Anti-Cancer Drugs最新文献

{"title":"9-Hexadecenoic acid inhibits the aggressiveness of gastric cancer via targeting PTPN1/FTH1 signaling.","authors":"Xin Wang, Haiyan Peng","doi":"10.1097/CAD.0000000000001724","DOIUrl":"https://doi.org/10.1097/CAD.0000000000001724","url":null,"abstract":"<p><p>9-Hexadecenoic acid (9-HA) possesses anti-tumor properties. However, the effects of 9-HA on gastric cancer are scarcely reported. The present study aimed to investigate the effects of 9-HA on gastric cancer. mRNA levels were detected by reverse transcription quantitative PCR. Protein expression was detected by western blot. Cell behaviors were analyzed using Cell Counting Kit-8, colony formation, transwell, and propidium iodide staining assays. Co-localization of PTPN1 and FTH1 was determined using fluorescence in situ hybridization assay. In vivo assay was conducted to further verify the effects of 9-HA on gastric cancer. 9-HA suppressed the malignant behavior of gastric cancer. Moreover, 9-HA promoted iron-overload-dependent ferroptosis of gastric cancer in vivo and in vitro. Traditional Chinese medicine systems pharmacology predicted that 9-HA could target PTPN1, which was upregulated in gastric cancer cells. PTPN1-mediated phosphorylation of FTH1 contributed to the latter degradation. Overexpressed PTPN1 alleviated the effects of 9-HA, promoting the aggressiveness of gastric cancer and suppressing tumor cell ferroptosis. Interestingly, overexpressed PTPN1 antagonized the effects of 9-HA, promoted tumor growth, and inhibited the ferroptosis of gastric cancer. In summary, 9-HA-mediated downregulation of PTPN1 drives ferroptosis and inhibit the aggressiveness of gastric cancer. Thence, 9-HA may be an alternative strategy for gastric cancer.</p>","PeriodicalId":7969,"journal":{"name":"Anti-Cancer Drugs","volume":" ","pages":""},"PeriodicalIF":1.8,"publicationDate":"2025-04-18","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143963184","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":"Complete regression of choroidal metastases from renal cancer under sunitinib with grade 3 hyperbilirubinemia.","authors":"Wala Ben Kridis, Raafat Ben Lassoued, Amira Trigui, Afef Khanfir","doi":"10.1097/CAD.0000000000001720","DOIUrl":"https://doi.org/10.1097/CAD.0000000000001720","url":null,"abstract":"<p><p>Sunitinib is a small molecule tyrosine kinase inhibitor that is taken by mouth. It works against several kinases, such as vascular endothelial growth factor receptor, c-Kit, and platelet-derived growth factor receptor. We report a case of total disappearance of choroid metastases from renal cell carcinoma after 6 months of sunitinib, with grade 3 hyperbilirubinemia.</p>","PeriodicalId":7969,"journal":{"name":"Anti-Cancer Drugs","volume":" ","pages":""},"PeriodicalIF":1.8,"publicationDate":"2025-04-18","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143963012","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 fatty acid metabolism-related gene signature can predict poor prognosis in glioma.","authors":"Chuanyu Li, Xinran Xue, Jiahui Kong, Jianjun Zhang","doi":"10.1097/CAD.0000000000001719","DOIUrl":"https://doi.org/10.1097/CAD.0000000000001719","url":null,"abstract":"<p><p>Gliomas, arising from supportive glial cells in the central nervous system, present significant challenges in oncology due to their varying aggressiveness and poor prognosis, particularly in high-grade forms. Understanding the molecular pathways involved in glioma progression is essential for developing effective treatment strategies. This study aimed to develop a fatty acid metabolism (FAM)-related gene signature to better predict poor prognosis in glioma patients, thereby facilitating more targeted therapeutic approaches. We employed the Least Absolute Shrinkage and Selection Operator regression analysis to identify a gene signature associated with FAM from The Cancer Genome Atlas and Chinese Glioma Genome Atlas RNA-seq datasets. Survival analyses, including Kaplan-Meier and Cox regression analyses, were conducted to assess the prognostic value of the identified genes. A total of seven FAM-related genes were associated with survival