International journal of oncology最新文献

{"title":"[Retracted] NR4A1‑induced increase in the sensitivity of a human gastric cancer line to TNFα‑mediated apoptosis is associated with the inhibition of JNK/Parkin‑dependent mitophagy.","authors":"Hongzhu Yan, Feng Xiao, Jue Zou, Chengmin Qiu, Weiwei Sun, Minmin Gu, Li Zhang","doi":"10.3892/ijo.2024.5666","DOIUrl":"10.3892/ijo.2024.5666","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 data shown in Figs. 2A and 4F were strikingly similar to data appearing in different form in other articles written by different authors at different research institutes that were submitted to their respective journals at around the same time; moreover, the same data had apparently been included in the western blots featured in Fig. 5A to show the Parkin and mito‑LCIII protein bands. As it was not clear what had been the original venue for the submission of the strikingly similar data here, the Editor requested that the authors send to us all the raw data underlying the affected figures; however, the authors were not able to comply with this request at the time of asking. Given that the authors were unable to provide the supporting data as requested, the Editor of <i>International Journal of Oncology</i> has decided that this paper should be retracted from the Journal on account of a lack of confidence in the presented data. The authors were asked for an explanation to account for these concerns, but the Editorial Office did not receive a satisfactory reply. The Editor apologizes to the readership for any inconvenience caused. [International Journal of Oncology 52: 367‑378, 2018; DOI: 10.3892/ijo.2017.4216].</p>","PeriodicalId":14175,"journal":{"name":"International journal of oncology","volume":"65 2","pages":""},"PeriodicalIF":4.5,"publicationDate":"2024-08-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11251739/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"141467869","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":"Microbial metabolites affect tumor progression, immunity and therapy prediction by reshaping the tumor microenvironment (Review).","authors":"Yuhang Zhou, Wenjie Han, Yun Feng, Yue Wang, Tao Sun, Junnan Xu","doi":"10.3892/ijo.2024.5661","DOIUrl":"10.3892/ijo.2024.5661","url":null,"abstract":"<p><p>Several studies have indicated that the gut microbiome and tumor microbiota may affect tumors. Emerging metabolomics research illustrates the need to examine the variations in microbial metabolite composition between patients with cancer and healthy individuals. Microbial metabolites can impact the progression of tumors and the immune response by influencing a number of mechanisms, including modulation of the immune system, cancer or immune‑related signaling pathways, epigenetic modification of proteins and DNA damage. Microbial metabolites can also alleviate side effects and drug resistance during chemotherapy and immunotherapy, while effectively activating the immune system to exert tumor immunotherapy. Nevertheless, the impact of microbial metabolites on tumor immunity can be both beneficial and harmful, potentially influenced by the concentration of the metabolites or the specific cancer type. The present review summarizes the roles of various microbial metabolites in different solid tumors, alongside their influence on tumor immunity and treatment. Additionally, clinical trials evaluating the therapeutic effects of microbial metabolites or related microbes on patients with cancer have been listed. In summary, studying microbial metabolites, which play a crucial role in the interaction between the microbiota and tumors, could lead to the identification of new supplementary treatments for cancer. This has the potential to improve the effectiveness of cancer treatment and enhance patient prognosis.