Anti-Cancer Drugs最新文献

{"title":"The PITX2/CKMT1B axis promotes lung adenocarcinoma stemness via lipid accumulation.","authors":"Longshan Zhou, Xiaoping Jin, Yuchao Shen, Lifeng Wang, Jianfeng Jing","doi":"10.1097/CAD.0000000000001811","DOIUrl":"10.1097/CAD.0000000000001811","url":null,"abstract":"<p><p>Dysregulated expression of mitochondrial creatine kinase 1B (CKMT1B), a member of the creatine kinase family, has been linked to tumor progression. However, its specific function in lung adenocarcinoma (LUAD) remains unclear. Bioinformatics analyses were performed to evaluate CKMT1B and its upstream transcription factor PITX2 in LUAD. CKMT1B and PITX2 expression levels were determined by quantitative PCR. The functional impact on cell stemness was subsequently evaluated using CCK-8, sphere formation assay, flow cytometry, and western blot. CKMT1B-mediated lipid accumulation was examined via BODIPY staining and measurements of triglyceride and glycerol concentration. The PITX2-CKMT1B interaction was validated through dual-luciferase reporter and chromatin immunoprecipitation (ChIP) assays, with the regulatory mechanism further substantiated by functional rescue experiments. CKMT1B was upregulated in LUAD and linked with poor prognosis. Its knockdown suppressed cell proliferation, sphere-forming capacity, and stemness-related protein expression (CD133, Bmi-1, SOX-2). Furthermore, CKMT1B overexpression facilitated lipid accumulation and stemness, effects that were reversible by the lipase inhibitor Orlistat. Mechanistically, PITX2 was identified as an upstream transcription factor of CKMT1B. PITX2 expression was positively correlated with CKMT1B, and high PITX2 expression predicted poor outcomes. In functional rescue experiments, PITX2 knockdown significantly reduced lipid accumulation and stemness, while these effects were partially restored by CKMT1B overexpression. PITX2 promotes lipid accumulation and enhances stemness in LUAD cells by transcriptionally activating CKMT1B, suggesting the PITX2/CKMT1B axis as a potential therapeutic target for LUAD treatment.</p>","PeriodicalId":7969,"journal":{"name":"Anti-Cancer Drugs","volume":" ","pages":"439-448"},"PeriodicalIF":2.0,"publicationDate":"2026-08-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145987714","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"The novel integrin-linked kinase inhibitor nilotinib suppresses cancer progression by promoting ubiquitylation of autoimmune regulator in oesophageal squamous cell carcinoma.","authors":"Xiaoli Ma, Yu Wei, LeiYu Cao, Yan Gao, Chengcheng Qu, Kalima Muhetaer, Li Zhang","doi":"10.1097/CAD.0000000000001828","DOIUrl":"10.1097/CAD.0000000000001828","url":null,"abstract":"<p><p>Integrin-linked kinase (ILK) is a key oncogenic driver in oesophageal squamous cell carcinoma (ESCC). This study evaluated the antitumour effects of the novel ILK inhibitor Nilotinib and explored its downstream mechanisms. In vitro , TE-1 and KYSE150 cells were assessed using Cell Counting Kit-8, lactate dehydrogenase release, colony formation, 5-ehynyl-2 ' -deoxyuridine incorporation, flow cytometry, Transwell assays, and Western blotting to confirm ILK targeting and determine functional changes. Electron microscopy and fluorescent probes with flow cytometry were used to analyse mitochondrial alterations. In vivo , a nude mouse subcutaneous xenograft model was established to examine tumour growth after peritumoural Nilotinib administration; hematoxylin and eosin staining assessed tissue changes, and immunohistochemistry measured Ki67 and cleaved-caspase 3 expression. ILK overexpression alleviated Nilotinib-induced cytotoxicity, restored proliferation, increased proliferating cell nuclear antigen (PCNA) and Ki67, and reduced cleaved-caspase 3 and cleaved poly(ADP-ribose) polymerase (PARP), supporting ILK as a primary target. Nilotinib dose-dependently inhibited proliferation, invasion, and metastasis while promoting apoptosis, accompanied by downregulation of PCNA, Ki67, [matrix metalloproteinase 2 (MMP2), MMP9, and