Pub Date : 2025-12-23DOI: 10.1016/j.semcancer.2025.12.008
Celestina Agyemang-Dua , Charles S. Chung , Cristina Espinosa-Diez
Cancer therapies save lives but often “break hearts” by damaging the cardiovascular system. As survival improves, therapy-induced cardiotoxicity has become a defining challenge of modern oncology. Recent discoveries reveal that long non-coding RNAs (lncRNAs), once dismissed as genomic noise, are the “RNA rebels” orchestrating cellular responses to cancer treatments. These molecules act as both heartbreakers and healers, amplifying or counteracting oxidative stress, mitochondrial dysfunction, apoptosis, and vascular injury. In anthracycline, radiation, and VEGF-targeted therapies, lncRNAs govern key processes that dictate whether cells succumb to damage or mount protective repair responses. Pro-injury lncRNAs exacerbate senescence and inflammation, while protective ones preserve mitochondrial homeostasis and limit cell death. Beyond mechanistic insight, these molecules hold clinical promise as biomarkers and therapeutic targets, guiding RNA-based strategies to predict, prevent, and treat cardiotoxicity. Understanding how they blur the line between protection and harm may redefine how we safeguard the heart in the era of precision cardio oncology.
{"title":"Heartbreakers and healers: RNA rebels in cardio-oncology","authors":"Celestina Agyemang-Dua , Charles S. Chung , Cristina Espinosa-Diez","doi":"10.1016/j.semcancer.2025.12.008","DOIUrl":"10.1016/j.semcancer.2025.12.008","url":null,"abstract":"<div><div>Cancer therapies save lives but often “break hearts” by damaging the cardiovascular system. As survival improves, therapy-induced cardiotoxicity has become a defining challenge of modern oncology. Recent discoveries reveal that long non-coding RNAs (lncRNAs), once dismissed as genomic noise, are the “RNA rebels” orchestrating cellular responses to cancer treatments. These molecules act as both heartbreakers and healers, amplifying or counteracting oxidative stress, mitochondrial dysfunction, apoptosis, and vascular injury. In anthracycline, radiation, and VEGF-targeted therapies, lncRNAs govern key processes that dictate whether cells succumb to damage or mount protective repair responses. Pro-injury lncRNAs exacerbate senescence and inflammation, while protective ones preserve mitochondrial homeostasis and limit cell death. Beyond mechanistic insight, these molecules hold clinical promise as biomarkers and therapeutic targets, guiding RNA-based strategies to predict, prevent, and treat cardiotoxicity. Understanding how they blur the line between protection and harm may redefine how we safeguard the heart in the era of precision cardio oncology.</div></div>","PeriodicalId":21594,"journal":{"name":"Seminars in cancer biology","volume":"119 ","pages":"Pages 1-11"},"PeriodicalIF":15.7,"publicationDate":"2025-12-23","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145834629","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}
Pub Date : 2025-12-18DOI: 10.1016/j.semcancer.2025.12.004
Yifan Chen , Xuejun Wang , Yihui Shen , Hui Zhang , Cheng Yu , Leilei Cheng , Junbo Ge
Advent of immune checkpoint inhibitors (ICIs) has renovated onco-immunotherapy, with around 50 % of cancer patients suitable for the treatment. However, patients treated by ICIs are in jeopardy for immune-related adverse events (irAEs) that attack any organ including the heart. ICIs-induced myocarditis (ICIIM) is an uncommon but possibly fatal irAE. With the increasing use of ICIs and improved diagnosis of this disease, the incidence of ICIIM is growing rapidly. In this review, we briefly overview roles of T cells and their immune checkpoints, and categorize the pathogenic process of ICIIM into three stages (upstream, midstream and downstream), with addressing recent research progress on the pathogenic mechanisms in each stage, particularly focusing on the downstream core pathogenic components and potential therapeutics for this disease.
