Journal of Cancer最新文献

{"title":"Bavachin suppresses proliferation of laryngopharyngeal cancer by regulating the STAT3 and MAPK signaling pathways.","authors":"Xiaonan Yang, Zhimin Ding, Hongting Hua, Ruijia Gan, Dongdong Meng, Yan Zang, Han Xiao, Dong Wang, Wanjin Jiang, Dongyu Si, Xiang Wei, Mei Zhang, Huabing Zhang, Chaobing Gao","doi":"10.7150/jca.92956","DOIUrl":"https://doi.org/10.7150/jca.92956","url":null,"abstract":"<p><p><b>Purpose:</b> The present study aimed to explore the underlying antitumor effects of bavachin on laryngopharyngeal cancer <i>in-vitro</i> and <i>in-vivo</i>. <b>Methods:</b> Tu212 and FaDu cells were cultured in the incubator. Cells were treated with 0.1% DMSO (control group) and different concentrations of bavachin (experimental groups) for exploring the results of proliferation and apoptosis. We revealed the underlying mechanism of bavachin on laryngopharyngeal cancer through western blotting, qRT-PCR assay and immunofluorescence staining. <b>Results:</b> Bavachin could suppress the proliferation and migration of laryngopharyngeal cancer cells <i>in-vitro</i> and <i>in-vivo</i>. Mechanistically, the results suggested that bavachin could downregulate the phosphorylation level of the signal transducer and activator of the transcription 3 (STAT3) and upregulate those of the mitogen-activated protein kinase (MAPK). Furthermore, bavachin also increased the expression level of Bax and suppressed those of Bcl-2, CDK4/6, and CyclinD1 in the laryngopharyngeal cancer cells. Additionally, the study also identified that bavachin promoted ferroptosis by decreasing the expression level of glutathione peroxidase 4 (GPX4) and increasing those of intracellular reactive oxygen species (ROS) and glutathione (GSH). <b>Conclusion:</b> Taken together, these results demonstrated that bavachin could suppress the growth and migration of laryngopharyngeal cancer cells and induce apoptosis and cell cycle arrest of the laryngopharyngeal cancer cells by regulating the MAPK/STAT3 signaling pathway. This study demonstrated that bavachin exhibited a clinical therapeutic potential for laryngopharyngeal cancer.</p>","PeriodicalId":15183,"journal":{"name":"Journal of Cancer","volume":"16 7","pages":"2339-2352"},"PeriodicalIF":3.3,"publicationDate":"2025-03-31","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12036085/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144006904","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}

{"title":"Construction of a Prognostic Model for Cervical Cancer Related to lncRNA Based on Differential Co-expression Network and Functional Study of Key Gene EGFR-AS1.","authors":"Kailong Du, Qian Chen, Hui Fan, Yunlong Lei, Jian Zhang","doi":"10.7150/jca.108429","DOIUrl":"https://doi.org/10.7150/jca.108429","url":null,"abstract":"<p><p>Cervical cancer is a common gynecological malignancy, and the average age of onset is decreasing gradually. Therefore, an effective predictive model is urgently needed to improve the personalized treatment of cervical cancer patients. Long non-coding RNAs (lncRNAs) play crucial roles in the occurrence, development, and prognosis of malignant tumors. In this study, we used cervical cancer multi-omics data and single-cell sequencing data for analysis, and established a 33-lncRNA-CESC model by using the random forest algorithm in ensemble learning and mRNA and lncRNA co-expression network technology. The results demonstrated that the model exhibited strong discriminative ability, accuracy, and clinical utility. Furthermore, we investigated the relationship between the model and immune cell infiltration. Enrichment analysis revealed associations between the model and cellular proliferation as well as epidermal growth factor receptor (EGFR) signaling pathways. Subsequently, attention was directed toward the gene EGFR-AS1 in the model, which was identified within the co-expression network and exhibited a significant association with patient prognosis. Additionally, EGFR-AS1 was found to be specifically associated with FAM83B. Analysis of single-cell data confirmed that FAM83B plays a role in the late stage of cervical cancer development mainly through the EGFR signaling pathway. Functional experiments showed that knockdown of either EGFR-AS1 or FAM83B inhibited cervical cancer cell proliferation and migration capabilities, and the phosphorylated ERK and AKT levels. In addition, there was a mutual regulatory effect between EGFR-AS1 and FAM83B expression. In conclusion, this study identifies that EGFR-AS1 served as a key factor in our 33-lncRNA-CESC model and potentially interacted with FAM83B to regulate the EGFR pathway which significantly impacting cervical cancer development.</p>","PeriodicalId":15183,"journal":{"name":"Journal of Cancer","volume":"16 7","pages":"2321-2338"},"PeriodicalIF":3.3,"publicationDate":"2025-03-31","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12036091/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143986439","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}

