Pub Date : 2025-06-23DOI: 10.1016/j.cpt.2025.06.006
Yuankai Shi
{"title":"Lighting the path against cancer with academic light: Forty years of growth with the Chinese Medical Association—Celebrating the 110th anniversary of the founding of the Chinese Medical Association","authors":"Yuankai Shi","doi":"10.1016/j.cpt.2025.06.006","DOIUrl":"10.1016/j.cpt.2025.06.006","url":null,"abstract":"","PeriodicalId":93920,"journal":{"name":"Cancer pathogenesis and therapy","volume":"3 5","pages":"Pages 361-363"},"PeriodicalIF":2.8,"publicationDate":"2025-06-23","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144911697","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Pub Date : 2025-06-20DOI: 10.1016/j.cpt.2025.06.005
Maryam Muhammad Akram , Junaid Mehmood Malik , Muhammad Ahsan
{"title":"Re: Nomogram for predicting the risk and prognosis of lung metastasis of four subtypes of breast cancer: A population-based study from SEER","authors":"Maryam Muhammad Akram , Junaid Mehmood Malik , Muhammad Ahsan","doi":"10.1016/j.cpt.2025.06.005","DOIUrl":"10.1016/j.cpt.2025.06.005","url":null,"abstract":"","PeriodicalId":93920,"journal":{"name":"Cancer pathogenesis and therapy","volume":"3 5","pages":"Pages 448-450"},"PeriodicalIF":2.8,"publicationDate":"2025-06-20","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144913323","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Pub Date : 2025-06-14DOI: 10.1016/j.cpt.2025.06.004
Jenna N. Duttenhefner, Katie M. Reindl
The mevalonate pathway plays a crucial role in the metabolic reprogramming of pancreatic ductal adenocarcinoma (PDAC), driving lipid biosynthesis, redox homeostasis, and oncogenic signaling, thereby sustaining tumor progression and therapeutic resistance. Its integration with Kirsten rat sarcoma viral oncogene homolog (KRAS)-driven signaling networks establishes it as a cornerstone of PDAC biology and a promising therapeutic target. The products of the pathway (sterols and isoprenoids) support key processes such as membrane biogenesis, protein prenylation, and immune evasion, facilitating tumor adaptation to the harsh microenvironment. Despite extensive research, therapeutic resistance and metabolic plasticity present considerable challenges in targeting this pathway. This review synthesizes current knowledge regarding the biochemical regulation of the mevalonate pathway in PDAC, its crosstalk with key oncogenic signaling networks, and emerging therapeutic strategies. In addition, we highlight critical knowledge gaps, including the complex regulatory crosstalk of the pathway with oncogenes, tumor suppressors, and nutrient-sensing pathways, and the mechanisms by which metabolic rewiring modulates tumor–immune interactions and therapy resistance. By integrating insights from pre-clinical and clinical studies, we highlighted promising novel combination therapies, including statins, bisphosphonates, and sterol regulatory element-binding protein (SREBP) inhibitors, as well as the potential for precision medicine approaches targeting mevalonate pathway vulnerabilities. Addressing these challenges may provide new avenues for improving therapeutic outcomes in PDAC.
