Cellular Oncology最新文献

{"title":"Retraction Note: Leptin promotes the migration and invasion of breast cancer cells by upregulating ACAT2.","authors":"Yunxiu Huang, Qianni Jin, Min Su, Feihu Ji, Nian Wang, Changli Zhong, Yulin Jiang, Yifeng Liu, Zhiqian Zhang, Junhong Yang, Lan Wei, Tingmei Chen, Bing Li","doi":"10.1007/s13402-025-01035-y","DOIUrl":"10.1007/s13402-025-01035-y","url":null,"abstract":"","PeriodicalId":9690,"journal":{"name":"Cellular Oncology","volume":" ","pages":"265"},"PeriodicalIF":6.6,"publicationDate":"2025-02-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143000855","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Fasting in combination with the cocktail Sorafenib:Metformin blunts cellular plasticity and promotes liver cancer cell death via poly-metabolic exhaustion.","authors":"Juan L López-Cánovas, Beatriz Naranjo-Martínez, Alberto Diaz-Ruiz","doi":"10.1007/s13402-024-00966-2","DOIUrl":"10.1007/s13402-024-00966-2","url":null,"abstract":"<p><strong>Purpose: </strong>Dual-Interventions targeting glucose and oxidative metabolism are receiving increasing attention in cancer therapy. Sorafenib (S) and Metformin (M), two gold-standards in liver cancer, are known for their mitochondrial inhibitory capacity. Fasting, a glucose-limiting strategy, is also emerging as chemotherapy adjuvant. Herein, we explore the anti-carcinogenic response of nutrient restriction in combination with sorafenib:metformin (NR-S:M).</p><p><strong>Results: </strong>Our data demonstrates that, independently of liver cancer aggressiveness, fasting synergistically boosts the anti-proliferative effects of S:M co-treatment. Metabolic and Cellular plasticity was determined by the examination of mitochondrial and glycolytic activity, cell cycle modulation, activation of cellular apoptosis, and regulation of key signaling and metabolic enzymes. Under NR-S:M conditions, early apoptotic events and the pro-apoptotic Bcl-xS/Bcl-xL ratio were found increased. NR-S:M induced the highest retention in cellular SubG1 phase, consistent with the presence of DNA fragments from cellular apoptosis. Mitochondrial functionality, Mitochondrial ATP-linked respiration, Maximal respiration and Spare respiratory capacity, were all found blunted under NR-S:M conditions. Basal Glycolysis, Glycolytic reserve, and glycolytic capacity, together with the expression of glycogenic (PKM), gluconeogenic (PCK1 and G6PC3), and glycogenolytic enzymes (PYGL, PGM1, and G6PC3), were also negatively impacted by NR-S:M. Lastly, a TMT-proteomic approach corroborated the synchronization of liver cancer metabolic reprogramming with the activation of molecular pathways to drive a quiescent-like status of energetic-collapse and cellular death.</p><p><strong>Conclusion: </strong>Altogether, we show that the energy-based polytherapy NR-S:M blunts cellular, metabolic and molecular plasticity of liver cancer. Notwithstanding the in vitro design of this study, it holds a promising therapeutic tool worthy of exploration for this tumor pathology.</p>","PeriodicalId":9690,"journal":{"name":"Cellular Oncology","volume":" ","pages":"161-182"},"PeriodicalIF":6.6,"publicationDate":"2025-02-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11850423/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"141578973","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Retraction Note: Downregulation of beta-catenin in chemo-tolerant TNBC through changes in receptor and antagonist profiles of the WNT pathway: Clinical and prognostic implications.","authors":"Saimul Islam, Hemantika Dasgupta, Mukta Basu, Anup Roy, Neyaz Alam, Susanta Roychoudhury, Chinmay Kumar Panda","doi":"10.1007/s13402-025-01036-x","DOIUrl":"10.1007/s13402-025-01036-x","url":null,"abstract":"","PeriodicalId":9690,"journal":{"name":"Cellular Oncology","volume":" ","pages":"267"},"PeriodicalIF":6.6,"publicationDate":"2025-02-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143000930","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Pre-existing cell