OncoTargets and therapy最新文献

{"title":"Multi‑cohort Validation Based on Disulfidptosis-Related lncRNAs for Predicting Prognosis and Immunotherapy Response of Esophageal Squamous Cell Carcinoma.","authors":"Zhongquan Yi, Xia Li, Yangyang Li, Yanan Ji, Jing Zhao, Heling Xu, Lei Zhou, JianXiang Song","doi":"10.2147/OTT.S519270","DOIUrl":"10.2147/OTT.S519270","url":null,"abstract":"<p><strong>Background: </strong>Disulfidptosis, a novel pattern of regulatory cell death, provides a valuable opportunity to gain deeper comprehension of tumor pathogenesis and treatment strategies. However, its biological mechanism in esophageal squamous cell carcinoma (ESCC) has yet to be completely elucidated.</p><p><strong>Materials and methods: </strong>From the Gene Expression Omnibus (GEO) GSE53625 dataset, we obtained RNA-seq data and clinical information. An analysis of Pearson correlation was utilized to screen disulfidptosis-related lncRNAs (DRLs), followed by LASSO and multivariate Cox regression analysis to construct a prognostic signature. The reliability and accuracy of this signature were verified on internal validation sets, including training (n= 90), testing (n= 89), and GSE53625 entire (n= 179) sets, as well as external sets, including TCGA-ESCC (n= 81) and GSE53624 (n= 119) sets. Additionally, mutation data comes from TCGA database was utilized for validating tumor mutation burden (TMB) analysis. In cell lines, an analysis of lncRNA differential expression was conducted using qRT-PCR.</p><p><strong>Results: </strong>Ultimately, six DRLs were utilized to construct a prognostic signature. Across all sets, Kaplan-Meier analysis indicated that high-risk ESCC patients have a poorer prognosis (<i>p</i> < 0.05), and ROC analysis showed that the AUC values at 1, 3, and 5 years all exceeded 0.6. Moreover, disparities were observed in immune phenotype scores, tumor infiltration of immune cells, functional enrichment, TIDE score, immune function, and TMB among the two risk groups. Additionally, individuals at high risk showed higher sensitivity to erlotinib, acetalax, gefitinib, lapatinib, sapitinib, and afatinib.</p><p><strong>Conclusion: </strong>Through bioinformatics analysis, a novel and robust DRLs signature for ESCC was established, providing new insights into the prognosis prediction and potential treatment strategies. Nevertheless, this study is retrospective and relies on public databases, with a limited sample size within the datasets. In the future, it is essential to conduct more extensive validation of the prognostic value and efficacy in real ESCC cohorts.</p>","PeriodicalId":19534,"journal":{"name":"OncoTargets and therapy","volume":"18 ","pages":"763-778"},"PeriodicalIF":2.7,"publicationDate":"2025-06-25","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12206906/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144529050","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":"Lidocaine as a Potential Therapeutic Agent in Colorectal Cancer: A Study of Gene Expression and Prognosis.","authors":"Wenyuan Li, Wenjie Gao, Chen Lu, Muhuo Ji, Yuan Yin, Hao Zhang, Cunming Liu, Chunzhao Yu","doi":"10.2147/OTT.S505753","DOIUrl":"10.2147/OTT.S505753","url":null,"abstract":"<p><strong>Background: </strong>Colorectal cancer (CRC) is a significant contributor to cancer-related mortality globally. Despite the availability of treatments such as surgery, chemotherapy, and radiotherapy, these interventions are often accompanied by severe side effects and suboptimal patient outcomes. Recent studies have suggested that lidocaine, a widely used local anesthetic, may possess anti-tumor properties in various cancer types. This study aims to explore the impact of lidocaine on CRC cell lines, HCT 116 and SW480, to evaluate its potential as a therapeutic agent.</p><p><strong>Methods: </strong>In vitro assays were conducted to assess the effect of lidocaine on the proliferation, migration, and invasion of CRC cells. The suppression of cell proliferation and induction of apoptosis were confirmed using colony formation, EdU, and TUNEL assays. RNA sequencing was performed on lidocaine-treated HCT 116 cells to identify differentially expressed genes and enriched biological pathways. A prognostic signature based on 16 genes was developed and validated using clinical data.