International journal of oncology最新文献

{"title":"[Retracted] Pro‑metastatic intracellular signaling of the elaidic <i>trans</i> fatty acid.","authors":"Kiyomu Fujii, Yi Luo, Rina Fujiwara-Tani, Shingo Kishi, Song He, Shuyun Yang, Takamitsu Sasaki, Hitoshi Ohmori, Hiroki Kuniyasu","doi":"10.3892/ijo.2026.5935","DOIUrl":"https://doi.org/10.3892/ijo.2026.5935","url":null,"abstract":"<p><p>Following the publication of the above paper, an interested reader has drawn the Editor's attention to the fact that the tubulin control blots featured in Fig. 3 on p. 88 were strikingly similar to the control blots subsequently featured in a figure in another paper that was published by the same research group in the journal <i>Oncotarget</i>, where the experimental conditions were reported to be different. A subsequent investigation of the data in this paper undertaken by the Editorial Office revealed that various of the western blots included in Figs. 2A and B, 3E and F, and 4C and D appeared to have been duplicated within and/or between these figure parts; moreover, various of the data in these figure parts were remarkably similar to data which appeared (either previously or subsequently relative to the publication date of this article) in other papers written by different authors at different research institutes. Given that the contentious data mentioned above have apparently re‑appeared in a range of other publications, the Editor of <i>International Journal of Oncology</i> has decided that this paper should be retracted from the Journal. The authors were asked for an explanation to account for these concerns, but the Editorial Office did not receive a reply. The Editor apologizes to the readership for any inconvenience caused. [International Journal of Oncology 50: 85‑92, 2017; DOI: 10.3892/ijo.2016.3797].</p>","PeriodicalId":14175,"journal":{"name":"International journal of oncology","volume":"69 5","pages":""},"PeriodicalIF":7.3,"publicationDate":"2026-11-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148891622","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Regulatory T cells in lung adenocarcinoma: Mechanisms of immune escape, prognostic significance and therapeutic opportunities (Review).","authors":"Lijuan Wang, Chenjin Ruan","doi":"10.3892/ijo.2026.5943","DOIUrl":"https://doi.org/10.3892/ijo.2026.5943","url":null,"abstract":"<p><p>Lung adenocarcinoma (LUAD) represents the most prevalent type of lung cancer, accounting for 35‑40% of all lung cancer cases. Regulatory T cells (Tregs), a CD4⁺ T cell subtype with immunosuppressive functions, play a pivotal role in maintaining self‑tolerance under physiological conditions. Recent evidence has increasingly highlighted their involvement in various cancers. In LUAD, Treg infiltration into tissues undermines the immune anticancer response, correlating with disease stage, treatment efficacy and prognosis. By inhibiting robust anti‑tumor immune mechanisms, Tregs facilitate tumor immune escape in LUAD. Furthermore, elevated Treg cell accumulation in LUAD has been linked to reduced overall survival rates. Tregs serve as independent predictors for LUAD diagnosis in patients at high risk of recurrence. Systematic depletion of all Tregs to enhance anticancer efficacy poses risks of inducing severe autoimmune pathologies. Consequently, understanding the precise structure of tumor‑infiltrating Tregs is essential for effective targeting of these cells in tumors. Additionally, identifying candidate targets or methods for the specific elimination of tumor‑infiltrating Tregs is necessary for developing efficient and safe combination immunotherapy strategies for LUAD. The present study focuses on the regulatory role of Tregs in LUAD prognosis, immune escape and targeted therapies, elucidating the molecular mechanisms of Treg involvement and presenting associated therapeutic targets.