outcomes in isocitrate dehydrogenase-1 wild-type glioblastoma. The constructed gene signature effectively stratified patients into high-risk and low-risk groups, with high-risk patients demonstrating significantly poorer survival. PTGR1 emerged as the core gene, closely linked to malignant progression and poor prognosis. The FAM-related gene signature developed in this study provides a reliable tool for predicting poor outcomes in glioma patients. PTGR1, identified as a pivotal gene within this signature, may serve as a potential target for future therapeutic interventions, offering promising avenues for enhancing patient survival.</p>","PeriodicalId":7969,"journal":{"name":"Anti-Cancer Drugs","volume":" ","pages":""},"PeriodicalIF":1.8,"publicationDate":"2025-04-18","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143974314","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":"Enhanced plasma and brain concentrations and medulloblastoma cytotoxicity of asciminib and nilotinib by P-glycoprotein inhibition with tariquidar.","authors":"Eric M Thompson, Lin Cheng, Ivan Spasojevic","doi":"10.1097/CAD.0000000000001728","DOIUrl":"https://doi.org/10.1097/CAD.0000000000001728","url":null,"abstract":"<p><p>ABL1 and ABL2 are putative drivers of medulloblastoma leptomeningeal dissemination. ABL1/ABL2 inhibitors, nilotinib and asciminib, are P-glycoprotein substrates. The purpose of this work is to elucidate P-glycoprotein expression in the brain/brain tumors and to determine if P-glycoprotein inhibition increases plasma and brain concentrations and medulloblastoma cytotoxicity of nilotinib and asciminib. ABCB1 (P-glycoprotein) mRNA expression was analyzed from multiple datasets of brain and brain tumor specimens. Cytotoxicity assays of medulloblastoma cells were conducted. In a mouse model, the pharmacokinetics of asciminib and nilotinib, with and without tariquidar, were determined using LC/MS. ABCB1 mRNA expression varied by brain region and was significantly lower in the cerebellum (P < 0.05). There was a bimodal increase in brain ABCB1 expression at ages 0-3 and 21-23 (P < 0.05). ABCB1 expression in pediatric brain tumors was similar to normal brain. The addition of tariquidar significantly reduced medulloblastoma cell viability compared to asciminib alone (P < 0.01). Tariquidar increased asciminib plasma and brain concentrations at 24 h (P = 0.0005 and P = 0.0002, respectively) and nilotinib brain concentrations at 3 h (P = 0.0009). Tariquidar increased the area under the curve (AUC) brain : plasma ratio of asciminib from 0.33 to 10.16% and of nilotinib from 1.16 to 9.61%. Tariquidar prolonged the plasma half-life of asciminib from 2.21 to 10.49 h and nilotinib from 7.63 to 14.64 h. P-glycoprotein inhibition increased the brain concentrations, AUC, and half-life of asciminib and nilotinib and increased cytotoxicity in medulloblastoma cells.</p>","PeriodicalId":7969,"journal":{"name":"Anti-Cancer Drugs","volume":" ","pages":""},"PeriodicalIF":1.8,"publicationDate":"2025-04-18","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143960422","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 effectiveness of sequential afatinib and furmonertinib in an advanced lung adenocarcinoma with rare compound EGFR mutation (L833V/H835L).","authors":"Yanqing Pan, Lingxin Yan, Yongyao Gu, Shaoxi Wang, Huiling Li, Pengli Yu, Quanfang Chen","doi":"10.1097/CAD.0000000000001692","DOIUrl":"10.1097/CAD.0000000000001692","url":null,"abstract":"<p><p>Uncommon atypical mutations account for 10-15% of all epidermal growth factor receptor (EGFR) activating mutations in nonsmall-cell lung cancer (NSCLC). Tumors harboring rare EGFR mutations show highly heterogeneous responses to EGFR tyrosine kinase inhibitors (TKIs). There is insufficient clinical evidence for uncommon types of EGFR mutations, especially those with compound EGFR mutations. In addition, for those with uncommon compound EGFR mutations, few studies have focused on acquired resistance mechanisms and subsequent treatment strategies after disease progression on EGFR-TKIs. Here, a 66-year-old smoking male was diagnosed with lung adenocarcinoma accompanied