</p><p><strong>Results: </strong>Lidocaine significantly inhibited the proliferation, migration, and invasion of CRC cells in a dose-dependent manner. The assays confirmed that lidocaine suppressed cell proliferation and induced apoptosis. RNA sequencing revealed 8002 differentially expressed genes in lidocaine-treated HCT 116 cells, with significant enrichment of key pathways such as the estrogen signaling pathway and MAPK pathway. A prognostic signature based on 16 genes was developed and validated, providing a predictive model for patient survival. These findings suggest that lidocaine has potential as a therapeutic agent for CRC treatment, although further in vivo studies are required to clarify its mechanisms and optimize its clinical application.</p>","PeriodicalId":19534,"journal":{"name":"OncoTargets and therapy","volume":"18 ","pages":"737-749"},"PeriodicalIF":2.7,"publicationDate":"2025-06-18","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12182729/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144476214","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":"Traditional Chinese Medicine Xiaoai Jiedu Recipe Suppresses the Development of Hepatocellular Carcinoma via Regulating the microRNA-29a/Signal Transducer and Activator of Transcription 3 Axis [Retraction].","authors":"","doi":"10.2147/OTT.S544657","DOIUrl":"https://doi.org/10.2147/OTT.S544657","url":null,"abstract":"<p><p>[This retracts the article DOI: 10.2147/OTT.S248797.].</p>","PeriodicalId":19534,"journal":{"name":"OncoTargets and therapy","volume":"18 ","pages":"735-736"},"PeriodicalIF":2.7,"publicationDate":"2025-06-11","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12170859/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144317554","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":"Crosstalk Between EGFR and Integrin Affects Invasion and Proliferation of Gastric Cancer Cell Line, SGC7901 [Retraction].","authors":"","doi":"10.2147/OTT.S544936","DOIUrl":"https://doi.org/10.2147/OTT.S544936","url":null,"abstract":"<p><p>[This retracts the article DOI: 10.2147/OTT.S35322.].</p>","PeriodicalId":19534,"journal":{"name":"OncoTargets and therapy","volume":"18 ","pages":"733-734"},"PeriodicalIF":2.7,"publicationDate":"2025-06-10","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12169025/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144310261","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":"Studying Immunogenic Cell Death in Human Colorectal Cancer Organoids.","authors":"Rebecca Lisandrelli, Matthias Winkler, Zlatko Trajanoski, Giorgia Lamberti","doi":"10.2147/OTT.S521346","DOIUrl":"10.2147/OTT.S521346","url":null,"abstract":"<p><strong>Purpose: </strong>Combination therapies of chemotherapeutic agents and immunotherapy have shown promising results in the treatment of cold tumors. Various chemotherapies trigger immunogenic cell death (ICD) and release of hallmarks immunogenic damage associated molecular patterns (DAMPs) that have been related with immunostimulatory activities, leading to better patient prognosis. We aim to optimize in vitro assays to detect DAMPs release in response to chemotherapeutic agents using a colorectal cancer (CRC) organoids model.</p><p><strong>Methods: </strong>CRC patient-derived organoids (PDOs) were treated either with oxaliplatin (OXA) or with 5-fluorouracil (5FU) and viability was measured with CellTiter-Glo3D Cell viability assay. Calreticulin (CALR) and high mobility group box 1 protein (HMGB1) intracellular translocation was assessed in immunofluorescence microscopy and quantified via co-localization with wheat germ agglutinin (WGA) and DAPI. Extracellular release of adenosine triphosphate (ATP) was quantified via specific luminescence assays.</p><p><strong>Results: </strong>The results showed that CRC PDOs release DAMPs in a patient-specific manner in response to OXA and 5FU treatments.