Cancer Biology & Therapy最新文献

{"title":"xinguangA preliminary characterization of PI4K/PIPK alterations across solid tumors: an exploratory framework for prognostic and therapeutic stratification.","authors":"Yaqiong Jie, Zhongyu Lu, Xiaoxuan Wang, Dongsheng Chen, Xing Zhang, Xinguang Han","doi":"10.1080/15384047.2026.2692173","DOIUrl":"10.1080/15384047.2026.2692173","url":null,"abstract":"<p><strong>Background: </strong>This study aimed to systematically characterize the genomic alteration landscape of phosphatidylinositol 4-kinase (PI4K) and phosphatidylinositol phosphate kinase (PIPK) family genes in solid tumors, assess the correlation of these alterations with patient clinical outcomes and the tumor immune microenvironment, and explore their potential as novel biomarkers or therapeutic targets.</p><p><strong>Methods: </strong>A retrospective analysis was conducted on whole-exome sequencing data from a cohort of 2,144 Chinese patients encompassing 18 solid tumor types. Genomic and transcriptomic data from The Cancer Genome Atlas (TCGA) pan-cancer project were integrated to perform survival analysis, correlating genomic alterations, gene expression levels, and patient overall survival. Associations between these gene alterations and tumor mutational burden (TMB), microsatellite instability (MSI), and levels of tumor-infiltrating immune cells were also evaluated.</p><p><strong>Results: </strong>We identified PI4K/PIPK alterations in 10.5% of 2,144 patients, with PIP4K2C amplification reaching 48%. While PI4K2B amplification and overexpression are consistently associated with poor prognosis in COAD, family-wide effects were highly heterogeneous across cancers. Alterations significantly correlated with higher TMB and MSI-H, and multi-omics analysis revealed tissue-specific immune landscapes, highlighting the family's potential for risk stratification and immunotherapy.</p><p><strong>Conclusions: </strong>This study provides the first systematic delineation of the genomic alteration landscape of PI4K and PIPK families at a pan-cancer scale within a Chinese population. It identifies PI4K2B as an amplification-driven prognostic biomarker in colorectal cancer, with potential clinical value analogous to HER2. These findings illuminate the significant roles of these kinases in cancer and provide novel insights for future precision oncology strategies.</p>","PeriodicalId":9536,"journal":{"name":"Cancer Biology & Therapy","volume":"27 1","pages":"2692173"},"PeriodicalIF":5.7,"publicationDate":"2026-12-31","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC13371475/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148435128","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":"<i>RET</i> fusion partners dictate oncogenic potential in undifferentiated spindle cell sarcomas.","authors":"Qi Gui, Ying Zhang, Mei Yang, Rongrui Liang, Man Huang, Xiaoshan Yang, Nan Chen, Xiaojun Chen, Mengyao Wu, Huafei Chen, Lijun Meng, Sheng Xiao, Min Tao","doi":"10.1080/15384047.2026.2683190","DOIUrl":"10.1080/15384047.2026.2683190","url":null,"abstract":"<p><strong>Background: </strong>Spindle cell tumors with <i>RET</i> rearrangements exhibit variable clinical behaviors, ranging from benign to highly aggressive malignancies. The underlying heterogeneity is suspected to be associated with distinct fusion partner genes. Understanding the impact of these fusion partners on oncogenic potential is crucial for precision therapy.</p><p><strong>Methods: </strong>We report a case of a spindle cell tumor harboring an <i>MYH10::RET</i> fusion, which initially responded to anti-RET therapy but relapsed due to an <i>NTRK1</i> fusion. Isogenic cell lines expressing MYH10::RET and CCDC6::RET were established. Functional assays, including cell proliferation, migration, invasion, and kinase activity assays, were performed. Genomic profiling was conducted using targeted DNA and RNA NGS and FISH.