</p>","PeriodicalId":14175,"journal":{"name":"International journal of oncology","volume":"69 5","pages":""},"PeriodicalIF":7.3,"publicationDate":"2026-11-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"149136647","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"[Corrigendum] TIP60 governs the auto‑ubiquitination of UHRF1 through USP7 dissociation from the UHRF1/USP7 complex.","authors":"Tanveer Ahmad, Waseem Ashraf, Abdulkhaleg Ibrahim, Liliyana Zaayter, Christian D Muller, Ali Hamiche, Yves Mély, Christian Bronner, Marc Mousli","doi":"10.3892/ijo.2026.5938","DOIUrl":"https://doi.org/10.3892/ijo.2026.5938","url":null,"abstract":"<p><p>Following the publication of the above article, and an Expression of Concern statement (doi: 10.3892/ijo.2026.5908) that was published in light of the fact that the GAPDH control western blots shown in Fig. 5A on p. 9 were strikingly similar to the GAPDH control western blots shown in Fig. 5D, the authors have responded to the queries raised by the Editorial Office. The GAPDH panels shown in Figs. 5A and 5D were generated from the same experiment and the same set of protein lysates: Fig. 5A presented the analysis of total protein expression, whereas Fig. 5D presented immunoprecipitation analyses performed using material derived from these same experimental samples. Consequently, the GAPDH loading control was legitimately shared between the two figures. However, given that the original figure legend did not explicitly state that the same GAPDH loading control was used for both analyses, to eliminate any possible ambiguity for readers, the authors have revised Fig. 5 by replacing the representative '-MG132 panel' in Fig. 5A with results obtained from an independent repeat experiment performed under identical experimental conditions. The revised version of Fig. 5 is shown on the next page. Note that this revised figure reproduces the original findings, and does not affect the quantitative analyses, the interpretation of the data, or the conclusions of the study. Regarding a query raised by the Editorial Office concerning the presentation of flow cytometric plots in Fig. 8, the authors explained that Fig. 8E was generated by applying an additional fluorescence gate to the parent flow cytometry dataset shown in Fig. 8B, which represents standard flow cytometric analysis, rather than duplication of experimental data, and so this figure was presented correctly, and as intended by the authors. The authors thank the Editor of <i>International Journal of Oncology</i> for granting them the opportunity to publish this corrigendum, and all the authors agree with its publication. [International Journal of Oncology 59: 89, 2021; DOI: 10.3892/ijo.2021.5269].</p>","PeriodicalId":14175,"journal":{"name":"International journal of oncology","volume":"69 5","pages":""},"PeriodicalIF":7.3,"publicationDate":"2026-11-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148989792","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Eomesodermin in renal cell carcinoma: Epigenetic and immune crosstalk driving tumor progression (Review).","authors":"Zhifei Che, Dongwen Huang, Jiaming Lin, Xincen Wang, Rongjin Feng, Xianping Che, Yubin Wang","doi":"10.3892/ijo.2026.5941","DOIUrl":"https://doi.org/10.3892/ijo.2026.5941","url":null,"abstract":"<p><p>Renal cell carcinoma (RCC) is the main pathological type of kidney cancer, which accounts for approximately 85‑95% of all cases of kidney cancer. Despite the emergence of targeted therapies and immunotherapies, however, the development of resistance remains common. Eomesodermin (Eomes) is a member of the T‑box transcription factor family that links both developmental biology and immune regulation with tumor‑associated programs. In RCC, its function appears to be context‑dependent. In tumor‑infiltrating leukocytes, Eomes has been shown to support mature natural killer cell and memory CD8⁺ T‑cell function, whereas persistent or dysregulated Eomes is associated with exhausted CD8⁺ T cells and Eomes‑positive type 1 regulatory T‑like immunosuppressive cells. In both intrinsic RCC tumor cells and stromal/endothelial compartments, current knowledge remains relatively limited, and what evidence there is has often been derived from indirect RCC pathway research, other tumor types or developmental models. The present review summarizes Eomes‑associated mechanisms in RCC through distinguishing among infiltrating leukocytes, tumor cells and stromal/endothelial compartments, and also through separating direct RCC evidence from indirectly derived mechanistic inferences. Epigenetic regulation, PI3K/Akt/mTOR signaling, Wnt/β‑catenin signaling, angiogenesis and therapeutic resistance are also discussed according to the strength of the available evidence. Current data support that Eomes stands as an exploratory biomarker and hypothesis‑generating therapeutic node, rather than as an established clinical target. Further research should be performed, however, to validate the cell‑type‑specific functions of Eomes in RCC tissues, single‑cell and spatial datasets, in addition to experimental RCC models.