</p><p><strong>Conclusion: </strong>This study successfully used immunofluorescence and luminescence methods to detect ICD-associated DAMPs release in CRC PDOs in response to chemotherapeutic treatments. This approach allows the recognition of patient-specific ICD activation and could help predict patient response to therapies.</p>","PeriodicalId":19534,"journal":{"name":"OncoTargets and therapy","volume":"18 ","pages":"705-715"},"PeriodicalIF":2.7,"publicationDate":"2025-06-06","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12152962/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144275526","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":"Lowering the Selinexor Dose within the Pomalidomide and Dexamethasone Combination Regimen Elicits Fewer Side Effects While Comparable Efficacy Against Relapsed/Refractory Multiple Myeloma.","authors":"Liying Peng, Tiantian Shan, Xinyi Zhou, Zhongyuan Feng, Wanting Qiang, Jing Lu, Haiyan He, Juan Du","doi":"10.2147/OTT.S516486","DOIUrl":"10.2147/OTT.S516486","url":null,"abstract":"<p><strong>Background: </strong>As a novel oral Exportin 1 (XPO1) inhibitor, selinexor at 80 or 100 mg has demonstrated efficacy in treating relapsed/refractory multiple myeloma (RRMM), nonetheless, this dosage has shown poor tolerability.</p><p><strong>Objective: </strong>To explore the optimal dosage of selinexor, we evaluated the efficacy and safety of 60 vs 40 mg selinexor, combine with regimen comprising pomalidomide and dexamethasone in RRMM.</p><p><strong>Design: </strong>21 patients with RRMM were enrolled to receive selinexor (60 or 40 mg once weekly), together with pomalidomide (4 mg/day on days 1-21) and dexamethasone (40 mg once weekly); the SPD-60 group (6 patients) vs SPD-40 group (15 patients).</p><p><strong>Methods: </strong>The clinical response and efficacy of the two groups were continuously followed up, and statistical analysis was carried out to screen out the dose group with fewer side effects and better efficacy. The primary endpoint was (objective response rates) ORR. The secondary endpoints included treatment safety and tolerability, progression-free survival (PFS) and overall survival (OS).</p><p><strong>Results: </strong>The ORR of the SPD-60 and SPD-40 groups were 33.3% and 46.7% respectively (<i>P</i>=0.773). With a median follow-up of 20.9 months, the median PFS was 6.2 months and the median OS was not achieved across all treated patients. The median PFS for SPD-60 group was 4.3 months, while for SPD-40 was 8.0 months (<i>P</i>=0.618). The 1-year OS rate were 66.7% for SPD-60 group and 85.1% for the SPD-40 group (<i>P</i>=0.308). The most common hematological adverse events were neutropenia (SPD-60 group 50% vs SPD-40 group 53.3%) and thrombocytopenia (50% vs 46.7%). Fatigue (83.3% vs 40%), infection (50% vs 53.3%), and nausea (83.3% vs 40%) were the most common non-hematologic adverse effects.</p><p><strong>Conclusion: </strong>The SPD-40 regimen may be more clinically applicable than SPD-60, as it elicited fewer adverse effects while demonstrating equivalent efficacy.</p><p><strong>Trial registration: </strong><i>ClinicalTrials.gov</i>: NCT04941937.</p>","PeriodicalId":19534,"journal":{"name":"OncoTargets and therapy","volume":"18 ","pages":"695-703"},"PeriodicalIF":2.7,"publicationDate":"2025-06-06","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12151071/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144266870","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":"IGFBP1 is One of 10 Metabolic Factors Predicting Recurrence Free Survival in Gastric Cancer and Promotes Cancer Progression via ZFX-IGFBP1 Axis.","authors":"Hui Liu, Yongming Huang, Guanghua Fu, Bo Lei, Ke Liu","doi":"10.2147/OTT.S499695","DOIUrl":"10.2147/OTT.S499695","url":null,"abstract":"<p><strong>Introduction: </strong>Metabolism-related genes (MRGs) critically influence cancer prognosis, yet their role in gastric carcinoma (GC) remains poorly understood.