by pleural metastasis. A rare L833V/H835L compound mutation in exon 21 of EGFR was detected in tumor biopsy by next-generation sequencing. Afatinib was used as first-line therapy and showed favorable efficacy. The patient continued afatinib treatment for a duration of 24 months. A new T790M mutation was detected with a rebiopsy after progression on afatinib. Then the patient received cryoablation therapy and a third-generation EGFR-TKI, furmonertinib. Our case suggests that a comprehensive screening for EGFR mutations should be conducted before and during treatment in clinical practice, and afatinib and furmonertinib could be first- and second-line treatment options in NSCLC patients harboring EGFR L833V/H835L mutations.</p>","PeriodicalId":7969,"journal":{"name":"Anti-Cancer Drugs","volume":" ","pages":"355-358"},"PeriodicalIF":1.8,"publicationDate":"2025-04-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143021879","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":"Real-life data on adjuvant trastuzumab emtansine treatment in early-stage HER2-positive breast cancer: a Turkish Oncology Group study.","authors":"Selin Akturk Esen, Ismet Seven, Gonca Akdere Ates, Rumeysa Colak, Oğuzcan Kinikoglu, Busra Akay Hacan, Yasemin Bakkal Temi, Nadiye Sever, Seda Kahraman, Haci Arak, Atakan Topcu, Seray Saray, Sinem Akbas, İsmail Beypinar, Omer Acar, Atike Pinar Erdoğan, Mesut Yilmaz, Deniz Isik, Ozturk Ates, Devrim Cabuk, Mehmet Ali Nahit Sendur, Dogan Uncu","doi":"10.1097/CAD.0000000000001717","DOIUrl":"https://doi.org/10.1097/CAD.0000000000001717","url":null,"abstract":"<p><p>In this Turkish Oncology Group study, we aimed to evaluate the effectiveness of trastuzumab emtansine (TDM1) in the adjuvant treatment of early-stage human epidermal growth factor receptor-2 (HER2)-positive breast cancer with residual disease using real-life data. A total of 13 Turkish centers participated in the study between September 2019 and October 2024. Patients with early-stage HER2-positive breast cancer who underwent surgery after completing neoadjuvant chemotherapy with HER2-targeted therapies had residual invasive disease in the breast or axillary lymph nodes and received adjuvant TDM1 therapy. The patients' files were retrospectively scanned from the hospitals' archives. The study included 79 female patients. The 36-month median disease-free survival rate was 92%, and the 36-month median overall survival rate was 85%. Neoadjuvant anthracyclines were administered to 93.6% of the patients. All patients received neoadjuvant trastuzumab and 86.1% of patients received neoadjuvant pertuzumab in addition to trastuzumab. Twelve (15.2%) patients developed progression during or after adjuvant TDM1 therapy. The most common adverse events were grade 1 fatigue (34.2%), grade 1 anemia (27.8%), and grade 1 AST increase (25.3%). Toxicity of grade 3 or above developed in five (5%) patients. TDM1 was stopped for one patient due to thrombocytopenia and for two patients due to cardiotoxicity. This study describes the sociodemographic and clinicopathological characteristics of patients with early-stage HER2-positive breast cancer with residual disease after neoadjuvant therapy and provides real-life data on treatment with adjuvant TDM1. The findings support the manageable safety profile of the adjuvant TDM1 regimen with a low discontinuation rate.</p>","PeriodicalId":7969,"journal":{"name":"Anti-Cancer Drugs","volume":" ","pages":""},"PeriodicalIF":1.8,"publicationDate":"2025-04-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143750783","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":"circ_0006528 promotes nonsmall cell lung cancer progression by sponging miR-892a and regulating NRAS expression.","authors":"Weixi Guo, Hongming Liu, Ming Zhong, Qinghua Qi, Yibin Li","doi":"10.1097/CAD.0000000000001439","DOIUrl":"10.1097/CAD.0000000000001439","url":null,"abstract":"<p><p>Micro-RNAs play essential roles in developing and progressing nonsmall cell lung cancer (NSCLC) and drug resistance. Nevertheless, the functions and mechanisms are partly explored. Therefore, the present study analyzes the effect of circ_0006528 and