</p>","PeriodicalId":14175,"journal":{"name":"International journal of oncology","volume":"69 5","pages":""},"PeriodicalIF":7.3,"publicationDate":"2026-11-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148989810","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"[Retracted] <i>In vitro</i> modulation of MMP‑2 and MMP‑9 in adult human sarcoma cell lines by cytokines, inducers and inhibitors.","authors":"M W Roomi, T Kalinovsky, J Monterrey, M Rath, A Niedzwiecki","doi":"10.3892/ijo.2026.5942","DOIUrl":"https://doi.org/10.3892/ijo.2026.5942","url":null,"abstract":"<p><p>Following the publication of the above paper, it was drawn to the Editor's attention by a concerned reader that the gelatinase zymography data shown in Figs. 6, 10 and 14 on p. 1792, 1794 and 1795 respectively had also been included in a paper written by the same research group which had already been published in the same journal (<i>International Journal of Oncology</i>). Even though these data appeared to have been included in the two papers to show the same experimental details, given the re‑use of these data in the above paper, the authors were requested to submit replacement data for these figures to be included in a corrigendum. Given the 13 years that have elapsed since the publication of these papers, the only available author was unable to verify and comply with this request; therefore, the Editor has decided that this paper should be retracted from the Journal on account of the re‑use of the abovementioned data. The Editor apologizes to the readership for any inconvenience caused. [International Journal of Oncology 43: 1787‑1798, 2013; DOI: 10.3892/ijo.2013.2113].</p>","PeriodicalId":14175,"journal":{"name":"International journal of oncology","volume":"69 5","pages":""},"PeriodicalIF":7.3,"publicationDate":"2026-11-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"149038531","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"[Expression of Concern] Ultraviolet exposure of melanoma cells induces fibroblast activation protein‑α in fibroblasts: Implications for melanoma invasion.","authors":"Petra Wäster, Inger Rosdahl, Brendan F Gilmore, Oliver Seifert","doi":"10.3892/ijo.2026.5940","DOIUrl":"10.3892/ijo.2026.5940","url":null,"abstract":"<p><p>Following the publication of the above paper, it was drawn to the Editor's attention by a concerned reader that the control β‑actin blots shown in Fig. 1D and G on p. 195 appeared to be very similar, albeit with rotation of one set of the blots through 180°, and with resizing of the bands. Similarly, certain of the β‑actin protein bands shown in Fig. 1G were strikingly similar to the control β‑actin protein bands shown in Fig. 5A on p. 200, suggesting that data in these figures had been assembled incorrectly. The authors were contacted by the Editorial Office to offer an explanation for the apparent anomalies in the presentation of the data in this paper, although up to this time, no response from them has been forthcoming. Owing to the fact that the Editorial Office has been made aware of potential issues surrounding the scientific integrity of this paper, we are issuing an Expression of Concern to notify readers of this potential problem while the Editorial Office conitnues to investigate this matter further. [International Journal of Oncology 39: 193‑202, 2011; DOI: 10.3892/ijo.2011.1002].</p>","PeriodicalId":14175,"journal":{"name":"International journal of oncology","volume":"69 5","pages":""},"PeriodicalIF":7.3,"publicationDate":"2026-11-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148989820","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"[Corrigendum] Influence of doxorubicin on apoptosis and oxidative stress in breast cancer cell lines.","authors":"Nesstor Pilco-Ferreto, Gloria M Calaf","doi":"10.3892/ijo.2026.5923","DOIUrl":"10.3892/ijo.2026.5923","url":null,"abstract":"<p><p>Subsequently to the publication of the above article, an interested reader drew to the authors' attention that, concerning the three breast cancer cell lines investigated in their study, it was surprising that they should have detected caspase‑3 expression in the MCF‑7 cell line, as reported for example in Fig. 6, since it has been shown that MCF‑7 cells do not express caspase‑3 (see the