</p><p><strong>Methods: </strong>We analyzed 24,991 genes from 407 GC patients in TCGA to identify a metabolic gene-based prognostic signature. In vitro and in vivo functional experiments validated key findings, while transcriptional regulation mechanisms were explored through promoter interaction assays.</p><p><strong>Results: </strong>A robust 10-metabolic gene signature was identified as strongly predictive of recurrence-free survival (RFS) in GC. Elevated insulin-like growth factor binding protein 1 (IGFBP1) expression correlated with reduced overall survival and disease-free survival. Functional studies demonstrated IGFBP1's oncogenic role in promoting GC proliferation and metastasis. Mechanistically, zinc finger protein X-linked (ZFX) activated IGFBP1 transcription by directly binding to its promoter.</p><p><strong>Discussion: </strong>We established a prognostic nomogram integrating the 10-metabolic gene signature for GC RFS prediction. IGFBP1 emerges as a potential therapeutic target and biomarker, with ZFX-driven transcriptional activation as a novel regulatory axis in GC progression.</p>","PeriodicalId":19534,"journal":{"name":"OncoTargets and therapy","volume":"18 ","pages":"717-732"},"PeriodicalIF":2.7,"publicationDate":"2025-06-05","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12148340/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144258653","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":"MAM Domain Containing 2 (MAMDC2) Affects Invasion and Metastasis of Human Gastric Cancer.","authors":"Jiaofeng Shen, Guangyu Gao, Songtao Liu","doi":"10.2147/OTT.S516982","DOIUrl":"10.2147/OTT.S516982","url":null,"abstract":"<p><strong>Background: </strong>Gastric cancer (GC) is the fifth most prevalent cancer worldwide and the fourth leading cause of cancer-related mortality. MAM Domain Containing 2 (MAMDC2) has been involved in many cancers. However, the impact of MAMDC2 on gastric cancer was unclear. This study aimed to investigate the role and mechanism of MAMDC2 in gastric cancer.</p><p><strong>Methods: </strong>Differential genes in gastric cancer are analyzed by GEO, TCGA, MSigDB database, R-packet limma, and Wilcoxon test. Survival analysis is performed through the R package survival. Construct a PPI network through the STRING database. Enrichment analysis is performed by Metascape. The infiltration level of gastric cancer immune cells is calculated by CIBERSORT. In addition, the expression of MAMDC2 was analyzed by immunohistochemistry and quantitative real-time polymerase chain reaction (RT-qPCR). siMAMDC2 was used to knock down the specific gene. Cell counting kit-8 (CCK-8) assay, colony formation assay, and cell migration were applied to evaluate the function of MAMDC2 in gastric cancer cells.</p><p><strong>Results: </strong>In the present study, we revealed a significant upregulation of MAMDC2 in gastric cancer tissues and cells. Knocking down MAMDC2 inhibited the proliferation and migration of gastric cancer cells, while overexpression of MAMDC2 produced the opposite results. Furthermore, MAMDC2 may be an independent factor in poor prognosis in gastric cancer patients.</p><p><strong>Conclusion: </strong>These results illustrated that MAMDC2 promoted the proliferation and migration of gastric cancer cells. The newly identified MAMDC2 provides novel insight into the pathogenesis of gastric cancer.</p>","PeriodicalId":19534,"journal":{"name":"OncoTargets and therapy","volume":"18 ","pages":"679-693"},"PeriodicalIF":2.7,"publicationDate":"2025-05-26","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12124315/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144199764","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 a Combined Prognostic Score Using Plasma Tumor DNA and Clinical Features in Metastatic Castration-Resistant Prostate Cancer Patients Treated with Taxanes.","authors":"Nicole Brighi, Giuseppe Schepisi, Vincenza Conteduca, Emanuela Scarpi, Paola Caroli, Federica Matteucci, Cristian Lolli","doi":"10.2147/OTT.S509285","DOIUrl":"10.2147/OTT.S509285","url":null,"abstract":"<p><strong>Purpose: </strong>There is an urgent need of biomarkers to personalize metastatic castration-resistant prostate cancer (mCRPC) treatment. A new prognostic model described by our group combines molecular characteristics (ptDNA levels), metabolic features from PET-scans (metabolic tumor volume), clinical parameters (visceral metastases), and lab tests (lactate-dehydrogenase levels) in abiraterone or enzalutamide-treated patients. This study aims to validate the score on mCRPC patients undergoing taxane treatment.