Nature cancerPub Date : 2025-06-05DOI: 10.1038/s43018-025-00992-5
Kang Qin, Carl M Gay, Lauren A Byers, Jianjun Zhang
{"title":"The current and emerging immunotherapy paradigm in small-cell lung cancer.","authors":"Kang Qin, Carl M Gay, Lauren A Byers, Jianjun Zhang","doi":"10.1038/s43018-025-00992-5","DOIUrl":"https://doi.org/10.1038/s43018-025-00992-5","url":null,"abstract":"<p><p>Small-cell lung cancer (SCLC) is a highly aggressive malignancy with poor prognosis. For decades, etoposide-platinum-based chemotherapy had been the mainstay treatment for SCLC; however, despite initial high response rates, most patients developed resistance. In 2019, the US Food and Drug Administration approved the anti-PD-L1 antibody atezolizumab in combination with etoposide-platinum as the new first-line standard of care for extensive-stage SCLC, heralding a paradigm shift in SCLC therapy. This Review aims to provide an overview of the current landscape and emerging treatment strategies of immunotherapies in SCLC as well as highlight the importance of developing biomarkers to facilitate patient selection.</p>","PeriodicalId":18885,"journal":{"name":"Nature cancer","volume":" ","pages":""},"PeriodicalIF":23.5,"publicationDate":"2025-06-05","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144234569","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}
Nature cancerPub Date : 2025-06-04DOI: 10.1038/s43018-025-00984-5
Fanzheng Meng, Hairui Li, Yabin Huang, Chunxu Wang, Yufeng Liu, Chunting Zhang, Danlei Chen, Taofei Zeng, Shenyu Zhang, Yunyun Li, Bo Zhang, Chuandong Lang, Jie Xia, Wanxiang Xiong, Shixiang Pan, Xuedan Sun, Rick F Thorne, Yao Liu, Jiabei Wang, Shugeng Zhang, Ruipeng Song, Jizhou Wang, Lianxin Liu
{"title":"RIOK1 phase separation restricts PTEN translation via stress granules activating tumor growth in hepatocellular carcinoma.","authors":"Fanzheng Meng, Hairui Li, Yabin Huang, Chunxu Wang, Yufeng Liu, Chunting Zhang, Danlei Chen, Taofei Zeng, Shenyu Zhang, Yunyun Li, Bo Zhang, Chuandong Lang, Jie Xia, Wanxiang Xiong, Shixiang Pan, Xuedan Sun, Rick F Thorne, Yao Liu, Jiabei Wang, Shugeng Zhang, Ruipeng Song, Jizhou Wang, Lianxin Liu","doi":"10.1038/s43018-025-00984-5","DOIUrl":"https://doi.org/10.1038/s43018-025-00984-5","url":null,"abstract":"<p><p>Resistance to tyrosine kinase inhibitors (TKIs) dampens their clinical efficacy in hepatocellular carcinoma (HCC). Stress granules formed by phase separation are essential to stress response and can be involved in therapy resistance, but their mechanisms in HCC are unclear. Here our screen shows that the atypical serine/threonine kinase RIOK1 is highly expressed in HCC, linked to poor prognosis, and transcriptionally activated by NRF2 under various stress conditions. RIOK1 undergoes liquid-liquid phase separation by incorporating IGF2BP1 and G3BP1 into stress granules that sequestrate PTEN messenger RNA reducing its translation. This process activates the pentose phosphate pathway, facilitating stress resolution and cytoprotection against TKI. We further show that the small-molecule inhibitor chidamide downregulates RIOK1 and enhances TKI efficacy. RIOK1-positive stress granules are found in donafenib-resistant tumors from patients with HCC. These findings reveal a link between stress granule dynamics, metabolic reprogramming and HCC progression, offering the potential means to improve TKI efficacy.</p>","PeriodicalId":18885,"journal":{"name":"Nature cancer","volume":" ","pages":""},"PeriodicalIF":23.5,"publicationDate":"2025-06-04","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144226008","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}
Nature cancerPub Date : 2025-06-03DOI: 10.1038/s43018-025-00977-4
En-Wei Tao, Ye Wang, Juan Tan, Yan Chen, Tian-Yue Sun, Yu Hao, Hao-Lian Wang, Qianqian Liu, Yun-Qian Wang, Linna Fu, Zhi-Qing Zhan, Haoyan Chen, Jie Hong, Qin-Yan Gao, Jing-Yuan Fang, Ying-Xuan Chen
