Cancer letters最新文献

{"title":"Immune checkpoint inhibitors rechallenge in non-small cell lung cancer: Current evidence and future directions","authors":"Xiaoyu Gang ,&nbsp;Jinshan Yan ,&nbsp;Xin Li ,&nbsp;Sha Shi ,&nbsp;Lu Xu ,&nbsp;Ruotong Liu ,&nbsp;Lutong Cai ,&nbsp;Heming Li ,&nbsp;Mingfang Zhao","doi":"10.1016/j.canlet.2024.217241","DOIUrl":"10.1016/j.canlet.2024.217241","url":null,"abstract":"<div><p>Immunotherapy, remarkably immune checkpoint inhibitors (ICIs), has significantly altered the treatment landscape for non-small cell lung cancer (NSCLC). Despite their success, the discontinuation of ICIs therapy may occur due to factors such as prior treatment completion, disease progression during ICIs treatment, or immune-related adverse events (irAEs). As numerous studies highlight the dynamic nature of immune responses and the sustained benefits of ICIs, ICIs rechallenge has become an attractive and feasible option. However, the decision-making process for ICIs rechallenge in clinical settings is complicated by numerous uncertainties. This review systematically analyses existing clinical research evidence, classifying ICIs rechallenge into distinct clinical scenarios, exploring methods to overcome ICIs resistance in rechallenge instances, and identifying biomarkers to select patients likely to benefit from rechallenge. By integrating recent studies and new technologies, we offer crucial recommendations for future clinical trial design and provide a practical guideline to maximize the therapeutic benefits of immunotherapy for NSCLC patients.</p></div>","PeriodicalId":9506,"journal":{"name":"Cancer letters","volume":"604 ","pages":"Article 217241"},"PeriodicalIF":9.1,"publicationDate":"2024-09-10","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.sciencedirect.com/science/article/pii/S0304383524006360/pdfft?md5=53c7e40945c977bb341fe976ce574e11&pid=1-s2.0-S0304383524006360-main.pdf","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142230168","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":1,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Bcl-xL is translocated to the nucleus via CtBP2 to epigenetically promote metastasis","authors":"Tiantian Zhang ,&nbsp;Sha Li ,&nbsp;Yingcai Adrian Tan ,&nbsp;Xiang Chen ,&nbsp;Cheryl Zhang ,&nbsp;Zhengming Chen ,&nbsp;Bikash Mishra ,&nbsp;Joseph HyungJoon Na ,&nbsp;Soyoung Choi ,&nbsp;Sandra J. Shin ,&nbsp;Priyadarshan Damle ,&nbsp;Kranthi Kumar Chougoni ,&nbsp;Steven R. Grossman ,&nbsp;Dunrui Wang ,&nbsp;Xuejun Jiang ,&nbsp;Yi Li ,&nbsp;Erika Hissong ,&nbsp;Yao-Tseng Chen ,&nbsp;Jenny Z. Xiang ,&nbsp;Yi-Chieh Nancy Du","doi":"10.1016/j.canlet.2024.217240","DOIUrl":"10.1016/j.canlet.2024.217240","url":null,"abstract":"<div><p>Nuclear Bcl-xL is found to promote cancer metastasis independently of its mitochondria-based anti-apoptotic activity. How Bcl-xL is translocated into the nucleus and how nuclear Bcl-xL regulates histone H3 trimethyl Lys4 (H3K4me3) modification have yet to be understood. Here, we report that C-terminal Binding Protein 2 (CtBP2) binds to Bcl-xL via its N-terminus and translocates Bcl-xL into the nucleus. Knockdown of CtBP2 by shRNA decreases the nuclear portion of Bcl-xL and reverses Bcl-xL-induced invasion and metastasis in mouse models. Furthermore, knockout of CtBP2 not only reduces the nuclear portion of Bcl-xL but also suppresses Bcl-xL transcription. The binding between Bcl-xL and CtBP2 is required for their interaction with MLL1, a histone H3K4 methyltransferase. Pharmacologic inhibition of the MLL1 enzymatic activity reverses Bcl-xL-induced H3K4me3 and TGFβ mRNA upregulation, as well as invasion. Moreover, the cleavage under targets and release using nuclease (CUT&amp;RUN) assay coupled with next-generation sequencing reveals that H3K4me3 modifications are particularly enriched in the promotor regions of genes encoding TGFβ and its signaling pathway members in cancer cells overexpressing Bcl-xL. Altogether, the metastatic function of Bcl-xL is mediated by its interaction with CtBP2 and MLL1 and this study offers new therapeutic strategies to treat Bcl-xL-overexpressing cancer.