</p>","PeriodicalId":14175,"journal":{"name":"International journal of oncology","volume":"65 1","pages":""},"PeriodicalIF":5.2,"publicationDate":"2024-07-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11173369/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"141283682","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":"Gallic acid suppresses the progression of clear cell renal cell carcinoma through inducing autophagy via the PI3K/Akt/Atg16L1 signaling pathway.","authors":"Tianxiang Zhang, Xi Zhang, Yang Fei, Jinsen Lu, Dairan Zhou, Li Zhang, Song Fan, Jun Zhou, Chaozhao Liang, Yang Su","doi":"10.3892/ijo.2024.5658","DOIUrl":"10.3892/ijo.2024.5658","url":null,"abstract":"<p><p>Clear cell renal cell carcinoma (ccRCC), the most common type of renal cell carcinoma (RCC), is not sensitive to traditional radiotherapy and chemotherapy. The polyphenolic compound Gallic acid (GA) can be naturally found in a variety of fruits, vegetables and plants. Autophagy, an intracellular catabolic process, regulates the lysosomal degradation of organelles and portions in cytoplasm. It was reported that autophagy and GA could affect the development of several cancers. Therefore, the aim of the present study was to evaluate the effects of GA on ccRCC development and clarify the role of autophagy in this process. In the present study, the effects of GA on the proliferation, migration and invasion of ccRCC cells were investigated <i>in vitro</i> by Cell Counting Kit‑8, colony formation, flow cytometry, wound healing and Transwell migration assays, respectively. Additionally, the effects of GA on ccRCC growth and metastasis were evaluated using hematoxylin‑eosin and immunohistochemical staining <i>in vivo</i>. Moreover, it was sought to explore the underlying molecular mechanisms using transmission electron microscopy, western blotting and reverse transcription‑quantitative PCR analyses. In the present study, it was revealed that GA had a more potent viability inhibitory effect on ccRCC cells (786‑O and ACHN) than the effect on normal renal tubular epithelial cell (HK‑2), which demonstrated that GA selectively inhibits the viability of cancer cells. Furthermore, it was identified that GA dose‑dependently inhibited the proliferation, migration and invasion of ccRCC cells <i>in vitro</i> and <i>in vivo</i>. It was demonstrated that GA promoted the release of autophagy markers, which played a role in regulating the PI3K/Akt/Atg16L1 signaling pathway. All the aforementioned data provided evidence for the great potential of GA in the treatment of ccRCC.</p>","PeriodicalId":14175,"journal":{"name":"International journal of oncology","volume":"65 1","pages":""},"PeriodicalIF":4.5,"publicationDate":"2024-07-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11173374/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"141179508","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":"Significance of signal recognition particle 9 nuclear translocation: Implications for pancreatic cancer prognosis and functionality.","authors":"Hiromichi Sato, Sikun Meng, Kazuki Sasaki, Shogo Kobayashi, Kansuke Kido, Yoshiko Tsuji, Yasuko Arao, Yoshiko Saito, Yoshifumi Iwagami, Daisaku Yamada, Yoshito Tomimaru, Takehiro Noda, Hidenori Takahashi, Daisuke Motooka, Shizuka Uchida, Ken Ofusa, Taroh Satoh, Yuichiro Doki, Hidetoshi Eguchi, Tomoaki Hara, Hideshi Ishii","doi":"10.3892/ijo.2024.5662","DOIUrl":"10.3892/ijo.2024.5662","url":null,"abstract":"<p><p>Signal recognition particles (SRPs) are essential for regulating intracellular protein transport and secretion. Patients with tumors with high SRP9 expression tend to have a poorer overall survival. However, to the best of our knowledge, no reports have described the relationship between SRP9 localization and prognosis in pancreatic cancer. Thus, the present study aimed to investigate this relationship. Immunohistochemical staining for SRP9 using excised specimens from pancreatic cancer surgery cases without preoperative chemotherapy or radiotherapy showed that SRP9 was preferentially expressed in the nucleus of the cancerous regions in some cases, which was hardly detected in other cases, indicating that SRP9 was transported to the nucleus in the former cases. To compare the prognosis of patients with SRP9 nuclear translocation, patients were divided into two groups: Those with a nuclear translocation rate of >50% and those with a nuclear translocation rate of ≤50%. The nuclear translocation rate of >50% group had a significantly better recurrence‑free survival than the nuclear translocation rate of ≤50% group (P=0.037). Subsequent <i>in vitro</i> experiments were conducted; notably, the nuclear translocation rate of SRP9 was reduced under amino acid‑deficient conditions, suggesting