subpopulations in primary prostate cancer tumors display surface fingerprints of docetaxel-resistant cells.","authors":"Stanislav Drápela, Barbora Kvokačková, Eva Slabáková, Anna Kotrbová, Kristína Gömöryová, Radek Fedr, Daniela Kurfürstová, Martin Eliáš, Vladimír Študent, Frederika Lenčéšová, Ganji Sri Ranjani, Vendula Pospíchalová, Vítězslav Bryja, Wytske M van Weerden, Martin Puhr, Zoran Culig, Jan Bouchal, Karel Souček","doi":"10.1007/s13402-024-00982-2","DOIUrl":"10.1007/s13402-024-00982-2","url":null,"abstract":"<p><strong>Purpose: </strong>Docetaxel resistance is a significant obstacle in the treatment of prostate cancer (PCa), resulting in unfavorable patient prognoses. Intratumoral heterogeneity, often associated with epithelial-to-mesenchymal transition (EMT), has previously emerged as a phenomenon that facilitates adaptation to various stimuli, thus promoting cancer cell diversity and eventually resistance to chemotherapy, including docetaxel. Hence, understanding intratumoral heterogeneity is essential for better patient prognosis and the development of personalized treatment strategies.</p><p><strong>Methods: </strong>To address this, we employed a high-throughput single-cell flow cytometry approach to identify a specific surface fingerprint associated with docetaxel-resistance in PCa cells and complemented it with proteomic analysis of extracellular vesicles. We further validated selected antigens using docetaxel-resistant patient-derived xenografts in vivo and probed primary PCa specimens to interrogate of their surface fingerprint.</p><p><strong>Results: </strong>Our approaches revealed a 6-molecule surface fingerprint linked to docetaxel resistance in primary PCa specimens. We observed consistent overexpression of CD95 (FAS/APO-1), and SSEA-4 surface antigens in both in vitro and in vivo docetaxel-resistant models, which was also observed in a cell subpopulation of primary PCa tumors exhibiting EMT features. Furthermore, CD95, along with the essential enzymes involved in SSEA-4 synthesis, ST3GAL1, and ST3GAL2, displayed a significant increase in patients with PCa undergoing docetaxel-based therapy, correlating with poor survival outcomes.</p><p><strong>Conclusion: </strong>In summary, we demonstrate that the identified 6-molecule surface fingerprint associated with docetaxel resistance pre-exists in a subpopulation of primary PCa tumors before docetaxel treatment. Thus, this fingerprint warrants further validation as a promising predictive tool for docetaxel resistance in PCa patients prior to therapy initiation.</p>","PeriodicalId":9690,"journal":{"name":"Cellular Oncology","volume":" ","pages":"205-218"},"PeriodicalIF":6.6,"publicationDate":"2025-02-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11850551/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142003719","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Next-generation BCMA-targeted chimeric antigen receptor CARTemis-1: the impact of manufacturing procedure on CAR T-cell features.","authors":"Belén Sierro-Martínez, Virginia Escamilla-Gómez, Laura Pérez-Ortega, Beatriz Guijarro-Albaladejo, Paola Hernández-Díaz, María de la Rosa-Garrido, Maribel Lara-Chica, Alfonso Rodríguez-Gil, Juan Luis Reguera-Ortega, Luzalba Sanoja-Flores, Blanca Arribas-Arribas, Miguel Ángel Montiel-Aguilera, Gloria Carmona, Maria Jose Robles, Teresa Caballero-Velázquez, Javier Briones, Hermann Einsele, Michael Hudecek, Jose Antonio Pérez-Simón, Estefanía García-Guerrero","doi":"10.1007/s13402-024-00984-0","DOIUrl":"10.1007/s13402-024-00984-0","url":null,"abstract":"<p><strong>Purpose: </strong>CAR therapy targeting BCMA is under investigation as treatment for multiple myeloma. However, given the lack of plateau in most studies, pursuing more effective alternatives is imperative. We present the preclinical and clinical validation of a new optimized anti-BCMA CAR (CARTemis-1). In addition, we explored how the manufacturing process could impact CAR-T cell product quality and fitness.