{"title":"Arachidonic acid promotes myeloid differentiation of splenic CD45- Ter119+ cells in myeloproliferative neoplasm.","authors":"Linlin Zhang, Yi Yang, Xiao Yu, Guodong Li, Peihua Zhang, Xiaomin Ren, Siyu Luo, Lin Li, Gustave Munyurangabo, Yachun Jia, Lingqin Song, Aili He, Guangyao Kong","doi":"10.7150/jca.110478","DOIUrl":"https://doi.org/10.7150/jca.110478","url":null,"abstract":"<p><p>Although splenic CD45^-Ter119⁺ cells promote cancer progression by secreting artemin, it remains unclear whether these cells play an important role in myeloproliferative neoplasm (MPN). Here, using a Kras^G12D/+-induced mouse model of MPN, we demonstrated that the number and cycling of CD45^-Ter119⁺ cells increased in the spleens of MPN mice. Moreover, these cells could differentiate into myeloid cells upon stimulation with GM-CSF and mIL-6. Through RNA sequencing, we further revealed that myeloid genes, such as Hoxa9, Mpo and Ms4a3, were highly expressed in CD45^-Ter119⁺ cells. Mechanistically, we showed that the arachidonic acid content was significantly elevated in splenic CD45^-Ter119⁺ cells, and exogenous arachidonic acid mediated the differentiation of splenic CD45^-Ter119⁺ cells into myeloid cells. Our results revealed that splenic CD45^-Ter119⁺ cells play a crucial role in myeloid leukemia and that arachidonic acid could be a potential therapeutic target for MPN treatment.</p>","PeriodicalId":15183,"journal":{"name":"Journal of Cancer","volume":"16 7","pages":"2289-2297"},"PeriodicalIF":3.3,"publicationDate":"2025-03-31","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12036098/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144007940","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}