{"title":"Immune checkpoint inhibitor-induced myocarditis: focus on the downstream pathogenic components and potential therapeutics","authors":"Yifan Chen , Xuejun Wang , Yihui Shen , Hui Zhang , Cheng Yu , Leilei Cheng , Junbo Ge","doi":"10.1016/j.semcancer.2025.12.004","DOIUrl":"10.1016/j.semcancer.2025.12.004","url":null,"abstract":"<div><div>Advent of immune checkpoint inhibitors (ICIs) has renovated onco-immunotherapy, with around 50 % of cancer patients suitable for the treatment. However, patients treated by ICIs are in jeopardy for immune-related adverse events (irAEs) that attack any organ including the heart. ICIs-induced myocarditis (ICIIM) is an uncommon but possibly fatal irAE. With the increasing use of ICIs and improved diagnosis of this disease, the incidence of ICIIM is growing rapidly. In this review, we briefly overview roles of T cells and their immune checkpoints, and categorize the pathogenic process of ICIIM into three stages (upstream, midstream and downstream), with addressing recent research progress on the pathogenic mechanisms in each stage, particularly focusing on the downstream core pathogenic components and potential therapeutics for this disease.</div></div>","PeriodicalId":21594,"journal":{"name":"Seminars in cancer biology","volume":"119 ","pages":"Pages 12-23"},"PeriodicalIF":15.7,"publicationDate":"2025-12-18","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145800820","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}
Pub Date : 2025-12-15DOI: 10.1016/j.semcancer.2025.12.006
M. Boschetti , I. Hasballa , I. Patelli , G. Piras , M. Albertelli
Gastroenteropancreatic neuroendocrine neoplasms (GEP-NEN) comprise a heterogeneous group of tumors differing according to the primary lesion site, histological features, clinical status and prognosis. The etiopathogenesis of GEP-NEN is not fully elucidated, however, excessive visceral adiposity may play a role in NEN oncogenesis and pose challenges to NEN therapeutic management. The interplay between obesity and GEP-NEN is complex and the potential carcinogenic mechanisms of obesity include chronic inflammation, abnormal immune function, hormone and metabolic dysregulation. Data regarding the prognostic impact of visceral adiposity on patients’ clinical and survival outcomes is still very limited and indeterminate. Molecular evidence predominantly supports the carcinogenic effects of obesity, although some studies have documented a potential protective role of excessive adiposity, i.e. the “obesity paradox” phenomenon, in NENs. Concerning therapeutic management of obesity in the setting of GEP-NENs, the current strategies to be considered include first-line nutritional and lifestyle intervention, followed by pharmacological and surgical treatment. This review aims to explore the intricate relationship between obesity and GEP-NENs, the potential impact on NEN outcomes, the current treatment approaches and future perspectives of the therapeutic landscape of individuals affected by GEP-NEN and obesity.
{"title":"Obesity and GEP-NEN: what’s new?","authors":"M. Boschetti , I. Hasballa , I. Patelli , G. Piras , M. Albertelli","doi":"10.1016/j.semcancer.2025.12.006","DOIUrl":"10.1016/j.semcancer.2025.12.006","url":null,"abstract":"<div><div>Gastroenteropancreatic neuroendocrine neoplasms (GEP-NEN) comprise a heterogeneous group of tumors differing according to the primary lesion site, histological features, clinical status and prognosis. The etiopathogenesis of GEP-NEN is not fully elucidated, however, excessive visceral adiposity may play a role in NEN oncogenesis and pose challenges to NEN therapeutic management. The interplay between obesity and GEP-NEN is complex and the potential carcinogenic mechanisms of obesity include chronic inflammation, abnormal immune function, hormone and metabolic dysregulation. Data regarding the prognostic impact of visceral adiposity on patients’ clinical and survival outcomes is still very limited and indeterminate. Molecular evidence predominantly supports the carcinogenic effects of obesity, although some studies have documented a potential protective role of excessive adiposity, i.e. the “obesity paradox” phenomenon, in NENs. Concerning therapeutic management of obesity in the setting of GEP-NENs, the current strategies to be considered include first-line nutritional and lifestyle intervention, followed by pharmacological and surgical treatment. This review aims to explore the intricate relationship between obesity and GEP-NENs, the potential impact on NEN outcomes, the current treatment approaches and future perspectives of the therapeutic landscape of individuals affected by GEP-NEN and obesity.</div></div>","PeriodicalId":21594,"journal":{"name":"Seminars in cancer biology","volume":"118 ","pages":"Pages 74-86"},"PeriodicalIF":15.7,"publicationDate":"2025-12-15","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145775562","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}
Pub Date : 2025-12-11DOI: 10.1016/j.semcancer.2025.12.005
Yaowen Zhang , Jianxiang Wang , Cong Li , Zhe Lei , Xiang Zhao , Xuan Xuan , Olga Sukocheva , Edmund Tse , Junqi Liu