that multiple factors are involved in this phenomenon. To further study the function of SRP9 nuclear translocation, <i>in vitro</i> experiments were performed by introducing SRP9 splicing variants (v1 and v2) and their deletion mutants lacking C‑terminal regions into MiaPaCa pancreatic cancer cells. The results demonstrated that both splicing variants showed nuclear translocation regardless of the C‑terminal deletions, suggesting the role of the N‑terminal regions. Given that SRP9 is an RNA‑binding protein, the study of RNA immunoprecipitation revealed that signaling pathways involved in cancer progression and protein translation were downregulated in nuclear‑translocated v1 and v2. Undoubtedly, further studies of the nuclear translocation of SRP9 will open an avenue to optimize the precise evaluation and therapeutic control of pancreatic cancer.</p>","PeriodicalId":14175,"journal":{"name":"International journal of oncology","volume":"65 1","pages":""},"PeriodicalIF":4.5,"publicationDate":"2024-07-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11173368/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"141283683","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] Fe₃O₄‑solamargine induces apoptosis and inhibits metastasis of pancreatic cancer cells.","authors":"Xiaodong Xie, Xiuming Zhang, Jun Chen, Xun Tang, Meiqin Wang, Lei Zhang, Zhen Guo, Wenrong Shen","doi":"10.3892/ijo.2024.5657","DOIUrl":"10.3892/ijo.2024.5657","url":null,"abstract":"<p><p>Following the publication of the above article, a concerned reader drew to the Editor's attention that certain of the Transwell invasion assay data shown in Fig. 5B on p. 911 were strikingly similar to data that had appeared in a previously published paper written by different authors at a different research institute. In view of the fact that certain of the data in the above article had already appeared in a previously published paper, the Editor of <i>International Journal of Oncology</i> has decided that this paper should be retracted from the publication. 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 54: 905‑915, 2019; DOI: 10.3892/ijo.2018.4637].</p>","PeriodicalId":14175,"journal":{"name":"International journal of oncology","volume":"65 1","pages":""},"PeriodicalIF":5.2,"publicationDate":"2024-07-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11155712/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"141087402","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":"Investigating the molecular mechanisms of microRNA‑409‑3p in tumor progression: Towards targeted therapeutics (Review).","authors":"Wenjie Xie, Zhichao Wang, Junke Wang, Xiu Wang, Hongzai Guan","doi":"10.3892/ijo.2024.5655","DOIUrl":"10.3892/ijo.2024.5655","url":null,"abstract":"<p><p>MicroRNAs (miRNAs) are a group of non‑coding RNAs that exert master regulatory functions in post‑-transcriptional gene expression. Accumulating evidence shows that miRNAs can either promote or suppress tumorigenesis by regulating different target genes or pathways and may be involved in the occurrence of carcinoma. miR‑409‑3p is dysregulated in a variety of malignant cancers. It plays a fundamental role in numerous cellular biological processes, such as cell proliferation, apoptosis, migration, invasion, autophagy, angiogenesis and glycolysis. In addition, studies have shown that miR‑409‑3p is expected to become a non‑invasive biomarker. Identifying the molecular mechanisms underlying miR‑409‑3p‑mediated tumor progression will help investigate miR‑409‑3p‑based targeted therapy for human cancers. The present review comprehensively summarized the recently published literature on miR‑409‑3p, with a focus on the regulation and function of miR‑409‑3p in various types of cancer, and discussed the clinical implications of miR‑409‑3p, providing new insight for the diagnosis and treatment of cancers.