{"title":"HPV Genotype, AGC Categories, and Age-Stratified Immediate Prevalence of Precancers and Cancers in Women with Atypical Glandular Cells with or without Concurrent Squamous Abnormal Cytology.","authors":"Xin Zhou, Zicheng Huang, Wanrun Lin, Suming Huang, Huijuan Zhang, Wenxin Zheng, Yudong Wang, Feng Zhou","doi":"10.7150/jca.105805","DOIUrl":"https://doi.org/10.7150/jca.105805","url":null,"abstract":"<p><p><b>Objectives:</b> Limited data exists on Papanicolaou (Pap) tests involving atypical glandular cells (AGC) with or without concurrent squamous cell abnormalities (Sq), hindering the reproducibility of results. This study aims to stratify the risk of precancers and cancers based on distinct high-risk human papillomavirus (hrHPV) genotyping, AGC categories, and age groups among women with AGC with or without concurrent squamous cell abnormalities. <b>Methods:</b> This retrospective analysis examined Pap smear patient data from January 2019 to December 2023, including 54 AGC + Sq cases and 974 cases with AGC-Alone. Among these, 799 patients (including 43 AGC + Sq cases and 756 AGC-Alone cases) had HPV testing results, and 769 (including 43 AGC + Sq cases and 726 AGC-Alone cases) had subsequent histological follow-up data. <b>Results:</b> In the total cohort, 5.25% (54 cases) were AGC + Sq, and 94.75% (974 cases) were AGC-Alone. The detection rates of high-grade glandular lesions (AIS+/AEH+) and adenocarcinoma (AC) were significantly higher in AGC patients over 65 years compared to other age groups (p = 0.000444 and p < 0.0001, respectively), while no significant differences were observed for high-grade squamous lesions (HSIL+) (p = 0.791) or squamous carcinoma (SCC) (p = 0.909). The prevalence of AIS+/AEH+ was significantly higher in HPV-16 (28.6%) and HPV-18 (50.0%) positive groups compared to the HPV-negative (10.4%) and other hrHPV types positive groups (6.3%) (p < 0.0001). Notably, the AGC + Sq group exhibited a higher prevalence of isolated squamous lesions, as well as glandular lesions with concurrent squamous involvement, compared to the AGC-Alone group (p = 0.001). Additionally, increased AC risk was observed in older AGC + Sq women at the 50-year cutoff, although no significant association was found between HPV genotype and immediate histology in the AGC + Sq group. <b>Conclusions:</b> A comprehensive approach that incorporates cytological results, hrHPV status, and age offers more effective stratification of AGC patients, leading to more precise management. While hrHPV testing and age provide valuable insights, relying solely on hrHPV results for triaging AGC + Sq cases is inadequate.</p>","PeriodicalId":15183,"journal":{"name":"Journal of Cancer","volume":"16 7","pages":"2250-2260"},"PeriodicalIF":3.3,"publicationDate":"2025-03-31","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12036100/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143998742","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}

{"title":"RBM39 Functions as a Potential Oncogene Through the NF-κB Signaling Pathway in Colorectal Cancer Cells.","authors":"YaTao Wang, XueSi Yang, ZhangQuan Yang, ZiRui Chen, HaiFeng Jiang, YiCong Wang, DongYan Shen, GuoQiang Su","doi":"10.7150/jca.105120","DOIUrl":"https://doi.org/10.7150/jca.105120","url":null,"abstract":"<p><p>Colorectal cancer (CRC) ranks as the third most frequently diagnosed cancer and is the second leading cause of cancer-related deaths globally. Recently, RNA-binding protein 39(RBM39), a critical factor in tumor-targeted mRNA and protein expression, has played a vital role in tumorigenesis and has broad development prospects in clinical treatment and drug research. However, the functional roles of RBM39 in the progression of CRC remain largely unexplored. This study found that RBM39 is notably overexpressed at both the mRNA and protein levels in CRC tissues compared with normal adjacent tissues. RBM39 was identified as a potential therapeutic target for colorectal cancer. Elevated RBM39 mRNA levels in CRC patients indicated worse survival probabilities. We show that RBM39 enhances the proliferation, migration, and invasion ability of CRC cells. Furthermore, we have made an innovative discovery that increased RBM39 inhibits apoptosis in CRC cells. Mechanistically, RNA-seq analysis indicated that RBM39 activates the NF-κB pathway, which plays a pivotal role in driving the malignant biological behaviors of colorectal cancer. Notably, these findings represent a novel contribution to our understanding of the mechanistic underpinnings of CRC, as they have not been previously documented in the literature. In the <i>in vivo</i> nude mouse xenograft model, our study demonstrates that the targeted knockdown of RBM39 markedly suppresses tumor formation, highlighting a novel therapeutic strategy for combating colorectal cancer. In conclusion, RBM39 emerges as a promising candidate for clinical diagnosis and targeted treatment of colorectal cancer, with implications for future research in tumor biology and therapeutic strategies.</p>","PeriodicalId":15183,"journal":{"name":"Journal of Cancer","volume":"16 7","pages":"2233-2249"},"PeriodicalIF":3.3,"publicationDate":"2025-03-29","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12036102/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144020576","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}