paper by Reiner U. Jänicke and colleagues entitled 'MCF‑7 breast carcinoma cells do not express caspase‑3'. Breast Cancer Res Treat vol. 117.1 (2009); p. 219‑221). In their response, the authors acknowledge that the prevailing consensus in the literature, established by the seminal work of Jänicke et al in an article they published in 1998 in <i>Journal of Biological Chemistry</i> holds that MCF‑7 cells harbor a 47‑bp deletion in exon 3 of the CASP3 gene, resulting in a frameshift mutation and a premature stop codon, with consequent absence of detectable functional protein. The authors' own article acknowledged this controversy by citing conflicting reports (references 13 and 39 compared with references 41‑43); however, they also recognize in retrospect that this should have prompted a more circumspect interpretation of their own data. Following a critical re‑evaluation of their methodology, the authors wish to draw attention to the following limitations of the present work: (1) The band detected in MCF‑7 cells using antibody H‑277 cannot be unambiguously attributed to caspase‑3, and cross‑reactivity with co‑expressed proteins of similar molecular weight, most notably caspase‑7, cannot be excluded. (2) The DDRT‑PCR amplicon obtained from MCF‑7 cells with the reported primers may correspond to the aberrant CASP3 transcript arising from the exon 3 deletion, and does not necessarily represent a translation‑competent mRNA. Sequencing of this amplicon was not performed, and would be required to resolve this question. (3) The conclusions of the article on caspase‑3 expression in MCF‑7 cells should therefore be read with these methodological caveats in mind. Importantly, these limitations do not affect the principal findings of the study concerning MDA‑MB‑231 and MCF‑10F cell lines, for which the experimental evidence remains methodologically sound.  The authors are grateful to the Editorial Board of <i>International Journal of Oncology</i> for the rigor of the review process, and also for the opportunity to address these concerns transparently. They also thank the reader of the article for drawing these concerns to their attention. [International Journal of Oncology 49: 753‑762, 2016; DOI: 10.3892/ijo.2016.3558].</p>","PeriodicalId":14175,"journal":{"name":"International journal of oncology","volume":"69 4","pages":""},"PeriodicalIF":7.3,"publicationDate":"2026-10-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC13471130/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148578445","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":"MicroRNA regulation of macrophage polarization in lung cancer: Regulatory networks and therapeutic potential (Review).","authors":"Zhao Yiming, Li Jie","doi":"10.3892/ijo.2026.5934","DOIUrl":"10.3892/ijo.2026.5934","url":null,"abstract":"<p><p>Lung cancer is among the most prevalent and fatal cancers worldwide, with its progression heavily shaped by the tumor microenvironment (TME). As key immune cell populations within the TME of lung cancer, macrophages are involved in the entire process of tumor initiation and development. Macrophage polarization serves as a critical link between inflammation and tumorigenesis and is broadly divided into classically activated M1 and alternatively activated M2 phenotypes. These phenotypes exert tumor‑suppressive and tumor‑promoting effects, respectively, by secreting distinct cytokine profiles. MicroRNAs (miRNAs/miRs) are a class of endogenous small non‑coding RNAs that play broad roles in the malignant progression of lung cancer by regulating various cellular processes, including proliferation, resistance to apoptosis, and metabolic reprogramming. Emerging evidence suggests that miRNAs such as miR‑335‑5p, miR‑106a‑5p and miR‑99b regulate M1/M2 macrophage polarization by targeting key pathways in lung cancer. Through these regulatory events, miRNAs exert synergistic effects on multiple tumor hallmarks, including proliferation, invasion, migration, apoptosis, angiogenesis, cell cycle progression, stemness maintenance, and epithelial‑mesenchymal transition. Collectively, these events drive lung cancer progression and influence therapeutic efficacy. The present review synthesizes recent discoveries to explore the relationship between macrophage polarization and lung cancer, with a specific focus on miRNA‑mediated regulatory mechanisms in lung cancer therapy. Ultimately, the present review aimed to provide new insight and a reference point to inform future prevention and treatment strategies for lung cancer.