International journal of oncology最新文献

{"title":"Beyond tumor‑associated macrophages involved in spheroid formation and dissemination: Novel insights for ovarian cancer therapy (Review).","authors":"Yuchen Liu, Haoyue Xiao, Hai Zeng, Ying Xiang","doi":"10.3892/ijo.2024.5705","DOIUrl":"10.3892/ijo.2024.5705","url":null,"abstract":"<p><p>Ovarian cancer (OC) is the most common and deadly malignant tumor of the female reproductive system. When OC cells detach from the primary tumor and enter the ascitic microenvironment, they are present as individual cells or multicellular spheroids in ascites. These spheroids, composed of cancer and non‑malignant cells, are metastatic units and play a crucial role in the progression of OC. However, little is known about the mechanism of spheroid formation and dissemination. Tumor‑associated macrophages (TAMs) in the center of spheroids are key in spheroid formation and metastasis and provide a potential target for OC therapy. The present review summarizes the key biological features of spheroids, focusing on the role of TAMs in spheroid formation, survival and peritoneal metastasis, and the strategies targeting TAMs to provide new insights in treating OC.</p>","PeriodicalId":14175,"journal":{"name":"International journal of oncology","volume":"65 6","pages":""},"PeriodicalIF":4.5,"publicationDate":"2024-12-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11575928/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142602067","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":"Hyperthermia reduces cancer cell invasion and combats chemoresistance and immune evasion in human bladder cancer.","authors":"Te-Fu Tsai, Thomas I-Sheng Hwang, Po-Chun Chen, Yen-Chen Chen, Kuang-Yu Chou, Chao-Yen Ho, Hung-En Chen, An-Chen Chang","doi":"10.3892/ijo.2024.5704","DOIUrl":"10.3892/ijo.2024.5704","url":null,"abstract":"<p><p>Bladder cancer (BC) is a common malignancy and its most prevalent type is urothelial carcinoma, which accounts for ~90% of all cases of BC. The current treatment options for BC are limited, which necessitates the development of alternative treatment strategies. Hyperthermia (HT), as an adjuvant cancer therapy, is known to improve the efficacy of chemotherapy or radiotherapy. The present study aimed to investigate the anti‑tumor effects of HT on cell survival, invasiveness, chemoresistance and immune evasion in human BC cell lines (5637, T24 and UMUC3). Calcein AM staining was performed to analyze the cytotoxicity of natural killer (NK) cells against human BC cells following HT treatment. Cell migration and invasion affected by HT were analyzed using Transwell migration and invasion assays. It was found that HT inhibited the proliferation of BC cells by downregulating the phosphorylation of protein kinase B. Moreover, HT effectively enhanced the sensitivity of BC cells to the chemotherapy drug cisplatin (DDP) and reduced the chemoresistance of DDP‑resistant cells by downregulating the expression of cadherin‑11. It was further demonstrated that HT inhibited the migration and invasion of BC cells and enhanced the cytotoxic effects of NK cells. In summary, the antineoplastic effects of HT were mediated through three main mechanisms: Enhancement of the chemosensitivity of BC cells and mitigation of DDP‑induced chemoresistance, suppression of the invasive potential of BC cells and reinforcement of the anticancer response of NK cells. Thus, HT appears to be a promising adjunctive therapy for human BC.</p>","PeriodicalId":14175,"journal":{"name":"International journal of oncology","volume":"65 6","pages":""},"PeriodicalIF":4.5,"publicationDate":"2024-12-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11575926/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142602089","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":"Melatonin and vitamin D as potential synergistic adjuvants for cancer therapy (Review).","authors":"Russel J Reiter, Luiz Gustavo De Almeida Chuffa, Vinícius Augusto Simão, Virna Margarita Martín Giménez, Natalia De Las Heras, Demetrios A Spandidos, Walter Manucha","doi":"10.3892/ijo.2024.5702","DOIUrl":"10.3892/ijo.2024.5702","url":null,"abstract":"<p><p>Significant advancements have been made in cancer therapy; however, limitations