</p><p><strong>Methods: </strong>CARTemis-1 optimizations were evaluated at the preclinical level both, in vitro and in vivo. CARTemis-1 generation was validated under GMP conditions, studying the dynamics of the immunophenotype from leukapheresis to final product. Here, we studied the impact of the manufacturing process on CAR-T cells to define optimal cell culture protocol and expansion time to increase product fitness.</p><p><strong>Results: </strong>Two different versions of CARTemis-1 with different spacers were compared. The longer version showed increased cytotoxicity. The incorporation of the safety-gene EGFRt into the CARTemis-1 structure can be used as a monitoring marker. CARTemis-1 showed no inhibition by soluble BCMA and presents potent antitumor effects both in vitro and in vivo. Expansion with IL-2 or IL-7/IL-15 was compared, revealing greater proliferation, less differentiation, and less exhaustion with IL-7/IL-15. Three consecutive batches of CARTemis-1 were produced under GMP guidelines meeting all the required specifications. CARTemis-1 cells manufactured under GMP conditions showed increased memory subpopulations, reduced exhaustion markers and selective antitumor efficacy against MM cell lines and primary myeloma cells. The optimal release time points for obtaining the best fit product were > 6 and < 10 days (days 8-10).</p><p><strong>Conclusions: </strong>CARTemis-1 has been rationally designed to increase antitumor efficacy, overcome sBCMA inhibition, and incorporate the expression of a safety-gene. The generation of CARTemis-1 was successfully validated under GMP standards. A phase I/II clinical trial for patients with multiple myeloma will be conducted (EuCT number 2022-503063-15-00).</p>","PeriodicalId":9690,"journal":{"name":"Cellular Oncology","volume":" ","pages":"219-237"},"PeriodicalIF":6.6,"publicationDate":"2025-02-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11850460/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142079286","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Regulatory mechanisms of steroid hormone receptors on gene transcription through chromatin interaction and enhancer reprogramming.","authors":"Ge Sun, Chunguang Zhao, Jing Han, Shaoya Wu, Yan Chen, Jing Yao, Li Li","doi":"10.1007/s13402-024-01011-y","DOIUrl":"10.1007/s13402-024-01011-y","url":null,"abstract":"<p><p>Regulation of steroid hormone receptors (SHRs) on transcriptional reprogramming is crucial for breast cancer progression. SHRs, including estrogen receptor (ER), androgen receptor (AR), progesterone receptor (PR), and glucocorticoid receptor (GR) play key roles in remodeling the transcriptome of breast cancer cells. However, the molecular mechanisms by which SHRs regulate chromatin landscape in enhancer regions and transcription factor interactions remain largely unknown. In this review, we summarized the regulatory effects of 3 types of SHRs (AR, PR, and GR) on gene transcription through chromatin interactions and enhancer reprogramming. Specifically, AR and PR exhibit bi-directional regulatory effects (both inhibitory and promoting) on ER-mediated gene transcription, while GR modulates the transcription of pro-proliferation genes in ER-positive breast cancer cells. In addition, we have presented four enhancer reprogramming mechanisms (transcription factor cooperation, pioneer factor binding, dynamic assisted loading, and tethering) and the multiple enhancer-promoter contact models. Based on these mechanisms and models, this review proposes that the combination of multiple therapy strategies such as agonists/antagonists of SHRs plus endocrine therapy and the adoption of the latest sequencing technologies are expected to improve the efficacy of ER positive breast cancer treatment.