COX2] and upregulation of cleaved-caspase 3 and cleaved-PARP. In xenografts, Nilotinib significantly reduced tumour size and weight, decreased Ki67, and increased cleaved-caspase 3.RNA sequencing identified autoimmune regulator (AIRE) as a markedly downregulated molecule following Nilotinib treatment. Cycloheximide chase assays indicated accelerated AIRE protein degradation, while MG132 partially rescued AIRE levels, implicating proteasome-dependent degradation. Overall, Nilotinib suppresses ESCC progression by inhibiting ILK and destabilising AIRE, suggesting its potential as a targeted therapy for ILK-positive ESCC.</p>","PeriodicalId":7969,"journal":{"name":"Anti-Cancer Drugs","volume":" ","pages":"449-461"},"PeriodicalIF":2.0,"publicationDate":"2026-08-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC13344393/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"147809809","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"The future of cancer treatment: integrating science, technology, and global collaboration.","authors":"Sergio Huerta","doi":"10.1097/CAD.0000000000001830","DOIUrl":"https://doi.org/10.1097/CAD.0000000000001830","url":null,"abstract":"","PeriodicalId":7969,"journal":{"name":"Anti-Cancer Drugs","volume":"37 7","pages":"411"},"PeriodicalIF":2.0,"publicationDate":"2026-08-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148417632","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Synergistic antitumor effect between Olaparib and Chidamide by regulation of MYBL2 in lung cancer.","authors":"Lila Zhu, Zhi Ji, Xia Wang, Jiaqi Xin, Lijun Ma, Runshi Zhang, Ting Deng, Yi Ba, Rui Liu","doi":"10.1097/CAD.0000000000001783","DOIUrl":"10.1097/CAD.0000000000001783","url":null,"abstract":"<p><p>Recently, various basic research and clinical studies have revealed the further potential of poly (adenosine diphosphate-ribose) polymerase (PARP) inhibitor Olaparib and histone deacetylase inhibitor Chidamide in lung cancer. However, no research available was found to report whether there is a synergistic effect of Olaparib in combination with Chidamide. This research was conducted to investigate whether there is a synergistic effect between the two drugs and the underlying mechanism in lung cancer cell lines. Here, we treat lung cancer cell lines with Olaparib with or without Chidamide in vivo and in vitro. Based on that, we found that there were synergistic effects between Olaparib and Chidamide. Combined use of them cooperatively downregulated the expression of MYBL2, which was responsible for the downregulation of BRCA1, a main member of DNA damage repair. Simultaneously, Olaparib-induced inhibition of PARP expression leads to the 'synthetic lethality' of cells. On the other hand, MYBL2 may regulate the expression of cycle protein dependent kinase 1, causing G2M cell cycle arrest. Consequently, the combination of Olaparib and Chidamide synergistically induces cell apoptosis through synthetic lethality and cell cycle arrest to exert an antitumor effect.</p>","PeriodicalId":7969,"journal":{"name":"Anti-Cancer Drugs","volume":" ","pages":"421-438"},"PeriodicalIF":2.0,"publicationDate":"2026-08-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"147809807","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Evaluation of the protective effect of chamomile oral solution on the incidence of neurotoxicity caused by paclitaxel in breast cancer patients.","authors":"Nasim Nikkhah, Hedyieh Karbasforooshan, Soodabeh Shahid Sales, Sare Hosseini, Saeed Akhlaghi, Zeinab Amiri Tehranizadeh, Sepideh Elyasi","doi":"10.1097/CAD.0000000000001804","DOIUrl":"10.1097/CAD.0000000000001804","url":null,"abstract":"<p><p>Neurotoxicity is one of the major complications in cancer patients following paclitaxel-containing regimens. Matricaria chamomilla L., isolated from the German chamomile, has anti-inflammatory and antioxidant features. In this study we evaluated the preventive impact of a chamomile oral formulation against paclitaxel-induced neurotoxicity in cancer patients. In this triple-blind