Oncology reports最新文献

{"title":"Molecular mechanisms and potential targeting strategies of ubiquitin‑proteasome system‑mediated PD‑1/PD‑L1 ubiquitination in tumor immune suppression (Review).","authors":"Li-Hui Gu, Ai Guo, Yi-Yue Ding, Xue-Jie Wang, Hong-Xing Zhang, Wan-Li Duan, Bao-Gang Zhang","doi":"10.3892/or.2025.9000","DOIUrl":"10.3892/or.2025.9000","url":null,"abstract":"<p><p>Cancer cells play a pivotal role in immune evasion by activating the programmed cell death protein 1 (PD‑1)/PD‑ligand (L)1 signaling pathway or immune cells within the tumor microenvironment. The ubiquitin‑proteasome system (UPS), the primary pathway for intracellular protein degradation, has been increasingly implicated in mediating tumor immune escape and resistance to anti‑PD‑1/PD‑L1 therapy. Targeting the UPS has demonstrated significant potential in improving the efficacy of tumor immunotherapy. Therefore, a deeper understanding of the molecular mechanisms by which UPS contributes to tumor resistance against PD‑1/PD‑L1 blockade, along with the optimization of UPS‑targeted small‑molecule drug design, holds scientific and clinical significance. In the present review, the role of UPS in tumor immune evasion through the regulation of PD‑1/PD‑L1 ubiquitination was discussed and potential therapeutic agents that may enhance the effectiveness of anti‑PD‑1/PD‑L1 treatment are summarized. These insights provide a theoretical foundation for advancing cancer immunotherapy and developing novel combination strategies.</p>","PeriodicalId":19527,"journal":{"name":"Oncology reports","volume":"54 6","pages":""},"PeriodicalIF":3.9,"publicationDate":"2025-12-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12511930/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145213294","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":"The silent players: Atypical <i>BCR‑ABL </i>isoforms as biomarkers and therapeutic hurdles in CML pathogenesis (Review).","authors":"Xin Zhou, Ai Li, Dexiao Kong, Yuqi Shi, Peipei Zhang, Ningning Shan","doi":"10.3892/or.2025.8995","DOIUrl":"10.3892/or.2025.8995","url":null,"abstract":"<p><p>Chronic myeloid leukemia (CML) is a hematological malignancy driven by diverse genetic aberrations, with the Philadelphia chromosome and its resultant <i>BCR‑ABL1 </i>fusion gene constituting key pathogenic drivers. Atypical <i>BCR‑ABL1</i> fusion transcripts have distinctive structural and functional properties. Structural divergence in these variants leads to functional alterations of encoded oncoproteins, potentially influencing disease progression and therapeutic responsiveness. Conventional diagnostic modalities, including reverse transcription‑PCR and fluorescence in situ hybridization, may fail to detect rare variants, necessitating complementary high‑sensitivity techniques such as next‑generation sequencing). Tyrosine kinase inhibitors (TKIs), including imatinib and dasatinib, remain cornerstone treatments; however, marked inter‑variant heterogeneity in TKI responsiveness is observed: Patients harboring <i>e13a3/e14a3</i> transcripts generally show favorable prognoses, while those with <i>e1a3/e6a2</i> variants demonstrate an increased risk of relapse and/or TKI resistance, often requiring multimodal strategies combining chemotherapy or allogeneic hematopoietic stem cell transplantation. Although Chimeric Antigen Receptor)‑T cell therapy has shown promise in treating (Philadelphia chromosome‑positive B‑cell Acute Lymphoblastic Leukemia, its application in CML, particularly in variants such as <i>e1a3</i> or <i>e6a2</i>, is not currently recommended as a first‑line treatment. Despite advances in elucidating the clinical implications of fusion gene heterogeneity in leukemogenesis, the prognostic value of atypical <i>BCR‑ABL1 </i>isoforms requires further validation through multicenter studies with extended cohorts. This review aimed to summarize cases of atypical fusion genes in CML, with analysis of clinical characteristics, therapeutic interventions, and prognostic outcomes, to provide clinicians with enhanced reference material for improved patient management.</p>","PeriodicalId":19527,"journal":{"name":"Oncology reports","volume":"54 6","pages":""},"PeriodicalIF":3.9,"publicationDate":"2025-12-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12498562/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145150040","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":"Relationship between amino acid transporter activity and radioactive iodine therapy efficacy in differentiated thyroid cancer.","authors":"Akihito Kotani, Yota Tatara, Riki Sakamoto, Andrzej Wojcik, Yasushi Mariya, Satoru Monzen","doi":"10.3892/or.2025.8993","DOIUrl":"10.3892/or.2025.8993","url":null,"abstract":"<p><p>Thyroid cancer is the most common malignant endocrine tumor. Differentiated thyroid cancer (DTC) accounts for 95% of thyroid cancer cases. The primary treatment for intermediate‑ and high‑risk DTC is total thyroidectomy. Postoperatively, serum thyroglobulin (Tg) and anti‑Tg antibody (Tg/Ab) levels are monitored to detect residual, recurrent or metastatic disease. Radioactive