</p></div>","PeriodicalId":9506,"journal":{"name":"Cancer letters","volume":"604 ","pages":"Article 217240"},"PeriodicalIF":9.1,"publicationDate":"2024-09-10","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142232333","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":1,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Hepatic stellate cells promote hepatocellular carcinoma development by regulating histone lactylation: Novel insights from single-cell RNA sequencing and spatial transcriptomics analyses","authors":"Yifan Yu ,&nbsp;Yongnan Li ,&nbsp;Long Zhou ,&nbsp;Xiaoli Cheng ,&nbsp;Zheng Gong","doi":"10.1016/j.canlet.2024.217243","DOIUrl":"10.1016/j.canlet.2024.217243","url":null,"abstract":"<div><p>This study evaluated the cellular heterogeneity and molecular mechanisms of hepatocellular carcinoma (HCC). Single cell RNA sequencing (scRNA-seq), transcriptomic data, histone lactylation-related genes were collected from public databases. Cell-cell interaction, trajectory, pathway, and spatial transcriptome analyses were executed. Differential expression and survival analyses were conducted. Western blot, Real-time reverse transcription PCR (qRT-PCR), and Cell Counting Kit 8 (CCK8) assay were used to detect the expression of <em>αSMA</em>, <em>AKR1B10</em> and its target genes, and verify the roles of <em>AKR1B10</em> in HCC cells. Hepatic stellate cell (HSC) subgroups strongly interacted with tumor cell subgroups, and their spatial distribution was heterogeneous. Two candidate prognostic genes (<em>AKR1B10</em> and <em>RMRP</em>) were obtained. <em>LONP1</em>, <em>NPIPB3</em>, and <em>ZSWIM6</em> were determined as <em>AKR1B10</em> targets. Besides, the expression levels of AKR1B10 and αSMA were significantly increased in LX-2 + HepG2 and LX-2 + HuH7 groups compared to those in LX-2 group, respectively. sh-<em>AKR1B10</em> significantly inhibited the HCC cell proliferation and change the expression of <em>AKR1B10</em> target genes, Bcl-2, Bax, Pan Kla, and H3K18la at protein levels. Our findings unveil the pivotal role of HSCs in HCC pathogenesis through regulating histone lactylation.</p></div>","PeriodicalId":9506,"journal":{"name":"Cancer letters","volume":"604 ","pages":"Article 217243"},"PeriodicalIF":9.1,"publicationDate":"2024-09-10","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142230037","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":1,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"The role of Hippo/YAP1 in cancer-associated fibroblasts: Literature review and future perspectives","authors":"Dipti Athavale ,&nbsp;Curt Balch ,&nbsp;Yanting Zhang ,&nbsp;Xiaodan Yao ,&nbsp;Shumei Song","doi":"10.1016/j.canlet.2024.217244","DOIUrl":"10.1016/j.canlet.2024.217244","url":null,"abstract":"<div><p>Cancer-associated fibroblasts (CAFs) are activated fibroblasts that play a role in numerous malignant phenotypes, including hyperproliferation, invasion, and metastasis. These phenotypes correlate with activity of the Hippo pathway oncoprotein, Yes-associated protein-1 (YAP1), and its paralog, transcriptional coactivator with PDZ-binding motif (TAZ). YAP1/TAZ are normally involved in organ growth, under the regulation of various kinases and upon phosphorylation, are retained in the cytoplasm by chaperone proteins, leading to their proteasomal degradation. In CAFs and tumor cells, however, a lack of YAP1 phosphorylation results in its translocation to the nucleus, binding to TEAD transcription factors, and activation of mitogenic pathways. In this review we summarize the literature discussing the central role of YAP1 in CAF activation, the upstream cues that promote YAP1-mediated CAF activation and extracellular matrix remodeling, and how CAFs mediate tumor-stroma crosstalk to support progression, invasion and metastasis in various cancer models. We further highlight YAP1⁺CAFs functions in modulating an immunosuppressive tumor microenvironment and propose evaluation of several YAP1 targets regarding their role in regulating intra-tumoral immune landscapes. Finally, we propose that co-administration of YAP1- targeted therapies with immune checkpoint inhibitors can improve therapeutic outcomes in patients with advanced tumors.