Oncology reports最新文献

{"title":"[Retracted] Tetramethylpyrazine inhibits prostate cancer progression by downregulation of forkhead box M1.","authors":"Yi Zhou, Zhigang Ji, Weigang Yan, Zhien Zhou, Hanzhong Li, Yu Xiao","doi":"10.3892/or.2024.8811","DOIUrl":"10.3892/or.2024.8811","url":null,"abstract":"<p><p>Following the publication of this paper, it was drawn to the Editor's attention by a concerned reader that certain of the Transwell invasion assay data shown in Fig. 3B on p. 839 were strikingly similar to data that had already appeared in another article written by different authors at different research institutes [Mao Y, Zhang L, Yuan L, Yan M and He Y: MiR‑218 suppresses cell progression by targeting APC in cervical cancer. Int J Clin Exp Pathol: 10, 2259‑2269, 2017]. Owing to the fact that the contentious data in the above article had already been published prior to its submission to <i>Oncology Reports</i>, the Editor 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. [Oncology Reports 38: 837‑842, 2017; DOI: 10.3892/or.2017.5768].</p>","PeriodicalId":19527,"journal":{"name":"Oncology reports","volume":"52 5","pages":""},"PeriodicalIF":3.8,"publicationDate":"2024-11-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11424923/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142292693","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":"Engineered extracellular vesicles with polypeptide for targeted delivery of doxorubicin against EGFR‑positive tumors.","authors":"Yuqing Yang, Fang Wang, Yuqin Li, Ruxi Chen, Xiangyu Wang, Jiahong Chen, Xi Lin, Haipeng Zhang, Youwei Huang, Rui Wang","doi":"10.3892/or.2024.8813","DOIUrl":"10.3892/or.2024.8813","url":null,"abstract":"<p><p>Lack of effective tumor‑specific delivery systems remains an unmet clinical challenge for the employment of chemotherapy using cytotoxic drugs. Extracellular vesicles (EVs) have recently been investigated for their potential as an efficient drug‑delivery platform, due to their good biodistribution, biocompatibility and low immunogenicity. In the present study, the formulation of GE11 peptide‑modified EVs (GE11‑EVs) loaded with doxorubicin (Dox‑GE11‑EVs), was developed to target epidermal growth factor receptor (EGFR)‑positive tumor cells. The results obtained demonstrated that GE11‑EVs exhibited highly efficient targeting and drug delivery to EGFR‑positive tumor cells compared with non‑modified EVs. Furthermore, treatment with Dox‑GE11‑EVs led to a significantly inhibition of cell proliferation and increased apoptosis of EGFR‑positive tumor cells compared with Dox‑EVs and free Dox treatments. In addition, it was observed that treatment with either free Dox or Dox‑EVs exhibited a high level of cytotoxicity to normal cells, whereas treatment with Dox‑GE11‑EVs had only a limited effect on cell viability of normal cells. Taken together, the findings of the present study demonstrated that the engineered Dox‑GE11‑EVs can treat EGFR‑positive tumors more accurately and have higher safety than traditional tumor therapies.</p>","PeriodicalId":19527,"journal":{"name":"Oncology reports","volume":"52 5","pages":""},"PeriodicalIF":3.8,"publicationDate":"2024-11-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11465103/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142351305","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":"Role and functional mechanisms of IL‑17/IL‑17R signaling in pancreatic cancer (Review).","authors":"Wanli Liu, Xianze Wang, Wenming Wu","doi":"10.3892/or.2024.8803","DOIUrl":"10.3892/or.2024.8803","url":null,"abstract":"<p><p>Interleukin‑17 (IL‑17), an inflammatory cytokine primarily secreted by T helper 17 cells, serves a crucial role in numerous inflammatory diseases and malignancies via its receptor, IL‑17R. In addition to stimulating inflammatory responses, IL‑17 exhibits dual functions in tumors, exerting both pro‑ and antitumor effects. Pancreatic ductal adenocarcinoma (PDAC) is the most common pancreatic malignancy and accounts for >90% of pancreatic cancer cases. PDAC is characterized by a prominent stromal microenvironment with significant heterogeneity, which contributes to treatment resistance. IL‑17/IL‑17R signaling has a notable effect on tumorigenesis, the tumor microenvironment and treatment efficacy in various cancer types, including PDAC. However, the specific mechanisms of IL‑17/IL‑17R signaling in pancreatic cancer remain uncertain. This review presents a brief overview of the current knowledge and recent advances in the role and functional mechanisms of IL‑17/IL‑17R signaling in pancreatic cancer. Furthermore, the potential of IL‑17‑targeted therapeutic strategies for PDAC treatment is also discussed.