{"title":"Network Pharmacology and Experimental Validation-based Investigation of the Underlying Mechanism of Yi-Yi-Fu-Zi-Bai-Jiang-San of Nasopharyngeal Carcinoma.","authors":"Zehua Lin, Ting Huang, Baoai Han, Zezhang Tao, Xiong Chen","doi":"10.7150/jca.109758","DOIUrl":"https://doi.org/10.7150/jca.109758","url":null,"abstract":"<p><p>Yi-Yi-Fu-Zi-Bai-Jiang-San (YYFZBJS) is a representative traditional Chinese medicine (TCM) formula. However, its potential anti-tumor effects in nasopharyngeal carcinoma (NPC) remains unclear. This study aims to investigate the monomers of YYFZBJS and their associated targets in the treatment of NPC. The primary active compounds of YYFZBJS and their corresponding targets were identified using the TCMSP, SEA, and Super-PRED databases. NPC-related target proteins were retrieved from OMIM, GeneCards, and TTD databases. A protein-protein interaction network was constructed using the common target proteins of YYFZBJS active compounds and NPC. Core genes were identified through three algorithms in CentiScape 2.2. Gene Ontology (GO) and Kyoto Encyclopedia of Genes and Genomes (KEGG) analyses were then performed on these core genes. Validation was conducted using the GSE53819 and GSE13597 datasets. Finally, interactions between core targets and active ingredients were confirmed through molecular docking, molecular dynamics simulations, and cell-based experiments. A total of 715 corresponding to YYFZBJS active compounds and 3159 NPC-related targets were screened. Among these, 143 intersection genes were identified, from which 32 core genes were selected based on degree centrality, closeness centrality, and betweenness centrality. GO and KEGG analyses of these core genes revealed relevant biological processes and pathways. Furthermore, these 32 core genes were cross-referenced with the GSE53819 and GSE13597 datasets, identifying PTGS2 and CCND1 as valid targets of active compounds. Molecular docking, molecular dynamics simulations and cell experiments confirmed the effectiveness of the Acacetin-PTGS2 pathway. Acacetin of the main active ingredient in YYFZBJS suppressed NPC by downregulating PTGS2 expression.</p>","PeriodicalId":15183,"journal":{"name":"Journal of Cancer","volume":"16 7","pages":"2212-2232"},"PeriodicalIF":3.3,"publicationDate":"2025-03-29","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12036090/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143972543","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}

{"title":"Extracellular vesicles-miR-205-5p inhibits lymphatic metastasis in pancreatic cancer through diffusely downregulating VEGFA.","authors":"Yuanyang Wang, Cheng Qin, Yutong Zhao, Bangbo Zhao, Zeru Li, Tianyu Li, Xiangyu Zhang, Weibin Wang","doi":"10.7150/jca.110659","DOIUrl":"https://doi.org/10.7150/jca.110659","url":null,"abstract":"<p><p>Pancreatic ductal adenocarcinoma (PDAC) is to become the second leading cause of cancer-related death by 2040. Many factors contribute to this dilemma, including lymphatic metastasis, which is the primary cause of PDAC metastasis. The inhibition of early lymph node metastasis, including the lymphangiogenic process, may be a novel strategy for PDAC treatment. Through miRNA sequencing of plasma extracellular vesicles (EVs) from PDAC patients, for the first time, we identified that plasma EV-miR-205-5p served as a non-invasive biomarker distinguishing lymphatic metastasis status (N0 vs. N2) in PDAC patients. Using tissue microarray and <i>in situ</i> hybridization, we discovered that miR-205-5p was highly expressed in PDAC, but negatively correlated with lymph node metastasis. By <i>in vivo</i> and <i>in vitro</i> experiments, we demonstrated its unique mechanism of action via EV-mediated transfer to human lymphatic endothelial cells (HLECs), leading to systematic downregulation of VEGFA and inhibition of the Akt/Erk pathway, which suppressed lymphangiogenesis. Delivering miR-205-5p via engineered EVs might be a promising strategy to eliminate PDAC lymphatic metastasis and improve prognosis.</p>","PeriodicalId":15183,"journal":{"name":"Journal of Cancer","volume":"16 7","pages":"2197-2211"},"PeriodicalIF":3.3,"publicationDate":"2025-03-29","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12036096/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143967233","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}