{"title":"Mevalonate pathway in pancreatic ductal adenocarcinoma: Mechanisms driving metabolic and cellular plasticity","authors":"Jenna N. Duttenhefner, Katie M. Reindl","doi":"10.1016/j.cpt.2025.06.004","DOIUrl":"10.1016/j.cpt.2025.06.004","url":null,"abstract":"<div><div>The mevalonate pathway plays a crucial role in the metabolic reprogramming of pancreatic ductal adenocarcinoma (PDAC), driving lipid biosynthesis, redox homeostasis, and oncogenic signaling, thereby sustaining tumor progression and therapeutic resistance. Its integration with Kirsten rat sarcoma viral oncogene homolog (<em>KRAS</em>)-driven signaling networks establishes it as a cornerstone of PDAC biology and a promising therapeutic target. The products of the pathway (sterols and isoprenoids) support key processes such as membrane biogenesis, protein prenylation, and immune evasion, facilitating tumor adaptation to the harsh microenvironment. Despite extensive research, therapeutic resistance and metabolic plasticity present considerable challenges in targeting this pathway. This review synthesizes current knowledge regarding the biochemical regulation of the mevalonate pathway in PDAC, its crosstalk with key oncogenic signaling networks, and emerging therapeutic strategies. In addition, we highlight critical knowledge gaps, including the complex regulatory crosstalk of the pathway with oncogenes, tumor suppressors, and nutrient-sensing pathways, and the mechanisms by which metabolic rewiring modulates tumor–immune interactions and therapy resistance. By integrating insights from pre-clinical and clinical studies, we highlighted promising novel combination therapies, including statins, bisphosphonates, and sterol regulatory element-binding protein (SREBP) inhibitors, as well as the potential for precision medicine approaches targeting mevalonate pathway vulnerabilities. Addressing these challenges may provide new avenues for improving therapeutic outcomes in PDAC.</div></div>","PeriodicalId":93920,"journal":{"name":"Cancer pathogenesis and therapy","volume":"4 2","pages":"Pages 110-123"},"PeriodicalIF":2.8,"publicationDate":"2025-06-14","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145885693","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Pub Date : 2025-06-10DOI: 10.1016/j.cpt.2025.06.003
Wei Guan , Ketao Wang , Yangliu Shao , Lei Zhou , Nan Wang , Wei Zhou , Maoquan Wang , Lili Wang , Yu Jing , Yonghui Li , Daihong Liu , Li Yu
Background
Fusion genes play a crucial role in the pathogenesis of acute myeloid leukemia (AML). This study investigated the utility of targeted next-generation sequencing (NGS) of RNA for detecting rare and unknown fusion genes in patients with AML.
Methods
A total of 85 adult AML samples previously identified as fusion gene-negative by multiplex nested reverse transcription-polymerase chain reaction (RT-PCR) were subjected to NGS analysis.
Results
Fusion genes were detected in 21 of 72 (29.2%) patients. Among the 26 primary refractory patients, 11 (42.3%) exhibited fusion genes, whereas among the 18 relapsed patients, fusion genes were identified in five (27.8%). Notably, KMT2A and NUP98 rearrangements were enriched in refractory/relapsed patients. Additionally, recurrent fusion transcripts involving EIF4A1 were observed. The identification of additional fusion genes resulted in an approximate 20.8% (11/53) reclassification of medium-risk karyotypes to the high-risk category, thereby enhancing diagnostic accuracy.
Conclusions
Targeted NGS may complement conventional methods for identifying novel fusions in refractory/relapsed AML; however, its prognostic utility requires verification in controlled trials.
{"title":"Insights into the biological features and improved diagnostics of adult acute myeloid leukemia via fusion genes identified through targeted next-generation sequencing","authors":"Wei Guan , Ketao Wang , Yangliu Shao , Lei Zhou , Nan Wang , Wei Zhou , Maoquan Wang , Lili Wang , Yu Jing , Yonghui Li , Daihong Liu , Li Yu","doi":"10.1016/j.cpt.2025.06.003","DOIUrl":"10.1016/j.cpt.2025.06.003","url":null,"abstract":"<div><h3>Background</h3><div>Fusion genes play a crucial role in the pathogenesis of acute myeloid leukemia (AML). This study investigated the utility of targeted next-generation sequencing (NGS) of RNA for detecting rare and unknown fusion genes in patients with AML.</div></div><div><h3>Methods</h3><div>A total of 85 adult AML samples previously identified as fusion gene-negative by multiplex nested reverse transcription-polymerase chain reaction (RT-PCR) were subjected to NGS analysis.</div></div><div><h3>Results</h3><div>Fusion genes were detected in 21 of 72 (29.2%) patients. Among the 26 primary refractory patients, 11 (42.3%) exhibited fusion genes, whereas among the 18 relapsed patients, fusion genes were identified in five (27.8%). Notably, <em>KMT2A</em> and <em>NUP98</em> rearrangements were enriched in refractory/relapsed patients. Additionally, recurrent fusion transcripts involving <em>EIF4A1</em> were observed. The identification of additional fusion genes resulted in an approximate 20.8% (11/53) reclassification of medium-risk karyotypes to the high-risk category, thereby enhancing diagnostic accuracy.</div></div><div><h3>Conclusions</h3><div>Targeted NGS may complement conventional methods for identifying novel fusions in refractory/relapsed AML; however, its prognostic utility requires verification in controlled trials.</div></div>","PeriodicalId":93920,"journal":{"name":"Cancer pathogenesis and therapy","volume":"4 1","pages":"Pages 64-71"},"PeriodicalIF":2.8,"publicationDate":"2025-06-10","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145684406","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Pub Date : 2025-05-20DOI: 10.1016/j.cpt.2025.05.002
Xiaojing Liu , Cheng Liu , Yuting Jin , Jing Xu , Chunyan Xu , Wei Zhu
Background
Resting tumor-associated macrophages (TAMs) are stimulated by the tumor microenvironment and can be primarily polarized into two subtypes: M1-and M2-like. M1-like TAMs promote inflammation and eradicate tumor cells, whereas M2-like TAMs suppress inflammation and facilitate tumor development. However, the mechanisms underlying phenotypic switching in these macrophages remain unclear. Therefore, we aimed to characterize the gene expression profiles of M1-like and M2-like TAMs in pan cancers.