</p><p><strong>Results: </strong>MYH10::RET-expressing cells showed significantly higher proliferation, migration, and invasion compared to CCDC6::RET-expressing cells. MYH10::RET exhibited approximately three-fold higher kinase activity. The patient's disease was managed through sequential targeted therapies, including combination therapy with third-generation inhibitors targeting RET and NTRK.</p><p><strong>Conclusion: </strong>Our findings suggest that distinct <i>RET</i> fusion partners significantly contribute to the clinical heterogeneity of <i>RET</i>-rearranged spindle cell tumors, likely through differential kinase activity. Continuous genomic monitoring is essential for identifying resistance mechanisms and guiding precision therapy. Future studies should explore the impact of different fusion partners on tumor behavior and therapeutic response.</p>","PeriodicalId":9536,"journal":{"name":"Cancer Biology & Therapy","volume":"27 1","pages":"2683190"},"PeriodicalIF":5.7,"publicationDate":"2026-12-31","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC13240951/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148155461","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":"KIF18A inhibitor prevents chromosomally unstable osteosarcoma growth by activating spindle assembly checkpoint.","authors":"Qiang Yan, Yan Zhang, Pengfei Wang, Yahui Fu, Chao Ke, Shuang Han, Jian Xing, Haoran Li, Kun Zhang","doi":"10.1080/15384047.2026.2689181","DOIUrl":"10.1080/15384047.2026.2689181","url":null,"abstract":"<p><strong>Background: </strong>Osteosarcoma survival rates have not improved significantly in decades, as complex gene mutations and intratumoral heterogeneity hinder new therapy development. To exploit the widespread chromosomal instability in osteosarcoma, we investigated targeting the essential mitotic motor protein KIF18A.</p><p><strong>Materials: </strong>Two whole-genome-doubling clones derived from the near-diploid SJSA1 osteosarcoma cell line were used to evaluate sensitivity to KIF18A knockout or pharmacological inhibition. The traditional osteosarcoma cell lines U2OS and MG63 were included in the study of the KIF18A inhibitor at both the cellular and xenograft (nude mice) levels.</p><p><strong>Results: </strong>Depletion of KIF18A significantly reduced cell viability, survival, and proliferation in the SPT cell, but not in the parental SJSA1 cell. Loss of KIF18A expression led to aberrant spindle assembly and mitotic delay through the activation of spindle assembly checkpoint (SAC) signaling. Therefore, the deficiency of SAC rescued the SPT cell growth. We then tested one of the latest KIF18A inhibitors, AM-1882, in SPT, U2OS, and MG63 cells. It showed potent anti-cancer activity and disruption of spindle assembly activity, just like the KIF18A knockout. In the mouse xenograft model, AM-1882 also apparently prevented tumor growth and, notably, did not show any toxicity when compared with chemotherapeutic drugs.</p><p><strong>Conclusion: </strong>Overall, our study demonstrated that KIF18A is a promising therapeutic target in osteosarcoma. The novel inhibitor AM-1882 offers exceptional anti-tumor efficacy paired with a favorable, low-toxicity safety profile.</p>","PeriodicalId":9536,"journal":{"name":"Cancer Biology & Therapy","volume":"27 1","pages":"2689181"},"PeriodicalIF":5.7,"publicationDate":"2026-12-31","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC13290091/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148293523","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":"Statement of retraction: Long non-coding RNA LINC01133 silencing exerts antioncogenic effect in pancreatic cancer through the methylation of DKK1 promoter and the activation of Wnt signaling pathway.","authors":"","doi":"10.1080/15384047.2026.2740282","DOIUrl":"10.1080/15384047.2026.2740282","url":null,"abstract":"","PeriodicalId":9536,"journal":{"name":"Cancer Biology & Therapy","volume":"27 1","pages":"2740282"},"PeriodicalIF":5.7,"publicationDate":"2026-12-31","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC13625708/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"149073616","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":"Elevated