remain with some conventional approaches. Adjuvants are agents used alongside primary treatments to enhance their efficacy and the treatment outcomes of patients. Modern lifestyles contribute to deficiencies in melatonin and vitamin D. Limited sun exposure affects vitamin D synthesis, and artificial light at night suppresses melatonin production. Both melatonin and vitamin D possess anti‑inflammatory, immune‑boosting and anticancer properties, rendering them potential adjuvants of interest. Studies suggest melatonin and vitamin D supplementation may address antioxidant imbalances in lip, oral and pharyngeal cancers. Moreover, promising results from breast, head and neck, brain, and osteosarcoma research indicate potential for tumor growth inhibition, improved survival, and a better quality of life of patients with cancer. The radioprotective properties of melatonin and vitamin D are another exciting area of exploration, potentially enhancing radiotherapy effectiveness while reducing side effects. For its part, the sleep‑promoting effects of melatonin may indirectly benefit patients with cancer by influencing the immune system. Thus, the prevalence of vitamin D and melatonin deficiencies highlights the importance of supplementation, as lower levels can worsen side‑effects from cancer treatments. The present review explores the potential of combining melatonin and vitamin D as synergistic adjuvants for cancer therapy. These agents have shown promise individually in cancer prevention and treatment, and their combined effects warrant investigation. Therefore, large‑scale controlled trials are crucial to definitively determine the optimal dosage, safety and efficacy of this combination in improving the lives of patients with cancer.</p>","PeriodicalId":14175,"journal":{"name":"International journal of oncology","volume":"65 6","pages":""},"PeriodicalIF":4.5,"publicationDate":"2024-12-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11575929/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142500441","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":"<i>SHARPIN</i> is a novel gene of colorectal cancer that promotes tumor growth potentially via inhibition of p53 expression.","authors":"Yusuke Nakano, Takaaki Masuda, Takeharu Sakamoto, Noritaka Tanaka, Taro Tobo, Masahiro Hashimoto, Takanari Tatsumi, Hideyuki Saito, Junichi Takahashi, Kensuke Koike, Tadashi Abe, Yuki Ando, Yuki Ozato, Kiyotaka Hosoda, Kosuke Hirose, Satoshi Higuchi, Tomohiko Ikehara, Yuichi Hisamatsu, Takeo Toshima, Yusuke Yonemura, Takayuki Ogino, Mamoru Uemura, Hidetoshi Eguchi, Yuichiro Doki, Koshi Mimori","doi":"10.3892/ijo.2024.5701","DOIUrl":"10.3892/ijo.2024.5701","url":null,"abstract":"<p><p>Colorectal cancer (CRC) is widely prevalent and represents a significant contributor to global cancer‑related mortality. There remains a pressing demand for advancements in CRC treatment modalities. The E3 ubiquitin ligase is a critical enzyme involved in modulating protein expression levels via posttranslational ubiquitin‑mediated proteolysis, and it is reportedly involved in the progression of various cancers, making it a target of recent interest in anticancer therapy. In the present study, using comprehensive expression analysis involving spatial transcriptomic analysis with single‑cell RNA sequencing in clinical CRC datasets, the ubiquitin‑associated protein Shank‑associated RH domain interactor (<i>SHARPIN</i>) was identified, located on amplified chromosome 8q, which could promote CRC progression. <i>SHARPIN</i> was found to be upregulated in tumor cells, with elevated expression observed in tumor tissues. This heightened expression of <i>SHARPIN</i> was positively associated with lymphatic invasion and served as an independent predictor of a poor prognosis in patients with CRC. <i>In vitro</i> and <i>in vivo</i> analyses using SHARPIN‑overexpressing or ‑knockout CRC cells revealed that SHARPIN overexpression upregulated MDM2, resulting in the downregulation of p53, while SHARPIN silencing or knockout downregulated MDM2, leading to p53 upregulation, which affects cell cycle progression, tumor cell apoptosis and tumor growth in CRC. Furthermore, <i>SHARPIN</i> was found to be overexpressed in several cancer types, exerting significant effects on survival outcomes. In conclusion, SHARPIN represents a newly identified novel gene with the potential to promote tumor growth following apoptosis inhibition and cell cycle progression in part by inhibiting p53 expression via MDM2 upregulation; therefore, SHARPIN represents a potential therapeutic target for CRC.