Methods
Three computational methods were used to estimate the infiltration score of TAMs in 9239 tumor samples across 31 solid cancer types, based on RNA sequencing databases. Tumor samples were divided into high- and low-score groups based on the median M1/M2 ratio. Furthermore, gene enrichment, protein interactions, and transcription factors were analyzed. Multiple pharmaco–omics profiles were used to identify potential drugs. Finally, binding between the compounds and drug targets was validated using molecular docking.
Results
Of the top 100 dysregulated genes in each cancer type, 70 and 82 genes with upregulated and downregulated expression, respectively, were consistently differentially expressed. We identified candidate drugs targeting protein phosphatase 2A (PP2A), a core protein. These included efaproxiral, hesperidin, ezetimibe, calcitriol, and linopirdine.
Conclusions
This study provides a pan-cancer characterization of the TAM polarization-related gene profile. Network pharmacology and molecular docking analyses revealed five promising therapeutic agents for TAM reprogramming. Thus, our findings provide valuable insights into the enhancement of immune responses to inhibit tumor immune escape and metastasis.
{"title":"Pan-cancer gene signature analysis of macrophage polarization and compound prediction for reprogramming tumor-associated macrophages toward M1-like macrophages","authors":"Xiaojing Liu , Cheng Liu , Yuting Jin , Jing Xu , Chunyan Xu , Wei Zhu","doi":"10.1016/j.cpt.2025.05.002","DOIUrl":"10.1016/j.cpt.2025.05.002","url":null,"abstract":"<div><h3>Background</h3><div>Resting tumor-associated macrophages (TAMs) are stimulated by the tumor microenvironment and can be primarily polarized into two subtypes: M1-and M2-like. M1-like TAMs promote inflammation and eradicate tumor cells, whereas M2-like TAMs suppress inflammation and facilitate tumor development. However, the mechanisms underlying phenotypic switching in these macrophages remain unclear. Therefore, we aimed to characterize the gene expression profiles of M1-like and M2-like TAMs in pan cancers.</div></div><div><h3>Methods</h3><div>Three computational methods were used to estimate the infiltration score of TAMs in 9239 tumor samples across 31 solid cancer types, based on RNA sequencing databases. Tumor samples were divided into high- and low-score groups based on the median M1/M2 ratio. Furthermore, gene enrichment, protein interactions, and transcription factors were analyzed. Multiple pharmaco–omics profiles were used to identify potential drugs. Finally, binding between the compounds and drug targets was validated using molecular docking.</div></div><div><h3>Results</h3><div>Of the top 100 dysregulated genes in each cancer type, 70 and 82 genes with upregulated and downregulated expression, respectively, were consistently differentially expressed. We identified candidate drugs targeting protein phosphatase 2A (PP2A), a core protein. These included efaproxiral, hesperidin, ezetimibe, calcitriol, and linopirdine.</div></div><div><h3>Conclusions</h3><div>This study provides a pan-cancer characterization of the TAM polarization-related gene profile. Network pharmacology and molecular docking analyses revealed five promising therapeutic agents for TAM reprogramming. Thus, our findings provide valuable insights into the enhancement of immune responses to inhibit tumor immune escape and metastasis.</div></div>","PeriodicalId":93920,"journal":{"name":"Cancer pathogenesis and therapy","volume":"4 2","pages":"Pages 136-144"},"PeriodicalIF":2.8,"publicationDate":"2025-05-20","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145927297","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Pub Date : 2025-05-19DOI: 10.1016/j.cpt.2025.05.003
Jinsong Liu , Liuliu Quan , Die Sang , Xiao Guan , Min Dou , Jian Yue , Peng Yuan