</p>","PeriodicalId":19527,"journal":{"name":"Oncology reports","volume":"52 5","pages":""},"PeriodicalIF":3.8,"publicationDate":"2024-11-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11378154/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142110423","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":"[Retracted] RNAi‑mediated EZH2 depletion decreases MDR1 expression and sensitizes multidrug‑resistant hepatocellular carcinoma cells to chemotherapy.","authors":"Bo Tang, Yi Zhang, Rui Liang, Zhenming Gao, Deguang Sun, Liming Wang","doi":"10.3892/or.2024.8809","DOIUrl":"https://doi.org/10.3892/or.2024.8809","url":null,"abstract":"<p><p>Following the publication of this paper, it was drawn to the Editor's attention by a concerned reader that the control western blotting data featured in Fig. 2C on p. 1039 and the cell cycle distribution images shown in Fig. 6A on p. 1041 were strikingly similar to data that had appeared in a pair of other articles written by different authors at different research institutes, one of which had already been submitted for publication when this article was received at <i>Oncology Reports</i>, the other of which was received some time afterwards, but which has subsequently been retracted. Owing to the fact that the abovementioned data had already been submitted for publication prior to its submission to <i>Oncology Reports</i>, the Editor 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. [Oncology Reports 29: 1037‑1042, 2013; DOI: 10.3892/or.2013.2222].</p>","PeriodicalId":19527,"journal":{"name":"Oncology reports","volume":"52 5","pages":""},"PeriodicalIF":3.8,"publicationDate":"2024-11-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11406480/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142292692","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":"[Retracted] MicroRNA-124-3p inhibits the growth and metastasis of nasopharyngeal carcinoma cells by targeting STAT3.","authors":"Shan Xu, Ning Zhao, Lian Hui, Min Song, Zi-Wei Miao, Xue-Jun Jiang","doi":"10.3892/or.2024.8807","DOIUrl":"10.3892/or.2024.8807","url":null,"abstract":"<p><p>Following the publication of this paper, it was drawn to the Editor's attention by a concerned reader that certain of the cell apoptotic data in Fig. 4 on p. 1389 and the migration and invasion assay data shown in Figs. 6 and 7 on p. 1391 were strikingly similar to data that were submitted for publication at around the same time in different articles written by different authors at different research institutes (several of which have subsequently been retracted). In addition, there appeared to be instances of duplication of the same data within Figs. 7 and 8, where data that were intending to have shown the results from differently performed experiments had apparently been derived from the same original sources. Owing to the fact that the contentious data in the above article had already been submitted for publication elsewhere prior to its submission to <i>Oncology Reports</i>, the Editor 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. [Oncology Reports 35: 1385-1394, 2016; DOI: 10.3892/or.2015.4524].