</p>","PeriodicalId":14175,"journal":{"name":"International journal of oncology","volume":"65 1","pages":""},"PeriodicalIF":5.2,"publicationDate":"2024-07-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11155714/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"140957383","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":"Complement regulatory protein CD46 promotes bladder cancer metastasis through activation of MMP9.","authors":"Thuy Nguyen Thi, Hien Duong Thanh, Van-Tan Nguyen, Se-Young Kwon, Changjong Moon, Eu Chang Hwang, Chaeyong Jung","doi":"10.3892/ijo.2024.5659","DOIUrl":"10.3892/ijo.2024.5659","url":null,"abstract":"<p><p>CD46, a transmembrane protein known for protecting cells from complement‑mediated damage, is frequently dysregulated in various types of cancer. Its overexpression in bladder cancers safeguards the cancer cells against both complement and antibody‑mediated cytotoxicity. The present study explored a new role of CD46 in facilitating cancer cell invasion and metastasis, examining its regulatory effect on matrix metalloproteases (MMPs) and their effect on the metastatic capability of bladder cancer cells. Specifically, CD46 alteration positively influenced MMP9 expression, but not MMP2, in several bladder cancer cell lines. Furthermore, CD46 overexpression triggered phosphorylation of p38 MAPK and protein kinase B (AKT), leading to enhanced activator protein 1 (AP‑1) activity via c‑Jun upregulation. The inhibition of p38 or AKT pathways attenuated the CD46‑induced MMP9 and AP‑1 upregulation, indicating that the promotion of MMP9 by CD46 involved activating both p38 MAPK and AKT. Functionally, the upregulation of MMP9 by CD46 translated to increased migratory and invasive capabilities of bladder cancer cells, as well as enhanced <i>in vivo</i> metastasis. Overall, the present study revealed a novel role for CD46 as a metastasis promoter through MMP9 activation in bladder cancers and highlighted the regulatory mechanism of CD46‑mediated MMP9 promotion via p38 MAPK and AKT activation.</p>","PeriodicalId":14175,"journal":{"name":"International journal of oncology","volume":"65 1","pages":""},"PeriodicalIF":4.5,"publicationDate":"2024-07-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11173367/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"141283681","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":"Daunorubicin induces GLI1‑dependent apoptosis in colorectal cancer cell lines.","authors":"Bo Ram Kim, Dae Yeong Kim, Na Ly Tran, Bu Gyeom Kim, Sun Il Lee, Sang Hee Kang, Byung Yook Min, Wooyoung Hur, Sang Cheul Oh","doi":"10.3892/ijo.2024.5654","DOIUrl":"10.3892/ijo.2024.5654","url":null,"abstract":"<p><p>Daunorubicin, also known as daunomycin, is a DNA‑targeting anticancer drug that is used as chemotherapy, mainly for patients with leukemia. It has also been shown to have anticancer effects in monotherapy or combination therapy in solid tumors, but at present it has not been adequately studied in colorectal cancer (CRC). In the present study, from a screening using an FDA‑approved drug library, it was found that daunorubicin suppresses GLI‑dependent luciferase reporter activity. Daunorubicin also increased p53 levels, which contributed to both GLI1 suppression and apoptosis. The current detailed investigation showed that daunorubicin promoted the β‑TrCP‑mediated ubiquitination and proteasomal degradation of GLI1. Moreover, a competition experiment using BODIPY‑cyclopamine, a well‑known Smo inhibitor, suggested that daunorubicin does not bind to Smo in HCT116 cells. Administration of daunorubicin (2 mg/kg, ip, qod, 15 days) into HCT116 xenograft mice profoundly suppressed tumor progress and the GLI1 level in tumor tissues. Taken together, the present results revealed that daunorubicin suppresses canonical Hedgehog pathways in CRC. Ultimately, the present study discloses a new mechanism of daunorubicin's anticancer effect and might provide a rationale for expanding the clinical application of daunorubicin.</p>","PeriodicalId":14175,"journal":{"name":"International journal of oncology","volume":"64 6","pages":""},"PeriodicalIF":4.5,"publicationDate":"2024-06-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11095621/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"140961454","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":"Decoding long non‑coding RNAs: Friends and foes in cancer development (Review).","authors":"Hequn Song, Joseph Adu-Amankwaah, Qizhong Zhao, Dongqi Yang, Kuntao Liu, Aisha Bushi, Jinming Zhao, Jinxiang Yuan, Rubin Tan","doi":"10.3892/ijo.2024.5649","DOIUrl":"10.3892/ijo.2024.5649","url":null,"abstract":"<p><p>Cancer remains a formidable adversary, challenging