clinical trial, cancer patients on paclitaxel were randomly allocated to chamomile oral solution ( n  = 40), or the placebo ( n  = 40) 5 ml three times a day for four courses of chemotherapy starting one day before the paclitaxel injection. At the end of each chemotherapy course, patients in both groups were evaluated and graded according to CTCAE (Common Terminology Criteria for Adverse Events). Also, anxiety and sleep disorder were evaluated at the beginning and end of the study based on Generalized Anxiety Disorder-7 and Pittsburgh Sleep Quality Index criteria, respectively. At the end of the four cycles of chemotherapy, there was no significant difference between the two groups in terms of the neuropathy CTCAE score. In terms of the various components of the sleep questionnaire, only the individual's overall description of sleep quality at the end of the study was significantly better in the treatment group ( P  = 0.026). Sleep quality was also significantly better ( P  = 0.027), and the chance of good sleep quality in the intervention group was 4.48 times higher. Regarding the anxiety score, despite a significant decrease in both groups, the difference between the two groups at the end of the fourth course was not significant. Neither group experienced any adverse effects. Although chamomile oral solution did not significantly lessen neuropathy, findings propose that it may significantly ameliorate sleep quality in patients receiving chemotherapy as a low-cost, low-risk treatment. It also has no significant impact on reducing the level of anxiety in cancer patients.</p>","PeriodicalId":7969,"journal":{"name":"Anti-Cancer Drugs","volume":" ","pages":"412-420"},"PeriodicalIF":2.0,"publicationDate":"2026-08-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145984318","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"A novel HEAT repeat protein 5B anaplastic lymphoma kinase fusion in lung adenocarcinoma confers sensitivity to ensartinib.","authors":"Guangyi Zhang, Di Wu, Haitao Deng, Qiuyun Xiao, Huiyun Peng","doi":"10.1097/CAD.0000000000001803","DOIUrl":"10.1097/CAD.0000000000001803","url":null,"abstract":"<p><p>Anaplastic lymphoma kinase (ALK) rearrangements are rare but highly actionable drivers in non-small cell lung cancer; however, uncommon fusion variants lack standard management. We report the clinical outcome of a novel HEAT repeat protein 5B (HEATR5B)-ALK fusion treated with ensartinib. A 52-year-old Chinese woman with stage IVA lung adenocarcinoma and left adrenal metastasis underwent tumor biopsy. Targeted DNA-based next-generation sequencing (NGS) identified HEATR5B(END..EX7)-ALK(IVS19..END) fusion; ALK protein expression was confirmed by immunohistochemistry (IHC). Ensartinib 225 mg orally once daily was initiated. Serial CT scans were evaluated according to RECIST 1.1; progression-free survival (PFS) and adverse events were recorded. The patient achieved a confirmed partial response at first restaging and maintained treatment for greater than 24 months without radiologic progression. No grade greater than or equal to 3 adverse events were observed; preexisting weight loss ceased. PFS is ongoing at the last follow-up (24+ months). The HEATR5B-ALK fusion is targetable by ensartinib, producing durable disease control and excellent tolerability. Comprehensive NGS and ALK IHC are essential for detecting rare actionable ALK variants.</p>","PeriodicalId":7969,"journal":{"name":"Anti-Cancer Drugs","volume":" ","pages":"462-468"},"PeriodicalIF":2.0,"publicationDate":"2026-08-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"147721651","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Ubiquitination mediated cisplatin resistance in bladder cancer.","authors":"Yuzhong Wang, Junfang Yuan, Shaowei Guo, Yongqiang Liu, Jianguo Ma","doi":"10.1097/CAD.0000000000001816","DOIUrl":"10.1097/CAD.0000000000001816","url":null,"abstract":"<p><p>Bladder cancer (BCa) patients frequently develop resistance to platinum-based therapies, particularly cisplatin. The link between