</p>","PeriodicalId":14175,"journal":{"name":"International journal of oncology","volume":"65 6","pages":""},"PeriodicalIF":4.5,"publicationDate":"2024-12-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11542962/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142500440","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":"Exosomal integrins in tumor progression, treatment and clinical prediction (Review).","authors":"Yu-Qing Shen, Lei Sun, Shi-Ming Wang, Xian-Yu Zheng, Rui Xu","doi":"10.3892/ijo.2024.5706","DOIUrl":"10.3892/ijo.2024.5706","url":null,"abstract":"<p><p>Integrins are a large family of cell adhesion molecules involved in tumor cell differentiation, migration, proliferation and neovascularization. Tumor cell‑derived exosomes carry a large number of integrins, which are closely associated with tumor progression. As crucial mediators of intercellular communication, exosomal integrins have gained attention in the field of cancer biology. The present review examined the regulatory mechanisms of exosomal integrins in tumor cell proliferation, migration and invasion, and emphasized their notable roles in tumor initiation and progression. The potential of exosomal integrins as drug delivery systems in cancer treatment was explored. Additionally, the potential of exosomal integrins in clinical tumor prediction was considered, while summarizing their applications in diagnosis, prognosis assessment and treatment response prediction. Thus, the present review aimed to provide guidance and insights for future basic research and the clinical translation of exosomal integrins. The study of exosomal integrins is poised to offer new perspectives and methods for precise cancer treatment and clinical prediction.</p>","PeriodicalId":14175,"journal":{"name":"International journal of oncology","volume":"65 6","pages":""},"PeriodicalIF":4.5,"publicationDate":"2024-12-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11575930/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142620454","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":"[Corrigendum] miR-382 inhibits migration and invasion by targeting ROR1 through regulating EMT in ovarian cancer.","authors":"Hong Tan, Qingnan He, Guanhui Gong, Yixuan Wang, Juanni Li, Junpu Wang, Ding Zhu, Xiaoying Wu","doi":"10.3892/ijo.2024.5698","DOIUrl":"https://doi.org/10.3892/ijo.2024.5698","url":null,"abstract":"<p><p>Following the publication of the above article, an interested reader drew to the authors' attention that certain of the Transwell migration and invasion assay data panels shown in Figs. 3E and G and 7E and G on p. 1754 and 1757 respectively contained overlapping data panels, both within Fig. 3 and between Figs. 3 and 7, such that data which were intended to represent the results of differently performed experiments had apparently been derived from the same original sources. Specifically, the 'con' and 'pre-con' data panels in Fig. 3 were overlapping, as were the 'pre-con' and 'pcDNA.1-ROR1' panels comparing Fig. 3 with Fig. 7, and the Editorial Office subsequently pointed out to the authors that the 'con' and 'pre-con' data panels in Fig. 3E also contained an overlapping edge. After having examined their original data, the authors realized that these figures were inadvertently assembled incorrectly. The corrected versions of Figs. 3 and 7 are shown on the next page, now showing the correct data for the 'con' experiment in Fig. 3E, the 'pre-con' experiment in Fig. 3G, and the 'pcDNA.1-ROR1' panel in Fig. 7G. 'The authors are grateful to 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; furthermore, they apologize to the readership of the journal for any inconvenience caused. [International Journal of Oncology 48: 181-190, 2016; DOI: 10.3892/ijo.2015.3241].