Lactylation, a recently recognized post-translational protein modification, is reshaping research in epigenetics and molecular medicine. Emerging evidence indicates that lactylation plays a critical role in the onset and progression of cancer, as well as in several pre-cancerous and metabolism-associated pathologies. This review summarizes the current understanding of the mechanisms and biological roles of lactylation in cancer and other diseases. Lactate has been shown to promote carcinogenesis both as an additional energy source and as a signaling molecule. Glycolysis and glucose transport—major sources of lactate and subsequent lactylation—are frequently targeted by anti-cancer therapies. Several small-molecule glucose transporter type 1 (GLUT1) inhibitors, including STF-31, WZB-117, and BAY-876, have demonstrated efficacy in suppressing tumor growth. During lactylation, lactate is covalently attached to histone lysine residues, leading to epigenetic modifications. This process is regulated by “writer” enzymes (p300 and HBO1) and “eraser” enzymes (HDAC1–3 and SIRT1–3), which participate in nuclear signaling networks associated with oncogenic transformation. Several inhibitors targeting “writer” enzymes, such as A485 and andrographolide, have been developed and shown to suppress angiogenesis. Inhibition of tumor immune evasion has also been explored using glycolytic enzyme inhibitors, including 2-deoxy-D-glucose and oxalate. Despite these advances, lactylation-targeted research remains in its early stages and faces notable limitations that warrant further investigation. This review provides insights into the role of lactylation in diverse diseases and highlights emerging therapeutic strategies aimed at modulating lactylation-associated molecular targets.
{"title":"Protein lactylation in cancer and other pathologies: Epigenetic regulation of glycolysis and its therapeutic perspectives","authors":"Yaowen Zhang , Jianxiang Wang , Cong Li , Zhe Lei , Xiang Zhao , Xuan Xuan , Olga Sukocheva , Edmund Tse , Junqi Liu","doi":"10.1016/j.semcancer.2025.12.005","DOIUrl":"10.1016/j.semcancer.2025.12.005","url":null,"abstract":"<div><div>Lactylation, a recently recognized post-translational protein modification, is reshaping research in epigenetics and molecular medicine. Emerging evidence indicates that lactylation plays a critical role in the onset and progression of cancer, as well as in several pre-cancerous and metabolism-associated pathologies. This review summarizes the current understanding of the mechanisms and biological roles of lactylation in cancer and other diseases. Lactate has been shown to promote carcinogenesis both as an additional energy source and as a signaling molecule. Glycolysis and glucose transport—major sources of lactate and subsequent lactylation—are frequently targeted by anti-cancer therapies. Several small-molecule glucose transporter type 1 (GLUT1) inhibitors, including STF-31, WZB-117, and BAY-876, have demonstrated efficacy in suppressing tumor growth. During lactylation, lactate is covalently attached to histone lysine residues, leading to epigenetic modifications. This process is regulated by “writer” enzymes (p300 and HBO1) and “eraser” enzymes (HDAC1–3 and SIRT1–3), which participate in nuclear signaling networks associated with oncogenic transformation. Several inhibitors targeting “writer” enzymes, such as A485 and andrographolide, have been developed and shown to suppress angiogenesis. Inhibition of tumor immune evasion has also been explored using glycolytic enzyme inhibitors, including 2-deoxy-<span>D</span>-glucose and oxalate. Despite these advances, lactylation-targeted research remains in its early stages and faces notable limitations that warrant further investigation. This review provides insights into the role of lactylation in diverse diseases and highlights emerging therapeutic strategies aimed at modulating lactylation-associated molecular targets.</div></div>","PeriodicalId":21594,"journal":{"name":"Seminars in cancer biology","volume":"118 ","pages":"Pages 28-43"},"PeriodicalIF":15.7,"publicationDate":"2025-12-11","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145752190","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}
Pub Date : 2025-12-11DOI: 10.1016/j.semcancer.2025.12.003
Jie Xu , Linlin Guo , Yi Wang , Xiaoping Li , Ping Yi , Chunming Cheng
Abnormal metabolism is a typical characteristic of malignant tumors, broadly influencing the outcome of cancer therapy. Research on tumor metabolism has increased exponentially in last decades. There is an urgent need to provide a blueprint or framework to accelerate the translation of cancer metabolism research into effective therapeutics. In this review, we summarize the impact of metabolism on cancer progression and emerging metabolic therapies, and systematically outline potential clinical applications in cancer prevention, early screening, diagnosis, treatment, and new challenges. Furthermore, we aim to provide researchers and clinicians with a clearer perspective on the immediate translation of clinical applications stemming from cancer metabolism research. It will revolutionize cancer management and significantly enhance patient survival.
