, we performed scRNA-seq on cells isolated from six cases of epithelial OC tissues (three cases of primary tumor and three of metastatic tumor), and we identified three mast cell subtypes, among which the proportion of the second group of mast cell subsets specifically expressing NR4A3 was significantly higher in the metastatic tissue than in the primary tissue, suggesting that NR4A3 expression of MC may be related to the metastasis and prognosis of OC. In vitro, the biological functions of constructed NR4A3^high bone-marrow-derived mast cells, such as degranulation response, showed a significant decline, but their secretion of high levels of CXCL16 and IL-8 promoted the polarization of macrophages to M2 through the STAT6 pathway, thus promoting the migration and invasion of OC. In ovarian tumor models in mice with mast cell deficiency (c-Kit W-sh/ W-sh), adoptive transfer of NR4A3^high mast cells can not only promote subcutaneous tumor growth, but also promote intraperitoneal tumor cell colonization, decrease the ratio of CD8+ T cells, and increase the ratio of M2 macrophages. These results indicate that NR4A3 can drive mast cells to release more CXCL16 and IL-8 and induce macrophage M2 polarization through STAT6 signaling pathway, thereby mediating the metastasis of ovarian cancer.</p>","PeriodicalId":23244,"journal":{"name":"Translational Oncology","volume":"60 ","pages":"102494"},"PeriodicalIF":4.1,"publicationDate":"2025-10-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12357255/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144822719","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Triptonide stabilizes BIM to enhance oxaliplatin-induced ferroptosis and apoptosis in colorectal cancer.","authors":"Ji Ma, Liyun Zheng, Shiji Fang, Wenjing Yang, Yiming Ding, Mengyuan Wang, Jiale Chen, Qiaoyou Weng, Zouying Yao, Chuan Jiang, Minjiang Chen, Hongtao Xu, Jiansong Ji","doi":"10.1016/j.tranon.2025.102491","DOIUrl":"10.1016/j.tranon.2025.102491","url":null,"abstract":"<p><p>Oxaliplatin (OXA) is a common chemotherapeutic agent for advanced colorectal cancer. However, its effectiveness is limited by drug resistance, highlighting the need for combination therapies. In this study, Triptonide (TN), a diterpenoid compound is used to enhance the sensitivity of OXA, and the underlying mechanisms are investigated. Our findings indicated the combination of TN and OXA demonstrated strong synergistic anti-tumor effects across a broad concentration range in both HCT116 and LoVo cell lines, particularly at ratios ranging from 1:312 to 1:156. The combination of TN and OXA at low doses effectively inhibits growth and induces cell death in HCT116 and LoVo cells. TN and OXA cotreatment causes severe mitochondrial damage in colorectal cancer cells, leading to intracellular reactive oxygen species (ROS) accumulation, which subsequently triggers apoptosis and ferroptosis. Mechanistically, TN directly binds to BIM, a pro-apoptotic and ferroptotic protein, and stabilizes it. TN treatment led to increased expression of BIM and knockdown of BIM alleviated the growth inhibition of OXA in colorectal cancer cells. Finally, TN and OXA cotreatment significantly reduced the tumor weight and volume of LoVo-bearing nude mice in vivo. Taken together, our findings indicate that TN may serve as a novel therapeutic agent to enhance the efficacy OXA in the treatment of colorectal cancer.</p>","PeriodicalId":23244,"journal":{"name":"Translational Oncology","volume":"60 ","pages":"102491"},"PeriodicalIF":4.1,"publicationDate":"2025-10-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12354971/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144800293","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Genetic polymorphisms of TRPA1 does affect risk of cisplatin induced nephrotoxicity in Chinese population.","authors":"Cong Wang, Guifei Deng, Siyu Niu, Xianglong Meng","doi":"10.1016/j.tranon.2025.102486","DOIUrl":"10.1016/j.tranon.2025.102486","url":null,"abstract":"<p><strong>Introduction: </strong>Irreversible acute kidney injury (AKI) caused by cisplatin limits its clinical use, and transient receptor potential anchor protein 1 (TRPA1) regulates cisplatin-induced nephrotoxicity (CIN) through NF-κB signaling pathway-mediated inflammation. Single nucleotide polymorphisms in TRPA1 and NF-κB1 genes may be associated with individual heterogeneous nephrotoxicity.</p><p><strong>Materials and methods: </strong>In this paper, we investigated the association of 17 single nucleotide polymorphisms (SNP) of TRPA1 and NF-κB1 genes with cisplatin-induced acute nephrotoxicity. Nephrotoxicity and its severity were assessed according to the Common Terminology Criteria for Adverse Events (CTCAE 5.0). SNPs were measured by 48-Plex SNPscan® high-throughput SNP typing echnology in DNA isolated from peripheral blood of 589 Chinese Han lung cancer patients (241 with CIN and 348 without CIN) treated with cisplatin regimen.</p><p><strong>Results: </strong>TRAP1 gene rs920829 locus T allele carriers had a reduced risk of nephrotoxicity relative to C allele carriers (OR 0.684, 95 % CI 0.524-0.894, p = 0.003), and their additive and dominant models showed similar trends as well. However, the SNPs of NF-κB1 were not observed to be correlated with nephrotoxicity.</p><p><strong>Conclusion: </strong>SNPs of TRPA1 have the potential as biomarkers for predicting cisplatin nephrotoxicity.