{"title":"SLC16A1 Inhibits Ferroptosis and Promotes the Progression of Head and Neck Squamous Cell Carcinoma.","authors":"Huaiyuan Zong, Luyao Teng, Lifang Chen, Jianxin Qiu, Chunhui Tian","doi":"10.7150/jca.110217","DOIUrl":"https://doi.org/10.7150/jca.110217","url":null,"abstract":"<p><p>The solute carrier family 16 member 1 (SLC16A1) gene demonstrates abnormally elevated expression levels in a variety of human malignant tumors, and it is pivotal in tumor initiation and progression. Nonetheless, the precise mechanisms through which this gene operates in head and neck squamous cell carcinoma (HNSCC) need to be elucidated. This study integrated bioinformatics analysis with clinical patient samples to elucidate that the mRNA and protein levels of SLC16A1 were significantly upregulated in patients with HNSCC, which was closely associated with poor patient prognosis. In addition, through the construction of stable SLC16A1 knockdown and overexpression models in HNSCC cells along with <i>in vitro</i> and <i>in vivo</i> experiments, the study comprehensively illuminated the pivotal role of SLC16A1 in promoting the proliferation, migration, and invasiveness of HNSCC cells, as well as enhancing their resistance to ferroptosis. <i>In vitro</i> experimental results demonstrated that when SLC16A1 was knocked down, the proliferation, migration, and invasion capabilities of HNSCC cell lines were significantly reduced and the extent of RAS-selective lethal 3-induced lipid peroxidation increased compared with control cells. Conversely, HNSCC cell lines overexpressing SLC16A1 exhibited enhanced proliferation, migration, and invasion capabilities, accompanied by lower levels of lipid peroxidation. <i>In vivo</i> experiments further corroborated the pivotal role of SLC16A1 in promoting HNSCC tumor growth. Our research findings indicate that SLC16A1 acts as an oncogene in HNSCC, and that abnormally high expression of SLC16A1 significantly accelerates the development and progression of HNSCC by conferring resistance to ferroptosis.</p>","PeriodicalId":15183,"journal":{"name":"Journal of Cancer","volume":"16 7","pages":"2184-2196"},"PeriodicalIF":3.3,"publicationDate":"2025-03-29","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12036106/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143967207","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}

{"title":"Erratum: CCT8 promotes cell migration and tumor metastasis in lung adenocarcinomas: Erratum.","authors":"Zhiqiang Wu, Liyuan Deng, Jin Tao, Yuhai Lu, Xiaofei Zeng, Weikun Jia, Hu Chen","doi":"10.7150/jca.113359","DOIUrl":"https://doi.org/10.7150/jca.113359","url":null,"abstract":"<p><p>[This corrects the article DOI: 10.7150/jca.87983.].</p>","PeriodicalId":15183,"journal":{"name":"Journal of Cancer","volume":"16 7","pages":"2182-2183"},"PeriodicalIF":3.3,"publicationDate":"2025-03-28","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12036095/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143997015","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}

{"title":"Erratum: Overexpression of TMEFF1 in Endometrial Carcinoma and the Mechanism Underlying its Promotion of Malignant Behavior in Cancer Cells: Erratum.","authors":"Xin Nie, Lingling Gao, Mingjun Zheng, Caixia Wang, Shuang Wang, Xiao Li, Yue Qi, Liancheng Zhu, Juanjuan Liu, Bei Lin","doi":"10.7150/jca.113036","DOIUrl":"https://doi.org/10.7150/jca.113036","url":null,"abstract":"<p><p>[This corrects the article DOI: 10.7150/jca.58524.].</p>","PeriodicalId":15183,"journal":{"name":"Journal of Cancer","volume":"16 7","pages":"2181"},"PeriodicalIF":3.3,"publicationDate":"2025-03-28","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12036089/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144009202","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}