miR-103b in exosomes derived from brain-metastatic triple-negative breast cancer cells remodels the brain pre-metastatic niche (PMN).","authors":"Li Zhou, Jin Ke, Shanlan Zhang, Sufang Xiao, Hui Zhang, Shan Liu, Li Liu, Mingan Liu, Zuohua Lu, Songguo Zheng","doi":"10.1080/15384047.2026.2725357","DOIUrl":"10.1080/15384047.2026.2725357","url":null,"abstract":"<p><strong>Background: </strong>Triple-negative breast cancer (TNBC) is a highly aggressive breast cancer with high brain metastatic (BM) potential. Tumor-derived exosomes are implicated as key modulators during the formation of the pre-metastatic niche (PMN). However, the regulation of TNBC-BM-derived exosomes on brain PMN remains enigmatic.</p><p><strong>Methods: </strong>The morphology and uptake of exosomes were identified using transmission electron microscopy and live-cell imaging, respectively. Differentially secreted miRNAs and mRNA were identified using high-throughput sequencing. The permeability of the blood‒brain barrier (BBB) and tight junction integrity were examined using immunofluorescence staining. Cell viability was examined using the CCK-8 assay. The apoptosis and intracellular ROS were investigated using fluorescence staining. The expression of mRNAs was examined using qPCR.</p><p><strong>Results: </strong>miR-103b was significantly increased in exosomes derived from TNBC-BM cells. miR-103b compromised the tight junctions of HUVECs and increased BBB permeability in mice. Additionally, miR-103b promoted apoptosis and increased intracellular ROS in HUVECs and U251 cells, two cell lines commonly used as surrogates for brain microvascular endothelial cells and astrocytes, respectively. miR-103b-regulated differentially expressed genes modulated tight junction, apoptosis, oxidative stress, inflammation, and metabolism. Target analysis identified 216 targets of miR-103b, among which hub targets were associated with biological processes involved in maintaining the BBB and the glucose metabolism signaling pathway.</p><p><strong>Conclusion: </strong>Collectively, our findings for the first time reveal that exosomal miR-103b from TNBC-BM cells potentially regulates the two major cellular constituents of the brain PMN, highlighting its role in the formation of the brain PMN during TNBC-BM and its potential as a promising therapeutic target.</p>","PeriodicalId":9536,"journal":{"name":"Cancer Biology & Therapy","volume":"27 1","pages":"2725357"},"PeriodicalIF":5.7,"publicationDate":"2026-12-31","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC13618856/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"149036614","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":"RecurIndex-derived molecular features associated with total pathological complete response in triple-negative breast cancer: An exploratory prospective cohort study with single-cell transcriptomic contextualization.","authors":"Meilin Chen, Xiwen Yan, Qifan Chen, Jiayi Bei, Zheng Pan, Tian Zhang, Weihao Cheng, Lu Xu, Feng Jin, Yan Gao, Zining Jin, Ang Zheng","doi":"10.1080/15384047.2026.2743407","DOIUrl":"10.1080/15384047.2026.2743407","url":null,"abstract":"<p><strong>Background: </strong>Reliable biomarkers for predicting neoadjuvant chemotherapy (NAC) response in triple-negative breast cancer (TNBC) remain limited. We explored whether RecurIndex-derived molecular features were associated with total pathological complete response (tpCR).</p><p><strong>Methods: </strong>Seventy-four patients with TNBC treated with dose-dense NAC were analyzed. Associations between RecurIndex risk scores, 18 core genes, and tpCR were assessed using logistic regression and ROC analyses. Clinical-molecular models were internally validated by bootstrap resampling. Public single-cell RNA-seq data were used for biological contextualization.</p><p><strong>Results: </strong>Twenty-nine patients (39.2%) achieved tpCR. The distant recurrence score, was significantly associated with tpCR. OBSL1, BLM, and CCR1 were identified as candidate tpCR-associated genes. The model combining OBSL1, BLM, and clinical nodal stage achieved an AUC of 0.838 and an optimism-corrected AUC of 0.799.