</p>","PeriodicalId":23244,"journal":{"name":"Translational Oncology","volume":"60 ","pages":"102486"},"PeriodicalIF":4.1,"publicationDate":"2025-10-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12355125/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144804871","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Ferroptosis and cellular senescence -Related Genes in Cervical Cancer: Mechanistic Insights from Multi-Omics and Clinical Sample Analysis.","authors":"Yongjin Luo, Lihua Tang, Zhonghong Zeng, DinhHuyen Trang, Dan Mo, Yihua Yang","doi":"10.1016/j.tranon.2025.102487","DOIUrl":"10.1016/j.tranon.2025.102487","url":null,"abstract":"<p><p>Mortality and treatment failure in cervical cancer (CC) patients are primarily due to extensive metastasis and chemoresistance. Immunotherapy has emerged as a crucial clinical treatment strategy for CC patients; however, the current methods and biomarkers are inadequate for accurately predicting immunotherapy responses and patient prognosis. This study comprehensively analyzed ferroptosis and cellular senescence, two processes intricately linked to tumorigenesis, progression, and therapy, utilizing multi-omics data from TCGA-CESC, GEO cohorts, and clinical data from CC patients. Based on ferroptosis- and cellular senescence -related patterns, two distinct clusters with divergent prognoses and tumor microenvironment (TME) characteristics were identified. A prognostic model was subsequntly constructed, demonstrating robust reliability in predicting CC prognosis and response to immunotherapy. Patients in the low-risk group exhibited enriched immune cell infiltration, lower TIDE scores, higher IPS scores, and higher expression levels of immune checkpoint inhibitor-related genes, such as PDCD1 and CTLA4, which were associated with improved overall outcomes. Validation with clinical samples confirmed the differential expression of model-associated genes in CC, further supporting the model's accuracy. This prognostic model provides valuable insights into predicting CC prognosis and optimizing immunotherapy, offering potential benefits for personalized treatment strategies.</p>","PeriodicalId":23244,"journal":{"name":"Translational Oncology","volume":"60 ","pages":"102487"},"PeriodicalIF":4.1,"publicationDate":"2025-10-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12357269/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144817486","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Investigation of MANF regulation of glioma stemness via STAT3/TGF-β/SMAD4/p38 pathway based on pan-cancer analysis.","authors":"Shi Feng, Ming Yang, Pengfei Dong, Fangfang Ding, Yang Hong, Huabao Cai, Xin Liu","doi":"10.1016/j.tranon.2025.102497","DOIUrl":"10.1016/j.tranon.2025.102497","url":null,"abstract":"<p><strong>Background: </strong>Glioma, particularly glioblastoma, is a highly aggressive brain tumor with poor prognosis and limited treatment options. Recent research highlights the role of MANF (Mesencephalic Astrocyte Derived Neurotrophic Factor) in tumor biology, yet its specific mechanisms in glioma remain underexplored. This study aims to elucidate the role of MANF in glioma and its underlying mechanisms of action.</p><p><strong>Methods: </strong>We conducted bioinformatics analysis using TCGA data to identify MANF-related pathways, followed by cellular assays and subcutaneous tumor models for functional validation. Experiments included Western blot and qRT-PCR analysis to investigate the effects of MANF on glioma cell proliferation, migration, and stemness gene expression.</p><p><strong>Results: </strong>MANF was found to be highly expressed in tumor tissues and associated with poor prognosis in glioma patients. Endogenous MANF regulates tumor cells by modulating the TGF-β/SMAD4/p38 pathway, promoting stemness and enhancing malignant behaviors, including migration and invasion. Exogenous MANF, however, did not significantly affect stemness gene expression but contributed to glioma cell proliferation.</p><p><strong>Conclusions: </strong>MANF emerges as a promising therapeutic target for glioma. This study clarifies MANF's specific mechanisms, offering insights into its potential for targeted glioma therapies.</p>","PeriodicalId":23244,"journal":{"name":"Translational Oncology","volume":"60 ","pages":"102497"},"PeriodicalIF":4.1,"publicationDate":"2025-10-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12357261/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144822718","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Diversity and inclusivity in oncology: A narrative review and orientation for institutional measures in Germany.","authors":"Hendrik Dapper, Sabine Oertelt-Prigione, Gertraud Stadler, Nina Weishaupt, Alexander Quaas, Vanessa Romotzky, Lena Haarmann, Emmanouil Fokas, Jiaqi Fan, Philipp Linde, Thomas Zander, Martin Görner, Laura Wortmann","doi":"10.1016/j.tranon.2025.102493","DOIUrl":"10.1016/j.tranon.2025.102493","url":null,"abstract":"","PeriodicalId":23244,"journal":{"name":"Translational Oncology","volume":"60 ","pages":"102493"},"PeriodicalIF":4.1,"publicationDate":"2025-10-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12355084/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144812442","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}