</p></div>","PeriodicalId":9506,"journal":{"name":"Cancer letters","volume":"604 ","pages":"Article 217244"},"PeriodicalIF":9.1,"publicationDate":"2024-09-10","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142171709","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":1,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"DNA repair status as a guide for pancreatic ductal adenocarcinoma treatment, an old view for a new future","authors":"Robert C.A.M. van Waardenburg","doi":"10.1016/j.canlet.2024.217222","DOIUrl":"10.1016/j.canlet.2024.217222","url":null,"abstract":"","PeriodicalId":9506,"journal":{"name":"Cancer letters","volume":"604 ","pages":"Article 217222"},"PeriodicalIF":9.1,"publicationDate":"2024-09-07","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142153176","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":1,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Combined inhibition of CDK4/6 and AKT is highly effective against the luminal androgen receptor (LAR) subtype of triple negative breast cancer","authors":"María Rosario Chica-Parrado ,&nbsp;Gun Min Kim ,&nbsp;Yasuaki Uemoto ,&nbsp;Fabiana Napolitano ,&nbsp;Chang-Ching Lin ,&nbsp;Dan Ye ,&nbsp;Emmanuel Bikorimana ,&nbsp;Yisheng Fang ,&nbsp;Kyung-min Lee ,&nbsp;Saurabh Mendiratta ,&nbsp;Ariella B. Hanker ,&nbsp;Carlos L. Arteaga","doi":"10.1016/j.canlet.2024.217219","DOIUrl":"10.1016/j.canlet.2024.217219","url":null,"abstract":"<div><p>Luminal Androgen Receptor (LAR) triple-negative breast cancers (TNBC) express androgen receptors (AR), exhibit high frequency of PIK3CA mutations and intact RB. Herein, we investigated combined blockade of the CDK4/6 and PI3K signaling with palbociclib, alpelisib, and capivasertib, which inhibit CDK4/6, PI3Kα, and AKT1-3, respectively. The combination of palbociclib/capivasertib, but not palbociclib/alpelisib, synergistically inhibited proliferation of MDA-MB-453 and MFM-223 LAR cells [synergy score 7.34 (p = 5.81x10⁻¹¹) and 4.78 (p = 0.012), respectively]. The AR antagonist enzalutamide was inactive against MDA-MB-453, MFM-223, and CAL148 cells and did not enhance the efficacy of either combination. Palbociclib/capivasertib inhibited growth of LAR patient-derived xenografts more potently than palbociclib/alpelisib. Treatment of LAR cells with palbociclib suppressed phosphorylated-RB and resulted in adaptive phosphorylation/activation of S473 pAKT and AKT substrates GSK3β, PRAS40, and FoxO3a. Capivasertib blocked palbociclib-induced phosphorylation of AKT substrates more potently than alpelisib. Treatment with PI3Kβ inhibitors did not block phosphorylation of AKT substrates, suggesting that PI3Kβ did not mediate the adaptive response to CDK4/6 inhibition. Phosphokinase arrays of MDA-MB-453 cells treated with palbociclib showed time-dependent upregulation of PDGFRβ, GSK3β, STAT3, and STAT6. RNA silencing of PDGFRβ in palbociclib-treated MDA-MB-453 and MFM-223 cells blocked the upregulation of S473 pAKT, suggesting that the adaptive response to CDK4/6 blockade involves PDGFRβ signaling. Finally, treatment with palbociclib and the PDGFR inhibitor CP637451 arrested growth of MDA-MB-453 and MFM-223 cells to the same degree as palbociclib/capivasertib. These findings support testing the combination of CDK4/6 and AKT inhibitors in patients with LAR TNBC, and further investigation of PDGFR antagonists in this breast cancer subtype.