{"title":"Leveraging cancer metabolism to translate into effective therapeutics","authors":"Jie Xu , Linlin Guo , Yi Wang , Xiaoping Li , Ping Yi , Chunming Cheng","doi":"10.1016/j.semcancer.2025.12.003","DOIUrl":"10.1016/j.semcancer.2025.12.003","url":null,"abstract":"<div><div>Abnormal metabolism is a typical characteristic of malignant tumors, broadly influencing the outcome of cancer therapy. Research on tumor metabolism has increased exponentially in last decades. There is an urgent need to provide a blueprint or framework to accelerate the translation of cancer metabolism research into effective therapeutics. In this review, we summarize the impact of metabolism on cancer progression and emerging metabolic therapies, and systematically outline potential clinical applications in cancer prevention, early screening, diagnosis, treatment, and new challenges. Furthermore, we aim to provide researchers and clinicians with a clearer perspective on the immediate translation of clinical applications stemming from cancer metabolism research. It will revolutionize cancer management and significantly enhance patient survival.</div></div>","PeriodicalId":21594,"journal":{"name":"Seminars in cancer biology","volume":"118 ","pages":"Pages 44-61"},"PeriodicalIF":15.7,"publicationDate":"2025-12-11","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145751985","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}
Pub Date : 2025-12-05DOI: 10.1016/j.semcancer.2025.12.002
Dongliang Wei , Yilan Sun , Jing Han , Jiannan Liu
The microbiota has emerged as a pivotal modulator of cancer immunotherapy, offering novel insights into the efficacy and toxicity of immune checkpoint inhibitors (ICIs). Recent evidence highlights that microbial communities and their metabolites dynamically regulate host immunity by priming dendritic cells, enhancing T-cell infiltration, and reprogramming the tumor microenvironment. Microbiome dysbiosis is implicated in immune-related adverse events (irAEs), underscoring its dual role in therapeutic outcomes. Leveraging these findings, precision microbiome interventions, including fecal microbiota transplantation, engineered probiotics, and dietary modulation, which demonstrate potential to enhance ICIs responsiveness and mitigate irAEs in preclinical and early-phase clinical studies. However, translating these strategies into clinical practice requires rigorous validation through multicenter trials to establish safety, efficacy, and standardized protocols. This review synthesizes current knowledge on the microbiome-immune-oncology axis, with a focus on mechanistic underpinnings, translational challenges, and innovative therapeutic strategies. By integrating microbiome profiling with patient-specific factors, proposing a roadmap for personalized immunotherapy, aligning with the emerging paradigm of precision oncology.