</p>","PeriodicalId":14175,"journal":{"name":"International journal of oncology","volume":"69 4","pages":""},"PeriodicalIF":7.3,"publicationDate":"2026-10-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC13553194/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148891609","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":"piR‑164552 promotes malignant progression in head and neck squamous cell carcinoma via the RBM4/EIF4E2 signaling axis: Insights from multi‑omics and functional analyses.","authors":"Shan Yang, Zhen Shang, Shunxian Xia, Hongbo Liu, Yanhan Dong, Xiaomin Wang, Wenhua Xu, Haijun Lu","doi":"10.3892/ijo.2026.5924","DOIUrl":"https://doi.org/10.3892/ijo.2026.5924","url":null,"abstract":"<p><p>Head and neck squamous cell carcinoma (HNSCC) is a highly aggressive malignancy with limited options for early diagnosis and poor clinical outcomes. In the present study, PIWI‑interacting RNA (piR)‑164552 was identified as a novel oncogenic regulator in HNSCC. piR‑164552 was found to be markedly upregulated in tumor tissues and serum exosomes and its expression promoted the proliferation, migration, invasion and tumorigenicity of HNSCC cells both <i>in vitro</i> and <i>in vivo</i>. Mechanistic analyses revealed that piR‑164552 interacted with RNA‑binding motif protein 4 (RBM4) and positively regulated RBM4 protein levels, which in turn enhanced the expression of eukaryotic initiation factor 4E‑like 2 (EIF4E2), forming a piR‑164552/RBM4/EIF4E2 axis. Integrated transcriptomic and translatomic profiling further demonstrated that this axis orchestrated extensive reprogramming of mRNA metabolism, ribosome biogenesis and cancer‑associated signaling pathways, underscoring its multilayered role in tumor progression. The present findings highlighted the diagnostic potential of piR‑164552 and uncovered its key contribution to the molecular network driving HNSCC, providing new insights into biomarker development and therapeutic strategies.</p>","PeriodicalId":14175,"journal":{"name":"International journal of oncology","volume":"69 4","pages":""},"PeriodicalIF":7.3,"publicationDate":"2026-10-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC13471134/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148758292","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":"Signaling pathways and targeted therapy in high‑risk refractory thyroid cancer: From bench to bedside (Review).","authors":"Jian Wang, Zhi Liu, Qing Zhang, Wei Sun","doi":"10.3892/ijo.2026.5927","DOIUrl":"10.3892/ijo.2026.5927","url":null,"abstract":"<p><p>Thyroid cancer is the most common endocrine malignancy worldwide, with its incidence increasing markedly over the past several decades, while mortality trends have shown complex patterns. High‑risk refractory thyroid cancers (including radioactive iodine‑refractory differentiated thyroid cancer, poorly differentiated thyroid cancer, anaplastic thyroid carcinoma, progressive medullary thyroid carcinoma and locally advanced disease) pose major challenges in clinical management. The present review systematically reviewed recent epidemiological trends in thyroid cancer and provided an in‑depth exploration of the molecular regulatory mechanisms of key signaling pathways, including MAPK, PI3K/AKT, Janus kinase/STAT, WNT/β‑catenin and NF‑κB, along with their roles in the pathogenesis and progression of thyroid cancer. Based on this, the latest clinical research advances in targeted therapies for high‑risk, refractory thyroid cancer are elaborated on, covering multikinase inhibitors, B‑Raf proto‑oncogene, serine/threonine kinase/mitogen‑activated protein kinase kinase inhibitors, immunotherapy combinations, innovative targeted strategies and redifferentiation approaches. Finally, future directions are discussed based on the 'total treatment' paradigm and strategies to overcome drug resistance, aiming to provide a systematic reference for basic research and clinical translation in thyroid cancer.</p>","PeriodicalId":14175,"journal":{"name":"International journal of oncology","volume":"69 4","pages":""},"PeriodicalIF":7.3,"publicationDate":"2026-10-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC13496938/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148764897","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}