</p></div>","PeriodicalId":9506,"journal":{"name":"Cancer letters","volume":"604 ","pages":"Article 217219"},"PeriodicalIF":9.1,"publicationDate":"2024-09-06","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.sciencedirect.com/science/article/pii/S0304383524006141/pdfft?md5=eced4d48c3e1e987fecdf3f21045f06b&pid=1-s2.0-S0304383524006141-main.pdf","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142145259","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":1,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Increasing membrane polyunsaturated fatty acids sensitizes non-small cell lung cancer to anti-PD-1/PD-L1 immunotherapy","authors":"Sofia La Vecchia ,&nbsp;Simona Fontana ,&nbsp;Iris Chiara Salaroglio ,&nbsp;Dario Pasquale Anobile ,&nbsp;Sabrina Digiovanni ,&nbsp;Muhlis Akman ,&nbsp;Niloufar Jafari ,&nbsp;Martina Godel ,&nbsp;Costanzo Costamagna ,&nbsp;Cyril Corbet ,&nbsp;Joanna Kopecka ,&nbsp;Chiara Riganti","doi":"10.1016/j.canlet.2024.217221","DOIUrl":"10.1016/j.canlet.2024.217221","url":null,"abstract":"<div><p>Immune checkpoints inhibitors (ICIs) as anti-PD-1/anti-PD-L1 have been approved as first-line treatment in patients with non-small cell lung cancer (NSCLC), but only 25 % of patients achieve durable response. We previously unveiled that estrogen receptor α transcriptionally up-regulates PD-L1 and aromatase inhibitors such as letrozole increase the efficacy of pembrolizumab. Here we investigated if letrozole may have additional immune-sensitizing mechanisms. We found that higher the level of PD-L1 in NSCLC, higher the activation of SREBP1c that transcriptionally increases fatty acid synthase and stearoyl-CoA desaturase enzymes, increasing the amount of polyunsaturated fatty acids (PUFAs). Letrozole further up-regulated SREBP1c-mediated transcription of lipogenic genes, and increased the amount of PUFAs, thereby leading to greater membrane fluidity and reduced binding between PD-L1 and PD-1. The same effects were observed upon supplementation with ω3-PUFA docosahexaenoic acid (DHA) that enhanced the efficacy of pembrolizumab in humanized NSCLC immune-xenografts. We suggest that PUFA enrichment in membrane phospholipids improves the efficacy of ICIs. We propose to repurpose letrozole or DHA as new immune-sensitizing agents in NSCLC.</p></div>","PeriodicalId":9506,"journal":{"name":"Cancer letters","volume":"604 ","pages":"Article 217221"},"PeriodicalIF":9.1,"publicationDate":"2024-09-06","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.sciencedirect.com/science/article/pii/S0304383524006165/pdfft?md5=670af3b5b5c9eb0194223861db9cd4d2&pid=1-s2.0-S0304383524006165-main.pdf","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142153177","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":1,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Evaluation of a new scoring system for assessing nerve invasion in resected pancreatic cancer: A single-center retrospective analysis","authors":"Rong Hua ,&nbsp;Hong-Fei Yao ,&nbsp;Zi-Yu Song ,&nbsp;Feng Yu ,&nbsp;Zhao-Yu Che ,&nbsp;Xiao-Fang Gao ,&nbsp;Yan-Miao Huo ,&nbsp;Wei Liu ,&nbsp;Yong-Wei Sun ,&nbsp;Min-Wei Yang ,&nbsp;Jian-Yu Yang ,&nbsp;Shan Zhang ,&nbsp;Jun-Feng Zhang","doi":"10.1016/j.canlet.2024.217213","DOIUrl":"10.1016/j.canlet.2024.217213","url":null,"abstract":"<div><p>Nerve invasion (NI) is a characteristic feature of pancreatic cancer. Traditional dichotomous statements on the presence of NI are unreasonable because almost all cases exhibit NI when sufficient pathological sections are examined. The critical implications of NI in pancreatic cancer highlight the need for a more effective criterion. This study included 511 patients, who were categorized into a training group and a testing group at a ratio of 7:3. According to the traditional definition, NI was observed in 91.2 % of patients using five pathological slides in our study. The prevalence of NI increased as more pathological slides were used. The