</p>","PeriodicalId":19527,"journal":{"name":"Oncology reports","volume":"52 5","pages":""},"PeriodicalIF":3.8,"publicationDate":"2024-11-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11391259/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142140701","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":"Enhanced capture system for mesenchymal‑type circulating tumor cells using a polymeric microfluidic device 'CTC‑Chip' incorporating cell‑surface vimentin.","authors":"Masatoshi Kanayama, Kazue Yoneda, Taiji Kuwata, Masataka Mori, Takehiko Manabe, Rintaro Oyama, Hiroki Matsumiya, Masaru Takenaka, Koji Kuroda, Takashi Ohnaga, Fumihiro Tanaka","doi":"10.3892/or.2024.8815","DOIUrl":"https://doi.org/10.3892/or.2024.8815","url":null,"abstract":"<p><p>CellSearch, the only approved epithelial cell adhesion molecule (EpCAM)‑dependent capture system approved for clinical use, overlooks circulating tumor cells (CTCs) undergoing epithelial‑mesenchymal transition (EMT‑CTCs), which is considered a crucial subtype responsible for metastasis. To address this limitation, a novel polymeric microfluidic device 'CTC‑chip' designed for the easy introduction of any antibody was developed, enabling EpCAM‑independent capture. In this study, antibodies against EpCAM and cell surface vimentin (CSV), identified as cancer‑specific EMT markers, were conjugated onto the chip (EpCAM‑chip and CSV‑chip, respectively), and the capture efficiency was examined using lung cancer (PC9, H441 and A549) and colon cancer (DLD1) cell lines, classified into three types based on EMT markers: Epithelial (PC9), intermediate (H441 and DLD1) and mesenchymal (A549). PC9, H441 and DLD1 cells were effectively captured using the EpCAM‑chip (average capture efficiencies: 99.4, 88.8 and 90.8%, respectively) when spiked into blood. However, A549 cells were scarcely captured (13.4%), indicating that EpCAM‑dependent capture is not suitable for mesenchymal‑type cells. The expression of CSV tended to be higher in cells exhibiting mesenchymal properties and A549 cells were effectively captured with the CSV‑chip (72.4 and 88.4% at concentrations of 10 and 100 µg/ml, respectively) when spiked into PBS. When spiked into blood, the average capture efficiencies were 27.7 and 46.8% at concentrations of 10 and 100 µg/ml, respectively. These results suggest that the CSV‑chip is useful for detecting mesenchymal‑type cells and has potential applications in capturing EMT‑CTCs.</p>","PeriodicalId":19527,"journal":{"name":"Oncology reports","volume":"52 5","pages":""},"PeriodicalIF":3.8,"publicationDate":"2024-11-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142372457","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":"Targeting adenocarcinoma and enzalutamide‑resistant prostate cancer using the novel anti‑androgen inhibitor ADA‑308.","authors":"Shaghayegh Nouruzi, Fraser Johnson, Sahil Kumar, Olena Sivak, Nakisa Tabrizian, Milla Koistinaho, Anu Muona, Amina Zoubeidi","doi":"10.3892/or.2024.8791","DOIUrl":"10.3892/or.2024.8791","url":null,"abstract":"<p><p>Prostate cancer (PCa) is the leading cause of cancer‑related death among men worldwide. PCa often develops resistance to standard androgen deprivation therapy and androgen receptor (AR) pathway inhibitors, such as enzalutamide (ENZ). Therefore, there is an urgent need to develop novel therapeutic strategies for this disease. The efficacy of ADA‑308 was evaluated through <i>in vitro</i> assessments of AR activity and cell proliferation, alongside <i>in vivo</i> studies. ADA‑308 has emerged as a promising candidate, demonstrating potent inhibition of AR‑sensitive adenocarcinoma as well as ENZ‑resistant PCa cell lines. The results of the study revealed that ADA‑308 effectively blocked AR activity, including its nuclear localization, and inhibited cell proliferation <i>in vitro</i>. Furthermore, ADA‑308 demonstrated notable efficacy <i>in vivo</i>, with a robust antitumor response in ENZ‑resistant models. These findings establish the role of ADA‑308 as a potent AR inhibitor that overcomes resistance to AR‑targeted therapies and highlights its potential as a novel therapeutic approach in advanced PCa management.