{"title":"Trastuzumab deruxtecan in advanced breast cancer patients with brain metastases or leptomeningeal metastases","authors":"Jinsong Liu , Liuliu Quan , Die Sang , Xiao Guan , Min Dou , Jian Yue , Peng Yuan","doi":"10.1016/j.cpt.2025.05.003","DOIUrl":"10.1016/j.cpt.2025.05.003","url":null,"abstract":"","PeriodicalId":93920,"journal":{"name":"Cancer pathogenesis and therapy","volume":"4 1","pages":"Pages 72-74"},"PeriodicalIF":2.8,"publicationDate":"2025-05-19","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145736167","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Pub Date : 2025-05-01DOI: 10.1016/j.cpt.2025.03.001
Gnanaprakash Jeyaraj
{"title":"Commentary on the “Relationship between visceral obesity and prognosis in patients with stage IVB cervical cancer receiving radiotherapy and chemotherapy”","authors":"Gnanaprakash Jeyaraj","doi":"10.1016/j.cpt.2025.03.001","DOIUrl":"10.1016/j.cpt.2025.03.001","url":null,"abstract":"","PeriodicalId":93920,"journal":{"name":"Cancer pathogenesis and therapy","volume":"3 3","pages":"Pages 269-270"},"PeriodicalIF":0.0,"publicationDate":"2025-05-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143887012","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Pub Date : 2025-05-01DOI: 10.1016/j.cpt.2024.09.006
Xingbin Hu , Wenhao Ouyang , Haizhu Chen , Zhihong Liu , Zijia Lai , Herui Yao
Background
Gastric cancer (GC) is a common malignancy characterized by the absence of reliable prognostic indicators and effective therapeutic targets. Claudin-9 (CLDN9) has been demonstrated to be upregulated in various cancers. However, its prognostic value, biological function, and regulatory mechanisms in GC remain unclear. Therefore, this study aimed to elucidate the role of CLDN9 in GC progression and its underlying mechanisms.
Methods
We utilized consensus cluster, random survival forest, and multivariate Cox regression analyses to identify CLDN9 in GC. Subsequently, we evaluated the mRNA and protein levels of CLDN9 in GC using quantitative real-time polymerase chain reaction (PCR) (qRT-PCR), Western blotting (WB), and immunohistochemistry (IHC). Furthermore, the role of CLDN9 in GC progression was investigated using a series of functional in vivo and in vitro experiments. Finally, we elucidated the molecular mechanisms of CLDN9 using bioinformatics, molecular biology, animal models, and patient tissue specimens.
Results
Two GC subtypes with survival and functional differences were identified based on glycolytic metabolic genes in the Cancer Genome Atlas (TCGA)- Stomach adenocarcinoma (STAD) dataset. A prognostic risk score was calculated using seven genes to assess the overall survival (OS) in GC. Using random survival forest and multivariate Cox analyses, we identified CLDN9 as the key gene linked to the glycolytic subtype and prognosis of GC. CLDN9 expression was significantly upregulated in patients with GC as well as in GC cells. CLDN9 knockdown inhibited tumor proliferation, invasion, and metastasis both in vivo and in vitro. Mechanistically, CLDN9 was found to regulate lactate dehydrogenase A (LDHA) expression and promote glycolytic metabolism by activating the phosphatidylinositol 3-kinase (PI3K)/protein kinase B (AKT)/hypoxia-inducible factor 1-alpha (HIF1α) signaling pathway. Additionally, lactate, a glycolytic metabolite, enhanced programmed cell death ligand 1 (PD-L1) lactylation and stability, which suppressed anti-tumor immunity in CD8+ T cells, thereby contributing to GC progression.
Conclusions
CLDN9 expression is associated with GC development and progression. Mechanistically, CLDN9 enhances the glycolysis pathway and facilitates PD-L1 lactylation through the PI3K/AKT/HIF1α signaling pathway, thereby suppressing anti-tumor immunity in CD8+ T cells. CLDN9 has the potential to serve as a novel prognostic marker and therapeutic target for GC.