the mechanism of regulation of NSCLC cell progression by sponging miR-892a to regulate neuroblastoma rat sarcoma viral oncogene (NRAS) expression. Initially, circ_0006528 is identified using divergent primers-based PCR and RNase R exonuclease treatments. After administration of the designed circ_0006528-specific siRNA, the RT-qPCR analysis is used to determine the interference efficiency of siRNA. At the same time, cell growth, invasion, and migration are assessed by 3-[4,5-dimethylthiazol-2-yl]-2,5 diphenyl tetrazolium bromide (MTT), Transwell, and scratch assays in the NSCLC cell lines [secretory pathway Ca2+-ATPase isoform 1 (SPCA-1) and A549] in vitro, respectively. Further, miR-892a inhibitor is added to the cells for functional recovery assay. Finally, the xenograft mouse model is constructed to explore the effect of circ_0006528 on tumor growth in vivo . The RT-qPCR analysis in 66 pairs of NSCLC cancer and noncancerous tissues revealed that circ_0006528 is highly expressed in NSCLC patient tissues. The RNase R experiments revealed that HSA_circ_0006528 is unaffected by RNase R exonuclease. MTT assay showed that knockdown of hsa_circ_0006528 by siRNA significantly decreased cell proliferation and viability in A549 and SPCA-1 cells. The luciferase reporter assay showed direct binding of hsa_circ_0006528 to miR-892a, and miR-892a targets binding NRAS. In addition, the miR-892a inhibitor terminated the hsa_circ_0006528 siRNA, triggering inhibition of proliferation, invasion, and migration of NSCLC cells. In summary, the study revealed that the knockout of hsa_circ_0006528 downregulation of NRAS expression by sponging miR-892a inhibited NSCLC cell growth and invasion.</p>","PeriodicalId":7969,"journal":{"name":"Anti-Cancer Drugs","volume":" ","pages":"261-270"},"PeriodicalIF":1.8,"publicationDate":"2025-04-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"138045992","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":"FSP1 expression as a predictor of platinum resistance and recurrence in epithelial ovarian cancer.","authors":"Hang Xing, Hai-Ning Bi, Qi Yin, Ji Zhang, Xue Zhang, Yao-Jiao Li, Xue-Mei Gong, Ji-Fang Shi","doi":"10.1097/CAD.0000000000001676","DOIUrl":"10.1097/CAD.0000000000001676","url":null,"abstract":"<p><p>The objective of this study is to assess the differential expression of ferroptosis suppressor protein 1 (FSP1) in relation to clinical features, platinum resistance, and recurrence in epithelial ovarian cancer (EOC). In addition, the potential significance of FSP1 in EOC as a predictor of platinum resistance and recurrence in EOC was explored. Patients with pathologically confirmed EOC who underwent surgical treatment were included in this analysis. Immunohistochemistry was employed to evaluate FSP1 expression in ovarian tissues, with quantitative analysis performed on the samples. Clinical data were collected during follow-up, and patients were categorized according to platinum resistance and recurrence criteria. Statistical analysis was conducted using SPSS version 27.0. A total of 40 tissue samples from patients with EOC were analyzed, along with 21 samples from benign ovarian tumors and 20 samples from normal ovarian tissues. The expression of FSP1 was significantly higher in the EOC group compared to both benign and normal tissue groups. Meanwhile, the expressions of FSP1 were higher in groups with clinically advanced stages, high-grade carcinoma, presence of cancerous ascites, lymph node metastasis, and in the clear cell EOC group, compared to those with clinically early stages, low-grade carcinoma, absence of cancerous ascites, no lymph node metastasis, and other pathological subtypes. A positive linear correlation was identified between FSP1 expression in EOC tissues and serum levels of CA125 and human epididymis protein 4 at the time of diagnosis. The elevated expression of FSP1 is positively correlated with serum CA125 and human epididymis protein 4 levels at the time of diagnosis, which is a risk factor for EOC drug resistance and recurrence. These findings suggest that FSP1 may serve as a valuable biomarker for predicting platinum resistance and recurrence in patients with EOC.