</p>","PeriodicalId":19527,"journal":{"name":"Oncology reports","volume":"52 4","pages":""},"PeriodicalIF":3.8,"publicationDate":"2024-10-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11332584/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"141917275","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":"A potential mechanism of tumor immune escape: Regulation and application of soluble natural killer group 2 member D ligands (Review).","authors":"Shuhao Huang, Zihao Qin, Feiyang Wang, Yiping Kang, Biqiong Ren","doi":"10.3892/or.2024.8796","DOIUrl":"10.3892/or.2024.8796","url":null,"abstract":"<p><p>The immune system is integral to the surveillance and eradication of tumor cells. Interactions between the natural killer group 2 member D (NKG2D) receptor and its ligands (NKG2DLs) are vital for activating NKG2D receptor‑positive immune cells, such as natural killer cells. This activation enables these cells to identify and destroy tumor cells presenting with NKG2DLs, which is an essential aspect of tumor immunity. However, tumor immune escape is facilitated by soluble NKG2DL (sNKG2DL) shed from the surface of tumor cells. The production of sNKG2DL is predominantly regulated by metalloproteinases [a disintegrin and metalloproteinases (ADAM) and matrix metalloproteinase (MMP) families] and exosomes. sNKG2DL not only diminish immune recognition on the tumor cell surface but also suppress the function of immune cells, such as NK cells, and reduce the expression of the NKG2D receptor. This process promotes immune evasion, progression, and metastasis of tumors. In this review, an in‑depth summary of the mechanisms and factors that influence sNKG2DL production and their contribution to immune suppression within the tumor microenvironment are provided. Furthermore, due to the significant link between sNKG2DLs and tumor progression and metastasis, they have great potential as novel biomarkers. Detectable via liquid biopsies, sNKG2DLs could assess tumor malignancy and prognosis, and act as pivotal targets for immunotherapy. This could lead to the discovery of new drugs or the enhancement of existing treatments. Thus, the application of sNKG2DLs in clinical oncology was explored, offering substantial theoretical support for the development of innovative immunotherapeutic strategies for sNKG2DLs.</p>","PeriodicalId":19527,"journal":{"name":"Oncology reports","volume":"52 4","pages":""},"PeriodicalIF":3.8,"publicationDate":"2024-10-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11358674/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142000447","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":"Metformin suppresses esophageal cancer progression through the radiation‑induced cellular senescence of cancer‑associated fibroblasts.","authors":"Yuya Sugimoto, Koichi Okamoto, Hiroto Saito, Takahisa Yamaguchi, Jun Kinoshita, Keishi Nakamura, Takahisa Takino, Yoshio Endo, Itasu Ninomiya, Tetsuo Ohta, Noriyuki Inaki","doi":"10.3892/or.2024.8788","DOIUrl":"10.3892/or.2024.8788","url":null,"abstract":"<p><p>Senescent cells are known to secrete proteins, including inflammatory cytokines and damage‑associated molecular patterns. This phenomenon is known as the senescence‑associated secretory phenotype (SASP). SASP in cancer stromal fibroblasts is involved in cancer growth and progression. Conversely, metformin, an antidiabetic drug, has been reported to inhibit SASP induction by inhibiting the activation of NF‑κB, a regulator of SASP. To date, at least to the best of our knowledge, there have been no reports regarding cellular senescence in fibroblasts and tumor progression via the SASP‑mediated paracrine pathway. The present study thus aimed to elucidate the induction mechanisms of SASP in radiation‑induced fibroblasts and to determine its effects on cancer progression via the paracrine pathway. Furthermore, the present study aimed to determine whether controlling SASP using metformin suppresses cancer progression. A well‑differentiated esophageal cancer cell line established by the authors' department and fibroblasts isolated and cultured from the non‑cancerous esophageal mucosa of resected esophageal cancer cases were used for the experiments. Fibroblasts were irradiated with 8 Gy radiation, and the changes in the expression of the senescence markers, SA‑β‑gal, p21, p16 and NF‑κB were evaluated using immunofluorescent staining and western blot analysis in the presence or absence of metformin treatment. The culture supernatants of irradiated fibroblasts treated