chemoresistance and glycolysis has been well documented. Emerging evidence suggests that Rac family small GTPase 3 ( RAC3 ) may play significant roles in cisplatin resistance. This study investigated the underlying molecular mechanisms. Clinical specimens (cisplatin-sensitive/resistant BCa tissues and matched adjacent normal tissues) were collected from hospital. Cisplatin-resistant cell lines [T24-derived cisplatin-resistant cells (T24-DDP) and 5637-derived cisplatin-resistant cells (5637-DDP)] were generated through stepwise dose escalation. RAC3 , Myc-binding protein 2 (MYCBP2 ), P21-activated kinase 1 ( PAK1 ), Ki-67, and glycolysis markers were analyzed by quantitative PCR, immunohistochemistry, and Western blot. RAC3 ubiquitination was assessed via co-immunoprecipitation. Cell viability, apoptosis, and glycolytic metabolism were evaluated using the cell counting kit-8 assay, terminal deoxynucleotidyl transferase deoxyuridine triphosphate/flow cytometry, and ATP/lactate assays, respectively. Glycolytic flux was measured by extracellular acidification rate. Additionally, BCa xenograft models were established for in-vivo detection. Elevated RAC3 expression and glycolytic activity were observed in BCa tissues, with further augmentation in cisplatin-resistant tumors. RAC3 overexpression promoted cell viability, glycolysis, invasion, and migration in cisplatin-treated T24 and 5637 cells. Conversely, RAC3 knockdown exerted the opposite effects and restored cisplatin sensitivity in resistant T24-DDP and 5637-DDP cells. Notably, the sensitizing effect of RAC3 knockdown was reversed by PAK1 overexpression. Furthermore, MYCBP2 regulated RAC3 stability, as MYCBP2 overexpression enhanced RAC3 ubiquitination, suppressed glycolysis, and sensitized resistant cells to cisplatin. These effects were abrogated by the proteasome inhibitor MG132, confirming proteasome-dependent degradation of RAC3 . MYCBP2 -mediated ubiquitination of RAC3 modulates the PAK1 /pyruvate dehydrogenase E1 subunit alpha axis to regulate glycolytic activity, ultimately determining cisplatin sensitivity in BCa.</p>","PeriodicalId":7969,"journal":{"name":"Anti-Cancer Drugs","volume":" ","pages":"386-400"},"PeriodicalIF":2.0,"publicationDate":"2026-07-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"147728141","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Aldehyde dehydrogenase 9A1 promotes cisplatin resistance in laryngeal squamous cell carcinoma by enhancing PTEN-induced kinase 1-Parkin-mediated mitophagy.","authors":"Jiawei Gui, Bo Wu, Yutong Fan, Xiaotong Liu, Yuzhe Liu, Haiying Wang, Jun An, Hao Wang, Ruoqing Wu, Liang Li, Jingchun Ge, Hui Xiao","doi":"10.1097/CAD.0000000000001799","DOIUrl":"10.1097/CAD.0000000000001799","url":null,"abstract":"<p><p>Cisplatin resistance remains a major challenge in laryngeal squamous cell carcinoma (LSCC) treatment. Aldehyde dehydrogenase 9A1 (ALDH9A1), a mitochondrial matrix protein, is dysregulated in various cancers, but its role in LSCC is unclear. This study demonstrates that ALDH9A1 is significantly downregulated in LSCC tissues, and low ALDH9A1 expression correlates with poor patient prognosis. Functionally, ALDH9A1 overexpression inhibits LSCC cell proliferation, migration, and invasion while promoting apoptosis. Mechanistically, ALDH9A1 interacts with and stabilizes PTEN-induced kinase 1 (PINK1), leading to activation of PINK1-Parkin-mediated mitophagy. Under cisplatin treatment, ALDH9A1 is upregulated and induces protective mitophagy, contributing to cisplatin resistance. Inhibition of mitophagy with chloroquine sensitizes LSCC cells to cisplatin. These findings identify ALDH9A1 as a key regulator of mitophagy and cisplatin resistance in LSCC, suggesting that targeting the ALDH9A1/PINK1 axis could provide a novel therapeutic strategy for overcoming cisplatin resistance.