</p>","PeriodicalId":14175,"journal":{"name":"International journal of oncology","volume":"65 5","pages":""},"PeriodicalIF":4.5,"publicationDate":"2024-11-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11436263/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142346617","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":"Molecular mechanisms and targeted therapy for the metastasis of prostate cancer to the bones (Review).","authors":"Yankai Xu, Gang Zhang, Yuanyuan Liu, Yangyang Liu, Aimin Tian, Jizhong Che, Zhengchao Zhang","doi":"10.3892/ijo.2024.5692","DOIUrl":"10.3892/ijo.2024.5692","url":null,"abstract":"<p><p>The incidence of prostate cancer (PCa) is increasing, making it one of the prevalent malignancies among men. Metastasis of PCa to the bones poses the greatest danger to patients, potentially resulting in treatment ineffectiveness and mortality. At present, the management of patients with bone metastasis focuses primarily on providing palliative care. Research has indicated that the spread of PCa to the bones occurs through the participation of numerous molecules and their respective pathways. Gaining knowledge regarding the molecular processes involved in bone metastasis may result in the development of innovative and well‑tolerated therapies, ultimately enhancing the quality of life and prognosis of patients. The present article provides the latest overview of the molecular mechanisms involved in the formation of bone metastatic tumors from PCa. Additionally, the clinical outcomes of targeted drug therapies for bone metastasis are thoroughly analyzed. Finally, the benefits and difficulties of targeted therapy for bone metastasis of PCa are discussed, aiming to offer fresh perspectives for treatment.</p>","PeriodicalId":14175,"journal":{"name":"International journal of oncology","volume":"65 5","pages":""},"PeriodicalIF":4.5,"publicationDate":"2024-11-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11419411/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142287176","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":"[Corrigendum] Adenoviral neutral endopeptidase gene delivery in combination with paclitaxel for the treatment of prostate cancer.","authors":"Katsuyuki Iida, Rong Zheng, Ruoqian Shen, David M Nanus","doi":"10.3892/ijo.2024.5694","DOIUrl":"10.3892/ijo.2024.5694","url":null,"abstract":"<p><p>Subsequently to the publication of the above article, an interested reader drew to the authors' attention that, for the immunostaining experiments shown in Fig. 3C on p. 1195, the 'NEP' and 'PTX' panels contained overlapping data, such that data which were intended to show the results of differently performed experiments had apparently been derived from the same original source. After re‑examining their original data, the authors have realized that the 'PTX' data panel in Fig. 3C had inadvertently been selected incorrectly. The revised and corrected version of Fig. 3, showing the correct data for the 'PTX' data panel in Fig. 3C, is shown on on the next page. The authors are grateful to the Editor of <i>International Journal of Oncology</i> for allowing them this opportunity to publish this Corrigendum, and all the authors agree with its publication. Furthermore, the authors apologize to the readership for any inconvenience caused. [International Journal of Oncology 41: 1192‑1198, 2012; DOI: 10.3892/ijo.2012.1586].</p>","PeriodicalId":14175,"journal":{"name":"International journal of oncology","volume":"65 5","pages":""},"PeriodicalIF":4.5,"publicationDate":"2024-11-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11436257/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142287172","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] Slug contributes to cancer progression by direct regulation of ERα signaling pathway.","authors":"Youqiang Li, Yanyuan Wu, Thomas C Abbatiello, Warren L Wu, Ju Ri Kim, Marianna Sarkissyan, Suren Sarkissyan, Seyung S Chung, Yahya Elshimali, Jaydutt V Vadgama","doi":"10.3892/ijo.2024.5689","DOIUrl":"10.3892/ijo.2024.5689","url":null,"abstract":"<p><p>Following the publication of the above paper, it was drawn to the Editor's attention by concerned readers that β‑actin bands shown in Figs. 1, 2 and 4 were strikingly similar, where the experimental conditions reported in Fig. 4 differed from those in Figs. 1 and 2; moreover, the Slug protein bands featured in Figs. 4a and 5a were remarkably similar in spite of the different experimental conditions that were reported in the respective figure legends, and the shape of the vimentin protein bands in Fig. 5e bore a strong similarity to the Slug protein bands that were featured in Fig. 2c, in spite of the bands being of slightly different sizes and arranged in a different orientation.  