</p>","PeriodicalId":9690,"journal":{"name":"Cellular Oncology","volume":" ","pages":"2073-2090"},"PeriodicalIF":6.6,"publicationDate":"2024-12-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142615398","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"USP28 promotes tumor progression and glycolysis by stabilizing PKM2/Hif1-α in cholangiocarcinoma.","authors":"Qian Qiao, Jifei Wang, Shuochen Liu, Jiang Chang, Tao Zhou, Changxian Li, Yaodong Zhang, Wangjie Jiang, Yananlan Chen, Xiao Xu, Mingyu Wu, Xiangcheng Li","doi":"10.1007/s13402-024-01002-z","DOIUrl":"10.1007/s13402-024-01002-z","url":null,"abstract":"<p><strong>Background: </strong>Ubiquitination is one of the important modification of proteins which can be reversed by deubiquitinating enzymes (DUBs). Ubiquitin specific protease 28 (USP28) belongs to the deubiquitinase family, which plays a cancer-promoting function in many types of cancers such as pancreatic cancer and breast cancer. So far, the molecular function and significance of USP 28 in cholangiocarcinoma remain unclear.</p><p><strong>Methods: </strong>In this study, we evaluated the expression of USP28 using tissue microarray (TMA), reverse transcription polymerase chain reaction (qRT-PCR), and online databases. We investigated the effect of USP28 on the progression of CCA through in vitro and in vivo functional experiments. In addition, we explored downstream molecular pathways using Western blotting (WB), immunofluorescence (IF), and mass spectrometry techniques.</p><p><strong>Results: </strong>Here, we found that cholangiocarcinoma tissue had higher USP 28 expression than normal bile duct tissue, and that high USP 28 levels were significantly associated with a malignant phenotype and poorer prognosis in cholangiocarcinoma patients. Both in vitro and in vivo, USP28 could mediate the deubiquitination of PKM2, thereby activating the downstream Hif1-α signaling pathway, promoting glycolysis and energy supply, and finally promoting tumor progression.</p><p><strong>Conclusion: </strong>In summary, USP28 activated downstream Hif1-α by reducing the ubiquitination level of PKM2, furthermore, promoting the level of glycolysis in CCA cells for tumor progression.</p>","PeriodicalId":9690,"journal":{"name":"Cellular Oncology","volume":" ","pages":"2217-2231"},"PeriodicalIF":6.6,"publicationDate":"2024-12-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142459017","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"HNRNPH1 stabilizes FLOT2 mRNA in a non-canonical m6A-dependent manner to promote malignant progression in nasopharyngeal carcinoma.","authors":"Qiguang Li, Jie Liu, Chong Zeng, Daogang Qin, Zijian Zhang, Qiaoli Lv, Jingao Li, Wei Huang","doi":"10.1007/s13402-024-01016-7","DOIUrl":"10.1007/s13402-024-01016-7","url":null,"abstract":"<p><strong>Purpose: </strong>The mechanism underlying the upregulation of FLOT2 in tumors, especially its regulatory mechanism at the RNA level, remains unclear. The purpose of this study is to investigate the regulatory mechanism of FLOT2 upregulation in tumors, particularly at the RNA level, and its role in nasopharyngeal carcinoma (NPC) progression.</p><p><strong>Methods: </strong>We identified the role of HNRNPH1 in maintaining FLOT2 mRNA stability and its dependency on the m6A modification. We explored the interaction between HNRNPH1 and METTL14, a key enzyme in m6A modification, and its impact on FLOT2 mRNA stability. We also assessed the expression levels of HNRNPH1 and METTL14 in NPC and their correlation with patient malignancy and prognosis. Experimental approaches included in vitro and in vivo assays to study the effects of HNRNPH1 knockdown on NPC cell proliferation and invasion.</p><p><strong>Results: </strong>HNRNPH1 is highly expressed in NPC and stabilizes FLOT2 mRNA through an m6A-dependent mechanism. HNRNPH1 interacts with METTL14 to prevent its degradation by STUB1 E3 ligases, leading to increased m6A modification of FLOT2 by METTL14. Additionally, IGF2BP3 was shown to recognize the m6A modification on FLOT2 mRNA, further stabilizing it. High expression of HNRNPH1 and METTL14 were observed in NPC and were positively associated with increased malignancy and poorer patient outcomes. HNRNPH1 knockdown significantly reduced the proliferation and invasive capabilities of NPC cells. Restoration of METTL14 in HNRNPH1-depleted cells could rescue FLOT2 expression and the malignant phenotype, but this effect was negated by the knockdown of FLOT2.