criterion of ‘two points of intraneural (endoneural) invasion in the case of four pathological slides’ has the highest receiver operating characteristic (ROC) score. Based on this new criterion, NI was proved to be an independent prognostic factor for overall survival (OS) and disease-free survival (DFS) and was also correlated with tumor recurrence (<em>P</em> = 0.004). Interestingly, gemcitabine-based chemotherapy regimen is an independent favorable factor for patients with high NI. In the high NI group, patients who received a gemcitabine-based regimen exhibited a better prognosis than those who did not receive the gemcitabine-based regimen for OS (<em>P</em> = 0.000) and DFS (<em>P</em> = 0.001). In conclusion, this study establishes assessment criteria to evaluate the severity of NI in order to predict patient outcomes.</p></div>","PeriodicalId":9506,"journal":{"name":"Cancer letters","volume":"603 ","pages":"Article 217213"},"PeriodicalIF":9.1,"publicationDate":"2024-09-05","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142145270","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":1,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"MIG6 loss increased RET inhibitor tolerant persister cells in RET-rearranged non-small cell lung cancer","authors":"Xinzhao Wei ,&nbsp;Ken Uchibori ,&nbsp;Nobuyuki Kondo ,&nbsp;Takahiro Utsumi ,&nbsp;Ai Takemoto ,&nbsp;Sumie Koike ,&nbsp;Satoshi Takagi ,&nbsp;Noriko Yanagitani ,&nbsp;Makoto Nishio ,&nbsp;Ryohei Katayama","doi":"10.1016/j.canlet.2024.217220","DOIUrl":"10.1016/j.canlet.2024.217220","url":null,"abstract":"<div><p>Recently approved RET tyrosine kinase inhibitors (TKIs) have shown promising therapeutic effects against RET-rearranged non-small cell lung cancer (NSCLC) or RET-mutated thyroid cancer. However, resistance develops, limiting long-term efficacy. Although many RET-TKI resistance mechanisms, such as secondary mutations in RET or activation of bypass pathways, are known, some primary or acquired resistance mechanisms are unclear. Here, human genome-wide CRISPR/Cas9 screening was performed to identify genes related to drug-tolerant persister cells. Patient-derived cells with RET-fusion were introduced genome-wide sgRNA library and treated with RET-TKI for 9 days, resulting in the discovery of several candidate genes. Knockout of MED12 or MIG6 significantly increased residual drug-tolerant persister cells under RET-TKI treatment. MIG6 loss induced significant EGFR activation even with low concentrations of EGFR ligands and led to resistance to RET-TKIs. EGFR inhibition with afatinib or cetuximab in combination with RET TKIs was effective in addressing drug persistence. By contrast, a KIF5B-RET positive cells established from a RET-rearranged NSCLC patient, showed significant resistance to RET-TKIs and high dependence on EGFR bypass signaling. Consistently, knocking out EGFR or RET led to high sensitivity to RET or EGFR inhibitor respectively. Here, we have provided a comprehensive analysis of adaptive and acquired resistance against RET-rearranged NSCLC.</p></div>","PeriodicalId":9506,"journal":{"name":"Cancer letters","volume":"604 ","pages":"Article 217220"},"PeriodicalIF":9.1,"publicationDate":"2024-09-05","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142145271","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":1,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Is tumor microenvironment important for targeted therapy in lung cancer?","authors":"Shi-Yong Sun","doi":"10.1016/j.canlet.2024.217203","DOIUrl":"10.1016/j.canlet.2024.217203","url":null,"abstract":"","PeriodicalId":9506,"journal":{"name":"Cancer letters","volume":"604 ","pages":"Article 217203"},"PeriodicalIF":9.1,"publicationDate":"2024-09-03","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142139389","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":1,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}