iodine (¹³¹I) therapy is administered orally when Tg and Tg/Ab levels exceed standard levels. Recombinant human thyroid‑stimulating hormone (rhTSH) administration methods that do not require thyroid hormone withdrawal treatment and hospitalization have been recommended. However, serum Tg levels, a biomarker of thyroid tissue ablation, are often disturbed by Tg/Ab interference, which is observed in one‑quarter of patients with DTC. The present study aimed to elucidate the molecular mechanisms underlying metabolic changes in patients with DTC treated with ¹³¹I, and to identify Tg/Ab‑independent biomarker candidates using the TPC‑1 cell model. Blood serum samples were collected from patients with DTC before and after administration of ¹³¹I, which was performed following stimulation with rhTSH. Intra‑individual variations in Tg and Tg/Ab levels were observed in the same patients before and after ¹³¹I administration. Serum metabolomic analysis showed elevated levels of branched‑chain amino acid (BCAA), including valine, leucine and isoleucine, in all 3 patients, who exhibited favorable clinical outcomes. Although the number of cases was limited, this may suggest a possible association between BCAA levels and treatment response. Additionally, while overall boronophenylalanine uptake decreased in the total cell population after ionizing radiation exposure, the surviving viable TPC‑1 cells exhibited relatively increased amino acid uptake, assessed using boronophenylalanine as a leucine analog, which corresponded to the findings presented in the cell‑based experiments. Higher expression levels of the CD98 cell surface antigen were observed in irradiated TPC‑1 cells compared with non‑irradiated controls, which may contribute to increased uptake of BCAAs. However, the mRNA expression levels of L‑type amino acid transporter type 1 (<i>LAT1</i>), L‑type amino acid transporter type 2 and <i>CD98hc</i> did not change upon exposure to IR. These results indicated that the increased BCAA uptake in IR‑exposed DTC cells was a transient response likely mediated by LAT1/CD98hc at the cell surface, as suggested by flow cytometry analysis, despite no corresponding increase in <i>LAT1</i> mRNA expression.</p>","PeriodicalId":19527,"journal":{"name":"Oncology reports","volume":"54 6","pages":""},"PeriodicalIF":3.9,"publicationDate":"2025-12-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12489427/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145150034","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":"Neuroscience in glioma biology (Review).","authors":"Chunzhi Zhang, Hanning Zhang, Jiahao Cao, Meili Liu","doi":"10.3892/or.2025.8999","DOIUrl":"10.3892/or.2025.8999","url":null,"abstract":"<p><p>Although our understanding of the molecular and cellular factors involved in the development and growth of glioma has increased, prognosis remains dismal in most patients. The emerging field of cancer neuroscience has revealed the intricate functional interplay between glioma and the cellular architecture of the brain, especially neural circuits. In recent years, studies have revealed that glioma cells integrate and remodel multicellular neural circuits. Neural circuits have thus emerged as critical regulators of glioma from initiation to malignant growth. In the present review, an updated framework was provided for understanding the construction of neuron‑glioma networks and the mechanisms by which neurons regulate the malignant phenotype of glioma. Readers will also obtain insights into the construction of glioma‑glioma networks formed by tumor microtubes. Furthermore, the present review reveals the complex interconnectivity among the nervous system, immune system and glioma that promotes tumor growth. Finally, some potential areas of clinical translation and new research directions were highlighted.</p>","PeriodicalId":19527,"journal":{"name":"Oncology reports","volume":"54 6","pages":""},"PeriodicalIF":3.9,"publicationDate":"2025-12-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12511927/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145149844","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":"Multiple roles of replication factor C family in pan‑cancer (Review).","authors":"Dan Luo, Bo Li, Xueping Jiang","doi":"10.3892/or.2025.8998","DOIUrl":"10.3892/or.2025.8998","url":null,"abstract":"<p><p>Due to the persistently high global incidence and mortality rates of cancer, developing novel therapeutic strategies is imperative. The replication factor C (RFC) family, a critical subset of DNA replication and repair, serves multifaceted roles in tumor progression. Despite its widely recognized importance, the pleiotropic mechanisms of the RFC family lack systematic illustration, particularly regarding each member specific contributions to cancer hallmarks. In the present review, mRNA expression of each RFC family member in pan‑cancer was profiled and the associations between their expression levels and tumor types evaluated. In addition, the effect of RFC expression on patients' survival across malignancies is assessed. Furthermore, the present review summarized current research on RFC family members in various malignancies with particular emphasis on the RFC‑like complexes, highlighting key findings and advancements in understanding their role in tumor biology. The signaling pathways associated with RFC family members are discussed and the molecular mechanisms elucidated. Finally, the clinical importance of RFC family members including prognosis, potential inhibitors and combination treatments are also discussed. The present review aimed to provide innovative perspectives for developing combinatorial molecular targeted therapies in the future.