</p><p><strong>Conclusion: </strong>Our study elucidates a novel mechanism where HNRNPH1 and METTL14 work together to maintain the stability of FLOT2 mRNA, thereby promoting NPC progression. Targeting this pathway presents a promising therapeutic strategy for the treatment of NPC.</p>","PeriodicalId":9690,"journal":{"name":"Cellular Oncology","volume":" ","pages":"2279-2295"},"PeriodicalIF":6.6,"publicationDate":"2024-12-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142680748","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Tumour cell-released autophagosomes promote lung metastasis by upregulating PD-L1 expression in pulmonary vascular endothelial cells in breast cancer.","authors":"Xu-Ru Wang, Xiao-He Zhou, Xiao-Tong Sun, Yu-Qing Shen, Yu-Yang Wu, Cheng-Dong Wu, Feng-Jiao Zhu, Yi-Ting Wei, Jin-Peng Chen, Jing Chen, Shi-Ya Zheng, Li-Xin Wang","doi":"10.1007/s13402-024-00994-y","DOIUrl":"10.1007/s13402-024-00994-y","url":null,"abstract":"<p><strong>Purpose: </strong>Establishing an immunosuppressive premetastatic niche (PMN) in distant organs is crucial for breast cancer metastasis. Vascular endothelial cells (VECs) act as barriers to transendothelial cell migration. However, the immune functions of PMNs remain unclear. Tumour cell-released autophagosomes (TRAPs) are critical modulators of antitumour immune responses. Herein, we investigated the mechanism through which TRAPs modulate the immune function of pulmonary VECs in lung PMN in breast cancer.</p><p><strong>Methods: </strong>Immortalised mouse pulmonary microvascular endothelial cells were incubated with TRAPs in vitro. RNA sequencing, flow cytometry, and western blotting were employed to assess immunosuppressive function and mechanism. In vivo, TRAP-trained and autophagy-deficient tumour mice were used to detect immunosuppression, and high-mobility group box 1 (HMGB1)-deficient TRAP-trained and TLR4 knockout mice were utilised to investigate the underlying mechanisms of pulmonary VECs. Additionally, the efficacy of anti-programmed cell death ligand-1 (PD-L1) immunotherapy was evaluated in early tumour-bearing mice.</p><p><strong>Results: </strong>HMGB1 on TRAPs surfaces stimulated VECs to upregulate PD-L1 via a TLR4-MyD88-p38/STAT3 signalling cascade that depended on the cytoskeletal movement of VECs. Importantly, PD-L1 on TRAP-induced VECs can inhibit T cell function, promote lung PMN immunosuppression, and result in more pronounced lung metastasis. Treatment with anti-PD-L1 reduces lung metastasis in early stage tumour-bearing mice.</p><p><strong>Conclusions: </strong>These findings revealed a novel role and mechanism of TRAP-induced immunosuppression of pulmonary VECs in lung PMN. TRAPs and their surface HMGB1 are important therapeutic targets for reversing immunosuppression, providing a new theoretical basis for the treatment of early stage breast cancer using an anti-PD-L1 antibody.</p>","PeriodicalId":9690,"journal":{"name":"Cellular Oncology","volume":" ","pages":"2147-2162"},"PeriodicalIF":6.6,"publicationDate":"2024-12-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142380113","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Retraction Note: The autocrine glycosylated-GREM1 interacts with TGFB1 to suppress TGFβ/BMP/SMAD-mediated EMT partially by inhibiting MYL9 transactivation in urinary carcinoma.","authors":"Ti-Chun Chan, Cheng-Tang Pan, Hsin-Yu Hsieh, Pichpisith Pierre Vejvisithsakul, Ren-Jie Wei, Bi-Wen Yeh, Wen-Jeng Wu, Lih-Ren Chen, Meng-Shin Shiao, Chien-Feng Li, Yow-Ling Shiue","doi":"10.1007/s13402-024-01006-9","DOIUrl":"10.1007/s13402-024-01006-9","url":null,"abstract":"","PeriodicalId":9690,"journal":{"name":"Cellular Oncology","volume":" ","pages":"2461-2462"},"PeriodicalIF":6.6,"publicationDate":"2024-12-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142459013","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}