</p><p><strong>Conclusions: </strong>RecurIndex-derived molecular features were associated with tpCR in TNBC. These exploratory findings warrant validation in independent cohorts.</p>","PeriodicalId":9536,"journal":{"name":"Cancer Biology & Therapy","volume":"27 1","pages":"2743407"},"PeriodicalIF":5.7,"publicationDate":"2026-12-31","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC13656812/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"149163960","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":"Glutamine transporter SLC1A5 inhibits autophagy-mediated CD276 degradation to promote esophageal cancer progression.","authors":"Chunyan Wang, Hongyan Zhang, Chaonan Guan, Yuying Li, Shengli Yang, Lan Huang","doi":"10.1080/15384047.2026.2621606","DOIUrl":"10.1080/15384047.2026.2621606","url":null,"abstract":"<p><strong>Background: </strong>CD276/B7-H3 is an immune checkpoint molecule often overexpressed in cancers, representing a potential therapeutic target. The underlying mechanisms for CD276 upregulation remain unclear. This study investigates how glutamine metabolism affects CD276 protein stability and esophageal squamous cell carcinoma (ESCC) progression.</p><p><strong>Methods: </strong>CD276 and SLC1A5 expression were analyzed in 90 ESCC clinical tissues and TCGA/GEO datasets. CCK-8, colony formation, wound healing and transwell assays were performed in KYSE150 and KYSE450 cells. Autophagy was quantified by immunofluorescence and western blot. Mitochondrial reactive oxygen species (ROS) levels measured by flow cytometry. Rescue experiments used <i>N</i>-acetylcysteine (NAC) and chloroquine (CQ). Finally, antitumor effects of SLC1A5 inhibitor V9302 in the presence or absence of CD276 were evaluated in NOD/SCID mice (<i>n</i> = 5 per group) bearing KYSE150 xenografts.</p><p><strong>Results: </strong>CD276 and SLC1A5 upregulated in ESCC tissues (<i>P</i> < 0.05). CD276 overexpression enhanced ESCC cell proliferation and migration by 42.3% and 58.7%, respectively (<i>P</i> < 0.01). CQ but not MG-132 increased CD276 expression in ESCC cells. SLC1A5 stabilized CD276 protein without altering CD276 mRNA levels, by suppressing ROS-dependent autophagic degradation. NAC reversed ROS-induced CD276 degradation, while CQ abrogated CD276 downregulation upon glutamine metabolism inhibition. Inhibiting glutamine metabolism could reverse ESCC cell proliferation induced by CD276 overexpression. Moreover, combination of V9302 and CD276 knockout significantly reduced KYSE150 cell-derived xenograft tumor volume by 65.2% (95% CI 58.3-72.1%, <i>P</i> < 0.001) in NOD/SCID mice, without affecting mouse body weight (<i>P</i> > 0.05).</p><p><strong>Conclusion: </strong>SLC1A5 enhances CD276 stability by suppressing ROS-autophagy signaling, promoting ESCC progression. Targeting glutamine metabolism to enhance CD276 degradation might be a novel therapeutic strategy for ESCC.</p>","PeriodicalId":9536,"journal":{"name":"Cancer Biology & Therapy","volume":"27 1","pages":"2621606"},"PeriodicalIF":5.7,"publicationDate":"2026-12-31","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12867364/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"146117555","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":"The MYBL2-GTSE1 axis promotes laryngeal squamous cell carcinoma progression by regulating PI3K/AKT-dependent glycolytic reprogramming.","authors":"Yiyin Liang, Cansi Wang, Tianjiao Ren, Bo Zhang, Yaqi Liu, Rong Fu, Juan Feng","doi":"10.1080/15384047.2026.2648193","DOIUrl":"10.1080/15384047.2026.2648193","url":null,"abstract":"<p><strong>Background: </strong>Laryngeal squamous cell carcinoma (LSCC) is a common head and neck malignancy with poor prognosis. The role of MYBL2, an oncogenic transcription factor, in the glycolytic reprogramming of LSCC remains unclear.