medical advancements with its dismal prognosis, low cure rates and high mortality rates. Within this intricate landscape, long non‑coding RNAs (lncRNAs) emerge as pivotal players, orchestrating proliferation and migration of cancer cells. Harnessing the potential of lncRNAs as therapeutic targets and prognostic markers holds immense promise. The present comprehensive review delved into the molecular mechanisms underlying the involvement of lncRNAs in the onset and progression of the top five types of cancer. By meticulously examining lncRNAs across diverse types of cancer, it also uncovered their distinctive roles, highlighting their exclusive oncogenic effects or tumor suppressor properties. Notably, certain lncRNAs demonstrate diverse functions across different cancers, confounding the conventional understanding of their roles. Furthermore, the present study identified lncRNAs exhibiting aberrant expression patterns in numerous types of cancer, presenting them as potential indicators for cancer screening and diagnosis. Conversely, a subset of lncRNAs manifests tissue‑specific expression, hinting at their specialized nature and untapped significance in diagnosing and treating specific types of cancer. The present comprehensive review not only shed light on the intricate network of lncRNAs but also paved the way for further research and clinical applications. The unraveled molecular mechanisms offer a promising avenue for targeted therapeutics and personalized medicine, combating cancer proliferation, invasion and metastasis.</p>","PeriodicalId":14175,"journal":{"name":"International journal of oncology","volume":"64 6","pages":""},"PeriodicalIF":5.2,"publicationDate":"2024-06-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11095623/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"140849427","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":"Current data and future perspectives on DNA methylation in ovarian cancer (Review).","authors":"Mengyu Fu, Fengying Deng, Jie Chen, Li Fu, Jiahui Lei, Ting Xu, Youguo Chen, Jinhua Zhou, Qinqin Gao, Hongmei Ding","doi":"10.3892/ijo.2024.5650","DOIUrl":"10.3892/ijo.2024.5650","url":null,"abstract":"<p><p>Ovarian cancer (OC) represents the most prevalent malignancy of the female reproductive system. Its distinguishing features include a high aggressiveness, substantial morbidity and mortality, and a lack of apparent symptoms, which collectively pose significant challenges for early detection. Given that aberrant DNA methylation events leading to altered gene expression are characteristic of numerous tumor types, there has been extensive research into epigenetic mechanisms, particularly DNA methylation, in human cancers. In the context of OC, DNA methylation is often associated with the regulation of critical genes, such as BRCA1/2 and Ras‑association domain family 1A. Methylation modifications within the promoter regions of these genes not only contribute to the pathogenesis of OC, but also induce medication resistance and influence the prognosis of patients with OC. As such, a more in‑depth understanding of DNA methylation underpinning carcinogenesis could potentially facilitate the development of more effective therapeutic approaches for this intricate disease. The present review focuses on classical tumor suppressor genes, oncogenes, signaling pathways and associated microRNAs in an aim to elucidate the influence of DNA methylation on the development and progression of OC. The advantages and limitations of employing DNA methylation in the diagnosis, treatment and prevention of OC are also discussed. On the whole, the present literature review indicates that the DNA methylation of specific genes could potentially serve as a prognostic biomarker for OC and a therapeutic target for personalized treatment strategies. Further investigations in this field may yield more efficacious diagnostic and therapeutic alternatives for patients with OC.</p>","PeriodicalId":14175,"journal":{"name":"International journal of oncology","volume":"64 6","pages":""},"PeriodicalIF":5.2,"publicationDate":"2024-06-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11095605/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"140957351","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}