Although the possibility of publishing a corrigendum was considered, software analysis of the highlighted bands performed independently by the Editorial Office demonstrated that the bands in question were likely to have been matching bands. Therefore, given the number of potential concerns that were identified with the assembly of various of the figures in this paper, the Editor of <i>International Journal of Oncology</i> has decided not to proceed with a corrigendum, and has determined that the paper should instead be retracted from the Journal on account of an overall lack of confidence in the originally 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 46: 1461‑1472, 2015; DOI: 10.3892/ijo.2015.2878].</p>","PeriodicalId":14175,"journal":{"name":"International journal of oncology","volume":"65 5","pages":""},"PeriodicalIF":4.5,"publicationDate":"2024-11-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11419408/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142287173","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":"Cinobufagin inhibits M2‑like tumor‑associated macrophage polarization to attenuate the invasion and migration of lung cancer cells.","authors":"Ying Sun, Yunfeng Lian, Xue Mei, Jinchan Xia, Long Feng, Jianfeng Gao, Huaming Xu, Xiaoyan Zhang, Huitong Yang, Xu Hao, Yilin Feng","doi":"10.3892/ijo.2024.5690","DOIUrl":"10.3892/ijo.2024.5690","url":null,"abstract":"<p><p>Macrophages have crucial roles in immune responses and tumor progression, exhibiting diverse phenotypes based on environmental cues. In the present study, the impact of cinobufagin (CB) on macrophage polarization and the consequences on tumor‑associated behaviors were investigated. Morphological transformations of THP‑1 cells into M0, M1 and M2 macrophages were observed, including distinct changes in the size, shape and adherence properties of these cells. CB treatment inhibited the viability of A549 and LLC cells in a concentration‑dependent manner, with an IC₅₀ of 28.8 and 30.12 ng/ml, respectively. CB at concentrations of <30 ng/ml had no impact on the viability of M0 macrophages and lung epithelial (BEAS‑2B) cells. CB influenced the expression of macrophage surface markers, reducing CD206 positivity in M2 macrophages without affecting CD86 expression in M1 macrophages. CB also altered certain expression profiles at the mRNA level, notably downregulating macrophage receptor with collagenous structure (MARCO) expression in M2 macrophages and upregulating tumor necrosis factor‑α and interleukin‑1β in both M0 and M1 macrophages. Furthermore, ELISA analyses revealed that CB increased the levels of pro‑inflammatory cytokines in M1 macrophages and reduced the levels of anti‑inflammatory factors in M2 macrophages. CB treatment also attenuated the migration and invasion capacities of A549 and LLC cells stimulated by M2 macrophage‑conditioned medium. Additionally, CB modulated peroxisome proliferator‑activated receptor γ (PPARγ) and MARCO expression in M2 macrophages and epithelial‑mesenchymal transition in A549 cells, which was partially reversed by rosiglitazone, a PPARγ agonist. Finally, CB and cisplatin treatments hindered tumor growth <i>in vivo</i>, with distinct impacts on animal body weight and macrophage marker expression in tumor tissues. In conclusion, the results of the present study demonstrated that CB exerted complex regulatory effects on macrophage polarization and tumor progression, suggesting its potential as a modulator of the tumor microenvironment and a therapeutic for cancer treatment.</p>","PeriodicalId":14175,"journal":{"name":"International journal of oncology","volume":"65 5","pages":""},"PeriodicalIF":4.5,"publicationDate":"2024-11-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11419410/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142287174","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}