{"title":"Claudin-9 (CLDN9) promotes gastric cancer progression by enhancing the glycolysis pathway and facilitating PD-L1 lactylation to suppress CD8+ T cell anti-tumor immunity","authors":"Xingbin Hu , Wenhao Ouyang , Haizhu Chen , Zhihong Liu , Zijia Lai , Herui Yao","doi":"10.1016/j.cpt.2024.09.006","DOIUrl":"10.1016/j.cpt.2024.09.006","url":null,"abstract":"<div><h3>Background</h3><div>Gastric cancer (GC) is a common malignancy characterized by the absence of reliable prognostic indicators and effective therapeutic targets. Claudin-9 (CLDN9) has been demonstrated to be upregulated in various cancers. However, its prognostic value, biological function, and regulatory mechanisms in GC remain unclear. Therefore, this study aimed to elucidate the role of <em>CLDN9</em> in GC progression and its underlying mechanisms.</div></div><div><h3>Methods</h3><div>We utilized consensus cluster, random survival forest, and multivariate Cox regression analyses to identify <em>CLDN9</em> in GC. Subsequently, we evaluated the mRNA and protein levels of <em>CLDN9</em> in GC using quantitative real-time polymerase chain reaction (PCR) (qRT-PCR), Western blotting (WB), and immunohistochemistry (IHC). Furthermore, the role of <em>CLDN9</em> in GC progression was investigated using a series of functional <em>in vivo</em> and <em>in vitro</em> experiments. Finally, we elucidated the molecular mechanisms of <em>CLDN9</em> using bioinformatics, molecular biology, animal models, and patient tissue specimens.</div></div><div><h3>Results</h3><div>Two GC subtypes with survival and functional differences were identified based on glycolytic metabolic genes in the Cancer Genome Atlas (TCGA)- Stomach adenocarcinoma (STAD) dataset. A prognostic risk score was calculated using seven genes to assess the overall survival (OS) in GC. Using random survival forest and multivariate Cox analyses, we identified <em>CLDN9</em> as the key gene linked to the glycolytic subtype and prognosis of GC. <em>CLDN9</em> expression was significantly upregulated in patients with GC as well as in GC cells. <em>CLDN9</em> knockdown inhibited tumor proliferation, invasion, and metastasis both <em>in vivo</em> and <em>in vitro</em>. Mechanistically, <em>CLDN9</em> was found to regulate lactate dehydrogenase A (LDHA) expression and promote glycolytic metabolism by activating the phosphatidylinositol 3-kinase (PI3K)/protein kinase B (AKT)/hypoxia-inducible factor 1-alpha (HIF1α) signaling pathway. Additionally, lactate, a glycolytic metabolite, enhanced programmed cell death ligand 1 (PD-L1) lactylation and stability, which suppressed anti-tumor immunity in CD8<sup>+</sup> T cells, thereby contributing to GC progression.</div></div><div><h3>Conclusions</h3><div><em>CLDN9</em> expression is associated with GC development and progression. Mechanistically, <em>CLDN9</em> enhances the glycolysis pathway and facilitates PD-L1 lactylation through the PI3K/AKT/HIF1α signaling pathway, thereby suppressing anti-tumor immunity in CD8<sup>+</sup> T cells. <em>CLDN9</em> has the potential to serve as a novel prognostic marker and therapeutic target for GC.</div></div>","PeriodicalId":93920,"journal":{"name":"Cancer pathogenesis and therapy","volume":"3 3","pages":"Pages 253-266"},"PeriodicalIF":0.0,"publicationDate":"2025-05-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143887014","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Pub Date : 2025-05-01DOI: 10.1016/j.cpt.2024.09.005
Yintao Li, Jianxin Xue, Li Zhang
{"title":"New advances in lung cancer treatment: Efficacy, safety, and future research directions","authors":"Yintao Li, Jianxin Xue, Li Zhang","doi":"10.1016/j.cpt.2024.09.005","DOIUrl":"10.1016/j.cpt.2024.09.005","url":null,"abstract":"","PeriodicalId":93920,"journal":{"name":"Cancer pathogenesis and therapy","volume":"3 3","pages":"Pages 181-182"},"PeriodicalIF":0.0,"publicationDate":"2025-05-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143887142","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
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