{"title":"Microbiota and cancer immunotherapy: Mechanisms, clinical implications, and precision therapeutics","authors":"Dongliang Wei , Yilan Sun , Jing Han , Jiannan Liu","doi":"10.1016/j.semcancer.2025.12.002","DOIUrl":"10.1016/j.semcancer.2025.12.002","url":null,"abstract":"<div><div>The microbiota has emerged as a pivotal modulator of cancer immunotherapy, offering novel insights into the efficacy and toxicity of immune checkpoint inhibitors (ICIs). Recent evidence highlights that microbial communities and their metabolites dynamically regulate host immunity by priming dendritic cells, enhancing T-cell infiltration, and reprogramming the tumor microenvironment. Microbiome dysbiosis is implicated in immune-related adverse events (irAEs), underscoring its dual role in therapeutic outcomes. Leveraging these findings, precision microbiome interventions, including fecal microbiota transplantation, engineered probiotics, and dietary modulation, which demonstrate potential to enhance ICIs responsiveness and mitigate irAEs in preclinical and early-phase clinical studies. However, translating these strategies into clinical practice requires rigorous validation through multicenter trials to establish safety, efficacy, and standardized protocols. This review synthesizes current knowledge on the microbiome-immune-oncology axis, with a focus on mechanistic underpinnings, translational challenges, and innovative therapeutic strategies. By integrating microbiome profiling with patient-specific factors, proposing a roadmap for personalized immunotherapy, aligning with the emerging paradigm of precision oncology.</div></div>","PeriodicalId":21594,"journal":{"name":"Seminars in cancer biology","volume":"118 ","pages":"Pages 62-73"},"PeriodicalIF":15.7,"publicationDate":"2025-12-05","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145696265","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}
Pub Date : 2025-12-04DOI: 10.1016/j.semcancer.2025.12.001
Luca Morelli
{"title":"Integrating biomarkers, experimental models, genomics, and novel therapeutics for pancreatic cancer precision medicine","authors":"Luca Morelli","doi":"10.1016/j.semcancer.2025.12.001","DOIUrl":"10.1016/j.semcancer.2025.12.001","url":null,"abstract":"","PeriodicalId":21594,"journal":{"name":"Seminars in cancer biology","volume":"118 ","pages":"Pages 1-2"},"PeriodicalIF":15.7,"publicationDate":"2025-12-04","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145692916","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}
Pub Date : 2025-12-01Epub Date: 2025-11-08DOI: 10.1016/j.semcancer.2025.11.018
{"title":"Expression of concern \"Decoding T cell senescence in cancer: Is revisiting required?\" [Semin. Cancer Biol. 108 (2025) 33-47].","authors":"","doi":"10.1016/j.semcancer.2025.11.018","DOIUrl":"https://doi.org/10.1016/j.semcancer.2025.11.018","url":null,"abstract":"","PeriodicalId":21594,"journal":{"name":"Seminars in cancer biology","volume":"117 ","pages":"114"},"PeriodicalIF":15.7,"publicationDate":"2025-12-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145715487","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}
Pub Date : 2025-12-01Epub Date: 2025-11-07DOI: 10.1016/j.semcancer.2025.11.003
{"title":"Expression of concern \"Navigating the paradox of senescence and chemoresistance in pancreatic cancer\" [Semin. Cancer Biol. 114 (2025) 60-72].","authors":"","doi":"10.1016/j.semcancer.2025.11.003","DOIUrl":"https://doi.org/10.1016/j.semcancer.2025.11.003","url":null,"abstract":"","PeriodicalId":21594,"journal":{"name":"Seminars in cancer biology","volume":"117 ","pages":"128"},"PeriodicalIF":15.7,"publicationDate":"2025-12-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145715522","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}
Pub Date : 2025-12-01Epub Date: 2025-11-07DOI: 10.1016/j.semcancer.2025.11.009
{"title":"Expression of concern \"Remodeling of tumor microenvironment by cellular senescence and immunosenescence in cervical cancer\" [Semin. Cancer Biol. 108 (2025) 17-32].","authors":"","doi":"10.1016/j.semcancer.2025.11.009","DOIUrl":"https://doi.org/10.1016/j.semcancer.2025.11.009","url":null,"abstract":"","PeriodicalId":21594,"journal":{"name":"Seminars in cancer biology","volume":"117 ","pages":"124"},"PeriodicalIF":15.7,"publicationDate":"2025-12-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145715527","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}
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