</p>","PeriodicalId":19527,"journal":{"name":"Oncology reports","volume":"54 6","pages":""},"PeriodicalIF":3.9,"publicationDate":"2025-12-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12512507/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145149880","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":"m6A reader IGF2BP2 mediates paclitaxel resistance in esophageal squamous cell carcinoma via FOXM1 mRNA stabilization.","authors":"Shiheng Ren, Jingru Wu, Lening Zhang, Guangyi Guan, Wenpeng Jiang","doi":"10.3892/or.2025.9002","DOIUrl":"10.3892/or.2025.9002","url":null,"abstract":"<p><p>Esophageal squamous cell carcinoma (ESCC) ranks among the primary contributors to cancer‑related mortality in China. Resistance to paclitaxel markedly diminishes its therapeutic effectiveness and outcomes. Anaerobic glycolysis is a pivotal mechanism in cancer progression. Insulin‑like growth factor 2 mRNA binding protein 2 (IGF2BP2) as a reader of RNA N6‑methyladenosine (m6A) modification ensures the stability of RNA at the post‑transcriptional level. Nonetheless, the role and mechanism of IGF2BP2 in mediating paclitaxel resistance and anaerobic glycolysis in ESCC remain unclear. The current study selected two ESCC cell lines (KYSE30 and KYSE150). Cell proliferation and clonogenic ability were assessed via functional experiments. Apoptosis was quantified through flow cytometry. The rate of anaerobic glycolysis was determined via glycolysis assays. The stability of Forkhead box M1 (FOXM1) mRNA was assessed through reverse transcription‑quantitative polymerase chain reaction following actinomycin D treatment. Protein levels were analyzed through western blotting. Bioinformatics analysis revealed an overexpression of IGF2BP2 in ESCC. Furthermore, IGF2BP2 silencing inhibited cell proliferation and clonogenic activity. RNA and m6A‑sequencing results suggested that FOXM1 is critical to IGF2BP2‑mediated paclitaxel resistance in ESCC. Additionally, it was discovered that the silencing of IGF2BP2 compromises FOXM1 mRNA stability, reduces anaerobic glycolysis, and diminishes paclitaxel resistance. Finally, FOXM1 overexpression mitigated the effects of IGF2BP2 silencing in ESCC cells. The current findings underscore the significant role of the IGF2BP2‑FOXM1 signaling pathway in modulating anaerobic glycolysis and paclitaxel resistance in ESCC, offering insights into future therapeutic approaches to this malignancy.</p>","PeriodicalId":19527,"journal":{"name":"Oncology reports","volume":"54 6","pages":""},"PeriodicalIF":3.9,"publicationDate":"2025-12-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145213311","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] Downregulation of miR‑145 contributes to lung adenocarcinoma cell growth to form brain metastases.","authors":"Chunyang Zhao, Yan Xu, Yongqiang Zhang, Weiwei Tan, Jianxin Xue, Zongze Yang, You Zhang, You Lu, Xun Hu","doi":"10.3892/or.2025.8991","DOIUrl":"10.3892/or.2025.8991","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, regarding the cell migration and invasion assay experiments shown in Fig. 4, the 'Mock' data panel in Fig. 4A‑a (A549 cell line, migration assay) was apparently identical to the 'Mock' data panel in Fig. 4B‑b (SPC‑A1 cell line, invasion assay), even though the reported experimental conditions were different. The authors were contacted by the Editorial Office to offer an explanation for this apparent data duplication; however, 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 continues to investigate this matter further. [Oncology Reports 30: 2027‑2034, 2013; DOI: 10.3892/or.2013.2728].</p>","PeriodicalId":19527,"journal":{"name":"Oncology reports","volume":"54 6","pages":""},"PeriodicalIF":3.9,"publicationDate":"2025-12-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12485591/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145086606","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":"[Expression of Concern] Reciprocal negative feedback loop between EZH2 and miR‑101‑1 contributes to miR‑101 deregulation in hepatocellular carcinoma.","authors":"Da Huang, Xiaobei Wang, Chunbo Zhuang, Wuhe Shi, Mu Liu, Qiming Tu, Detai Zhang, Lihua Hu","doi":"10.3892/or.2025.8997","DOIUrl":"10.3892/or.2025.8997","url":null,"abstract":"<p><p>Following the publication of this paper, it was drawn to the Editor's attention by a concerned reader that, for the Transwell assay data shown in Fig. 5B on p. 1088, the rightmost panels in the top and the bottom rows appeared to contain a small overlapping section, suggesting that data which were intended to show the results of differently performed experiments had been derived from the same original source. The authors were contacted by the Editorial Office to offer an explanation for this apparent anomaly in the presentation of the data in this paper; however, 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 continues to investigate this matter further. [Oncology Reports 35: 1083‑1090, 2016; DOI: 10.3892/or.2015.4467].