</p>","PeriodicalId":7969,"journal":{"name":"Anti-Cancer Drugs","volume":" ","pages":"366-375"},"PeriodicalIF":2.2,"publicationDate":"2026-07-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145817486","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Comparative study of the efficacy and safety of PSOX and SOX plus sintilimab regimens as first-line treatments for advanced gastric cancer.","authors":"Tao Zhang, Wenbin Yang, Chenguang Zhang, Kedi Wang, Hao Li","doi":"10.1097/CAD.0000000000001800","DOIUrl":"10.1097/CAD.0000000000001800","url":null,"abstract":"<p><p>Advanced gastric cancer (AGC) remains associated with poor survival despite advances in multimodal treatment. Recent trials suggest that adding programmed death-1 inhibitors to chemotherapy may improve outcomes in HER2-negative AGC, but real-world evidence-particularly in surgical settings-remains limited. This retrospective study evaluated the efficacy and safety of SOX plus sintilimab compared with P-SOX in patients with AGC undergoing perioperative chemotherapy followed by standard D2 gastrectomy. A total of 242 patients were included, of whom 161 received P-SOX and 81 received SOX plus sintilimab. Short-term response, long-term survival outcomes, and treatment-related adverse events were compared between groups. Prognostic factors for progression-free survival (PFS) were further analyzed in patients treated with SOX plus sintilimab. The SOX plus sintilimab regimen achieved superior short-term efficacy, with higher objective response rates by the Response Evaluation Criteria in Solid Tumors (RECIST) version 1.1 (70.4% vs. 47.2%) and higher tumor regression grades (91.4% vs. 72.7%) compared with P-SOX (both P < 0.001). Median overall survival was significantly longer in the SOX plus sintilimab group (32.0 vs. 29.0 months; HR = 0.617, P  = 0.006), while PFS showed a borderline improvement. Treatment-related adverse events were mostly grade 1-2, with comparable rates of severe toxicities between groups; immune-related events were infrequent. Poor perioperative treatment response, larger tumor size, poor differentiation, and advanced stage were independently associated with worse PFS. In conclusion, SOX plus sintilimab offers improved efficacy with acceptable safety compared with P-SOX, providing supportive real-world evidence for its use in AGC.</p>","PeriodicalId":7969,"journal":{"name":"Anti-Cancer Drugs","volume":" ","pages":"376-385"},"PeriodicalIF":2.0,"publicationDate":"2026-07-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC13148506/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145916726","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Dual checkpoint inhibition achieves successful treatment of diffuse bilateral lung metastasis in giant advanced liver cancer: a case report.","authors":"Ting-Ting Xie, Wang Chen, Zi-Han Zeng, Ji-Hang Luo, Yan Wang, Xiao-Min Peng, Ming-Dong Lin, Jian Song, Meng Xu, Yin Li","doi":"10.1097/CAD.0000000000001796","DOIUrl":"10.1097/CAD.0000000000001796","url":null,"abstract":"<p><p>Advanced hepatocellular carcinoma (HCC) with extensive metastases is associated with a poor prognosis, highlighting the need for individualized, multimodal treatment strategies. We present the case of a 54-year-old male with advanced HCC (cT3NxM1, Child-Pugh B) and spinal as well as bilateral pulmonary metastases who experienced disease progression after multiple lines of therapy. A dynamically adjusted, multidisciplinary regimen was implemented, incorporating transarterial chemoembolization (TACE), surgery, immunotherapy, and targeted therapy. The final regimen - combining nivolumab plus ipilimumab (O+Y) with TACE and lenvatinib - achieved a partial response in lung metastases, with a progression-free survival exceeding one year and overall survival of over 24 months. This case underscores the therapeutic potential of O+Y in later-line settings and demonstrates the clinical value of an integrated, personalized treatment paradigm for advanced HCC.</p>","PeriodicalId":7969,"journal":{"name":"Anti-Cancer Drugs","volume":" ","pages":"401-406"},"PeriodicalIF":2.0,"publicationDate":"2026-07-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"146058890","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}