</p>","PeriodicalId":7969,"journal":{"name":"Anti-Cancer Drugs","volume":" ","pages":"338-346"},"PeriodicalIF":1.8,"publicationDate":"2025-04-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143381579","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":"Clinical efficacy of pyrotinib combined with chemotherapy for neoadjuvant treatment in HER2-positive breast cancer: a single-center study.","authors":"Benkai Wei, Huanhuan Yan, Fan Li, Jun Shen","doi":"10.1097/CAD.0000000000001690","DOIUrl":"10.1097/CAD.0000000000001690","url":null,"abstract":"<p><p>This study aimed to evaluate the efficacy of pyrotinib, an orally administered small molecule tyrosine kinase inhibitor, combined with neoadjuvant chemotherapy in treating patients with human epidermal growth factor receptor 2 (HER2)-positive breast cancer. Pyrotinib works by inhibiting the HER2 signaling pathway, thereby preventing tumor cell growth. This single-arm clinical trial aimed to assess the total pathological complete response (tpCR; ypT0/is and ypN0) rate as the primary endpoint. A total of 27 patients were enrolled, each receiving 4-8 cycles of pyrotinib in combination with neoadjuvant chemotherapy. Pyrotinib combined with neoadjuvant chemotherapy demonstrated notable antitumor activity in patients with HER2-positive breast cancer. Among 26 patients, the tpCR rate was 26% (7/26), while the breast pathological complete response rate was 30% (8/26), indicating complete inhibition of the primary tumor in some cases. Notably, patients with HR-negative breast cancer demonstrated a higher tpCR rate compared with those with HR-positive breast cancer. The treatment regimen was well-tolerated. Diarrhea was the most common adverse event, occurring in 92.3% of patients, with 46.2% experiencing grade 3 or higher diarrhea. No severe adverse events or treatment-related fatalities were reported.</p>","PeriodicalId":7969,"journal":{"name":"Anti-Cancer Drugs","volume":" ","pages":"347-354"},"PeriodicalIF":1.8,"publicationDate":"2025-04-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142982537","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":"Preclinical evidence that fibroblast growth factor receptor pathway inhibition by BGJ398 enhances small cell lung cancer response to chemotherapy.","authors":"Yingying Shen, Yan Jiang, Junyao Wu, Chenyu Wang, Jiao Bo Kun Huang, Jie Liu, Sen Chen","doi":"10.1097/CAD.0000000000001683","DOIUrl":"10.1097/CAD.0000000000001683","url":null,"abstract":"<p><p>Small cell lung cancer (SCLC) is a highly aggressive form of lung cancer with limited therapeutic options and poor prognosis. In this study, we explored the therapeutic potential of BGJ398, a selective fibroblast growth factor receptor (FGFR) inhibitor, alone and in combination with standard chemotherapy (cisplatin and paclitaxel) in SCLC. High-throughput screening of kinase inhibitors was performed on three SCLC cell lines (NCI-H446, NCI-H69, and NCI-H182), identifying BGJ398 as one of the most potent and selective inhibitors. BGJ398 demonstrated significant synergy with cisplatin and paclitaxel in vitro , as indicated by combination index values below 1. In vivo , combination treatments significantly inhibited tumor growth and extended survival in SCLC xenograft models compared to monotherapies. Notably, the combination of BGJ398 with cisplatin exhibited the most pronounced tumor suppression and survival benefits. Immunohistochemistry analysis confirmed that BGJ398 effectively inhibited FGFR signaling pathways, reducing levels of phosphorylated FGFR, protein kinase B, signal transducer and activator of transcription 3, and extracellular signal-regulated kinase. These findings suggest that BGJ398, particularly in combination with chemotherapy, holds significant promise as a treatment strategy for SCLC, providing enhanced anti-tumor efficacy and improved survival outcomes.</p>","PeriodicalId":7969,"journal":{"name":"Anti-Cancer Drugs","volume":" ","pages":"290-296"},"PeriodicalIF":1.8,"publicationDate":"2025-04-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142998840","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}