</p>","PeriodicalId":19527,"journal":{"name":"Oncology reports","volume":"54 6","pages":""},"PeriodicalIF":3.9,"publicationDate":"2025-12-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12512520/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145149855","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":"miR‑100‑5p and miR‑203a‑3p suppress esophageal squamous cell carcinoma progression by targeting FKBP5.","authors":"Hiroto Tanaka, Suguru Maruyama, Katsutoshi Shoda, Yoshihiko Kawaguchi, Yudai Higuchi, Takaomi Ozawa, Takashi Nakayama, Ryo Saito, Wataru Izumo, Koichi Takiguchi, Kensuke Shiraishi, Shinji Furuya, Hidetake Amemiya, Hiromichi Kawaida, Daisuke Ichikawa","doi":"10.3892/or.2025.9003","DOIUrl":"https://doi.org/10.3892/or.2025.9003","url":null,"abstract":"<p><p>Poorly differentiated cancers, including esophageal squamous cell carcinoma (ESCC), exhibit higher malignant potential and worse prognoses than well‑differentiated types. The present study aimed to identify microRNAs (miRNAs or miRs) involved in ESCC progression and their target mRNAs, focusing on tumor differentiation. miRNA candidates were selected using a miRNA array‑based approach and GEO datasets, comparing expression levels between poorly and non‑poorly differentiated ESCC. Clinical samples (n=61) and cell lines were analyzed to determine the significance and function of the selected miRNAs and their target mRNA. miR‑100‑5p and miR‑203a‑3p were significantly downregulated in poorly differentiated ESCC, with lower expression strongly associated with poorer overall survival (OS) (miR‑100‑5p: P=0.02; miR‑203a‑3p: P=0.05) and relapse‑free survival (RFS) (miR‑100‑5p: P=0.04; miR‑203a‑3p: P=0.12). Overexpression of these miRNAs suppressed cell migration and invasion. <i>FKBP5</i> was identified as a common target, with its expression significantly reduced upon double‑transfection with miR‑100‑5p and miR‑203a‑3p. <i>FKBP5</i> downregulation reduced tumor aggressiveness in KYSE70 cells, and clinical samples showed significantly worse survival rates in patients with high <i>FKBP5</i> expression (OS: P=0.02; RFS: P=0.04). These findings suggest that miR‑100‑5p and miR‑203a‑3p act as tumor suppressors by targeting <i>FKBP5</i>, highlighting <i>FKBP5</i> as a potential therapeutic target in ESCC.</p>","PeriodicalId":19527,"journal":{"name":"Oncology reports","volume":"54 6","pages":""},"PeriodicalIF":3.9,"publicationDate":"2025-12-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145213291","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] Effects and mechanisms of fatty acid metabolism‑mediated glycolysis regulated by betulinic acid‑loaded nanoliposomes in colorectal cancer.","authors":"Gang Wang, Yang Yu, Yu-Zhu Wang, Zhi-Min Zhu, Pei-Hao Yin, Ke Xu","doi":"10.3892/or.2025.8994","DOIUrl":"10.3892/or.2025.8994","url":null,"abstract":"<p><p>Following the publication of this paper, it was drawn to the Editor's attention by a concerned reader that, regarding the western blot experiments shown in Figs. 6E and 7C, a pair of the gel slices were strikingly similar in appearance, suggesting that the same data had been included in these figures to show the results with different proteins. Moreover, two additional gel slices in these figures had apparently been re‑used in a pair of subsequent papers published by the same research group, where the experimental conditions were indicated to be different, and it was noted by the Editorial Office that one of the gel slices may have contained an anomaly in the form of a break in the continuity of the gel. Upon asking the authors to provide the Editorial Office with an explanation of the above issues, they did supply us with revised versions of Figs. 6E and 7C; however, it was subsequently pointed out to the authors that certain of the western blot data in Fig. 6E had apparently reappeared in a further paper by the same authors, in the journal <i>Integrative Cancer Therapies</i>. Owing to the lack of a further response from the authors in relation to the latter query, the Editor of <i>Oncology Reports</i> has decided that this paper should now be retracted from the Journal on account of a lack of confidence in the presented data. The Editor apologizes to the readership for any inconvenience caused. [Oncology Reports 44: 2595‑2609, 2020; DOI: 10.3892/or.2020.7787].</p>","PeriodicalId":19527,"journal":{"name":"Oncology reports","volume":"54 6","pages":""},"PeriodicalIF":3.9,"publicationDate":"2025-12-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12489532/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145149911","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}