</p><p><strong>Methods: </strong>We integrated RNA-sequencing with public databases (TCGA, GEO) and tissue microarrays to assess MYBL2 expression and its clinical significance. Transcriptional regulation was verified by ChIP-qPCR and luciferase reporter assays. Signaling pathways and metabolic profiles were examined using Western blotting and Seahorse analysis (ECAR/OCR). Biological functions were evaluated by <i>in vitro</i> functional assays and <i>in vivo</i> xenograft models in female BALB/c nude mice.</p><p><strong>Results: </strong>MYBL2 was significantly overexpressed in LSCC tissues and correlated with poor prognosis. Mechanistically, MYBL2 directly activates GTSE1 transcription. This regulation stimulates PI3K/AKT signaling to upregulate key glycolytic proteins (PKM2, HK2, GLUT1, LDHA), thereby driving metabolic reprogramming characterized by elevated glycolysis (ECAR) and suppressed mitochondrial respiration (OCR). Functionally, MYBL2 overexpression enhanced the proliferation, migration, and invasion of LSCC cells <i>in vitro</i> and promoted tumor growth <i>in vivo</i>. Importantly, these oncogenic effects were effectively reversed by GTSE1 knockdown or PI3K inhibition with LY294002, validating the pathway's functional significance.</p><p><strong>Conclusion: </strong>The MYBL2-GTSE1 axis promotes LSCC progression through PI3K/AKT-mediated metabolic reprogramming, representing a promising therapeutic target.</p>","PeriodicalId":9536,"journal":{"name":"Cancer Biology & Therapy","volume":"27 1","pages":"2648193"},"PeriodicalIF":5.7,"publicationDate":"2026-12-31","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC13011630/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"147497641","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":"The role of copper and cuproptosis in digestive system cancers: novel therapeutic strategies and mechanistic insights.","authors":"Guoshuai Xu, Nan Yao, Renjia Cheng, Lin Yang, Fuzhou Han, Jun Qu, Wenqiang Li","doi":"10.1080/15384047.2026.2644674","DOIUrl":"10.1080/15384047.2026.2644674","url":null,"abstract":"<p><p>Recent research has highlighted the critical role of copper metabolism and a novel form of copper-dependent cell death, termed cuproptosis, in the progression and treatment of these cancers. Copper, an essential trace element, plays a crucial role in various cellular processes, including mitochondrial function, antioxidant defense, and angiogenesis. However, the dysregulation of copper homeostasis in cancer cells can exacerbate genomic instability, promote angiogenesis, and reshape the immune microenvironment, thereby driving tumor progression. This review systematically explores the mechanisms of copper homeostasis and cuproptosis in digestive system cancers. We also explore innovative strategies for overcoming drug resistance and reshaping immune responses through copper chelators, copper ionophores, and nanomedicines that induce cuproptosis. By integrating basic research with clinical evidence, this review aims to provide a scientific perspective on understanding the biological significance of cuproptosis and developing new anticancer strategies, while also stimulating in-depth thinking on the intersection of metabolic intervention and cell death.</p>","PeriodicalId":9536,"journal":{"name":"Cancer Biology & Therapy","volume":"27 1","pages":"2644674"},"PeriodicalIF":5.7,"publicationDate":"2026-12-31","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12998029/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"147466843","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":"Statement of Retraction: Upregulation of long non-coding RNA NNT-AS1 promotes osteosarcoma progression by inhibiting the tumor suppressive miR-320a.","authors":"","doi":"10.1080/15384047.2026.2740298","DOIUrl":"10.1080/15384047.2026.2740298","url":null,"abstract":"","PeriodicalId":9536,"journal":{"name":"Cancer Biology & Therapy","volume":"27 1","pages":"2740298"},"PeriodicalIF":5.7,"publicationDate":"2026-12-31","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC13641516/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"149079660","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}