</p><p><strong>Patients and methods: </strong>Twenty-eight patients affected by mCRPC, pre-treated with abiraterone or enzalutamide, candidate for taxane-based treatments, have been prospectively evaluated. All patients underwent a basal PET/CT scan with F-choline and blood samples. The prognostic model previously described was applied to this population; based on the partial results of the parameters, we assigned the patients into three risk groups.</p><p><strong>Results: </strong>In the 28 patients evaluated, we observed a different median OS among the three risk groups (risk group I, 18.1 months [95% CI: 15.2-33.1 months]; risk group II, 12.7 months [4.9-18.6 months]; and risk group III, 10.1 months [3.4-15.4 months]; p = 0.012). Statistically significant differences were also observed for PFS.</p><p><strong>Conclusion: </strong>The prognostic score has confirmed to be a good prognostic tool also in a more advanced cohort of patients treated with taxanes. This tool may represent a valid method to refine prognostication and treatment selection in a cohort of patients where biomarkers are scarce.</p>","PeriodicalId":19534,"journal":{"name":"OncoTargets and therapy","volume":"18 ","pages":"667-677"},"PeriodicalIF":2.7,"publicationDate":"2025-05-23","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12117575/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144174358","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":"CXCL11: A Novel Biomarker in Colorectal Cancer as Metastasis Predictor.","authors":"Riyadi Wibowo, Yunia Sribudiani, Kiki Lukman, Reno Rudiman, Tommy Ruchimat, Bambang Am Am Setya Sulthana, Andriana Purnama, Alma Wijaya, Etis Primastari, Prapanca Nugraha","doi":"10.2147/OTT.S515119","DOIUrl":"10.2147/OTT.S515119","url":null,"abstract":"<p><strong>Objective: </strong>CXCL11 (C-X-C motif chemokine ligand 11) encodes a chemokine, a small signaling protein involved in immune and inflammatory responses. This study aims to evaluate the association between CXCL11 gene expression variations and metastasis in colorectal cancer (CRC) patients, highlighting its potential as a biomarker for metastasis.</p><p><strong>Methods: </strong>This is observational laboratory-based study utilized tissue samples from colorectal cancer (CRC) patients stored in the Tissue Bank of the Research Unit, Division of Digestive Surgery, Faculty of Medicine, Universitas Padjadjaran. Conducted between January and August 2024, data collection involved pathological and anatomical assessments of tissue samples obtained through biopsies or tumor resections. Gene expression analysis was performed on 60 fresh tumor tissues using PCR at the Biomolecular Laboratory, Faculty of Medicine, Universitas Padjadjaran.</p><p><strong>Results: </strong>The findings revealed a significant variation in CXCL11 expression among CRC patients based on cancer stage (P = 0.015) and metastasis status (P = 0.017). However, no significant differences in CXCL11 expression were observed concerning age, gender, anatomical pathology, or tumor location.</p><p><strong>Conclusion: </strong>This study identifies a relationship between CXCL11 gene expression differences and metastasis in CRC patients. Further studies with larger sample sizes are recommended to validate CXCL11's role as a biomarker for CRC metastasis. Additionally, future research should explore the potential application of CXCL11 in antitumor therapy.</p>","PeriodicalId":19534,"journal":{"name":"OncoTargets and therapy","volume":"18 ","pages":"657-665"},"PeriodicalIF":2.7,"publicationDate":"2025-05-14","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12085893/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144094486","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}