with metformin and those treated without metformin were collected and added to the cancer cells to evaluate their proliferative, invasive and migratory abilities. Vimentin and E‑cadherin expression levels were also evaluated using immunofluorescent staining and western blot analysis. The expression levels of p16, p21 and NF‑κB in irradiated fibroblasts were attenuated by treatment with metformin. Supernatants collected from irradiated fibroblasts exhibited the proliferative activity of esophageal cancer cells, and the promotion of migratory and invasion abilities, which may be due to epithelial‑mesenchymal transition and changes in cell morphology. These reactions were confirmed to be suppressed by the addition of the supernatant of cultured fibroblasts pre‑treated with metformin. On the whole, the present study demonstrates that fibroblasts in the cancer stroma may be involved in tumor progression through cellular senescence.</p>","PeriodicalId":19527,"journal":{"name":"Oncology reports","volume":"52 4","pages":""},"PeriodicalIF":3.8,"publicationDate":"2024-10-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11332583/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"141875488","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":"DNA methylation and mRNA expression of ZNF577 as biomarkers for the detection and prognosis of lung adenocarcinoma.","authors":"Batkhishig Munkhjargal, Kazuya Kondo, Shiho Soejima, Bilguun Tegshee, Michiko Yamashita, Naoya Kawakita, Hiroaki Toba, Hiromitsu Takizawa","doi":"10.3892/or.2024.8790","DOIUrl":"10.3892/or.2024.8790","url":null,"abstract":"<p><p>Despite advances in science and technology, lung cancer remains a major public health issue. The discovery of early diagnostic and prognostic markers is still needed to reduce the mortality rate of lung cancer, which is the highest among all cancer types. Aberrations in the DNA methylation system have an important role in human cancer and are promising for the development of early diagnostic and prognostic markers. The present study focused on zinc finger protein (ZNF)577, whose encoding gene was indicated to exhibit promoter hypermethylation together with 9 other genes in lung adenocarcinoma (LADC) in a previous study by our group. ZN577 is a member of the ZNG family and its functional role has so far remained elusive. LADC tissue samples surgically resected at Tokushima University Hospital (Tokushima, Japan) between April 1999 and November 2013 were collected. A total of 73 tumors and 27 paired tumor-adjacent normal tissues were examined for DNA methylation and mRNA expression of ZNF577. A total of 149 LADC tissue samples were collected and evaluated by immunohistochemistry (IHC) for the tissue expression of ZNF577. High methylation (n=27, P<0.0001) and low mRNA expression levels (n=27, P<0.031) of ZNF577 were identified in LADC tissues, and it was demonstrated that methylation levels were inversely correlated with mRNA expression levels (P=0.0116, ρ=-0.2515). Among the LADC tissues, lepidic-patterned samples had lower methylation levels of ZNF577 than other pathological types. In addition, mRNA expression levels of ZNF577 were significantly higher in females, non-smokers and stage I samples. Overall survival [P<0.0001; area under curve (AUC)=0.8658] and disease-free survival (DFS; P<0.0004; AUC=0.7232) rates were significantly higher in the ZNF577 high mRNA expression group than in the ZNF577 low mRNA expression group. Among the 149 LADC samples examined by IHC, 105 were negative and 44 were positive for the tissue expression of ZNF577. Cox regression analysis showed poorer DFS (hazard ratio: 3.917; P=0.023) in patients with lower expression of ZNF577. In conclusion, higher methylation levels of ZNF577 were observed in LADC tissues than in normal lung tissue and low mRNA expression of ZNF577 was associated with unfavorable prognosis.</p>","PeriodicalId":19527,"journal":{"name":"Oncology reports","volume":"52 4","pages":""},"PeriodicalIF":3.8,"publicationDate":"2024-10-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"141917273","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}