{"title":"TRMT6-mediated tRNA m<sup>1</sup>A modification acts as a translational checkpoint of histone synthesis and facilitates colorectal cancer progression.","authors":"En-Wei Tao, Ye Wang, Juan Tan, Yan Chen, Tian-Yue Sun, Yu Hao, Hao-Lian Wang, Qianqian Liu, Yun-Qian Wang, Linna Fu, Zhi-Qing Zhan, Haoyan Chen, Jie Hong, Qin-Yan Gao, Jing-Yuan Fang, Ying-Xuan Chen","doi":"10.1038/s43018-025-00977-4","DOIUrl":"https://doi.org/10.1038/s43018-025-00977-4","url":null,"abstract":"<p><p>Transfer RNA modifications have emerged as critical regulators of translational reprogramming, yet their roles in colorectal cancer (CRC) remain largely elusive. Here, we find that tRNA N1-methyladenosine (m<sup>1</sup>A) methyltransferase TRMT6 is upregulated in human CRC tissues and high TRMT6 expression correlates with poor survival in patients with CRC. Using orthotopic, metastatic and conditional knockout mouse models, we establish the oncogenic role of TRMT6 in CRC. Mechanistically, TRMT6 increases tRNA m<sup>1</sup>A levels by maintaining the stability of the TRMT6-TRMT61A complex. Targeting TRMT6-mediated tRNA m<sup>1</sup>A modification in CRC cells destabilizes tRNA-Lys-TTT-1-1 and impairs histone mRNA translation in a codon-biased manner, thereby restricting histone synthesis and hindering cell cycle progression. Our study provides evidence that TRMT6 functions as a translational checkpoint in the accelerated histone synthesis of CRC cells, highlighting TRMT6 as a promising target for potential anti-CRC therapies.</p>","PeriodicalId":18885,"journal":{"name":"Nature cancer","volume":" ","pages":""},"PeriodicalIF":23.5,"publicationDate":"2025-06-03","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144216388","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}
Nature cancerPub Date : 2025-05-29DOI: 10.1038/s43018-025-00985-4
Sangjo Kang, Mary E Ughetta, Jack Y Zhang, Valerie J Marallano, Anirudh Sattiraju, Theodore Hannah, Shalaka Wahane, Aarthi Ramakrishnan, Molly Estill, Nadejda M Tsankova, Li Shen, Alexander M Tsankov, Roland H Friedel, Hongyan Zou
{"title":"Glioblastoma shift from bulk to infiltrative growth is guided by plexin-B2-mediated microglia alignment in invasive niches.","authors":"Sangjo Kang, Mary E Ughetta, Jack Y Zhang, Valerie J Marallano, Anirudh Sattiraju, Theodore Hannah, Shalaka Wahane, Aarthi Ramakrishnan, Molly Estill, Nadejda M Tsankova, Li Shen, Alexander M Tsankov, Roland H Friedel, Hongyan Zou","doi":"10.1038/s43018-025-00985-4","DOIUrl":"https://doi.org/10.1038/s43018-025-00985-4","url":null,"abstract":"<p><p>Glioblastoma (GBM) lethality stems from uncontrolled growth and infiltration. Using an immunocompetent murine model, we mapped GBM invasion and tumor-associated microglia and macrophage (TAM) interactions. We show that microglia are mobilized ahead of invasion, transforming morphologically and functionally-first forming glial nets around tumor infiltrates and then organizing into 'oncostreams' guiding collective migration. Single-cell RNA sequencing revealed three distinct states for tumor cells and microglia, corresponding to invasive niches versus tumor bulk. The invasive patterns and niche-specific gene signatures of tumor cells and TAMs were validated in human GBMs. We further identified a critical role of plexin-B2 in TAMs for resolving cell collision, aligning GBM cells and restructuring the extracellular matrix. Plexin-B2 ablation in TAMs disrupted invasion tracks, shifting GBM growth from infiltrative to bulk expansion. Understanding niche-specific TAM mobilization and anatomical-functional invasion units opens new strategies to target GBM invasion.</p>","PeriodicalId":18885,"journal":{"name":"Nature cancer","volume":" ","pages":""},"PeriodicalIF":23.5,"publicationDate":"2025-05-29","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144182770","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}
Nature cancerPub Date : 2025-05-29DOI: 10.1038/s43018-025-00988-1
Man Nie, Dexin Lei, Zhou Liu, Kuan Zeng, Xinyan Liang, Peng Huang, Yu Wang, Peng Sun, Hang Yang, Panpan Liu, Runcong Nie, Silan Huang, Erwei Song, Wenqi Jiang, Zhiming Li, Yanqi Yang, Yi Xia, Linbin Yang
{"title":"Cardiomyocyte-localized CCDC25 senses NET DNA to promote doxorubicin cardiotoxicity by activating autophagic flux.","authors":"Man Nie, Dexin Lei, Zhou Liu, Kuan Zeng, Xinyan Liang, Peng Huang, Yu Wang, Peng Sun, Hang Yang, Panpan Liu, Runcong Nie, Silan Huang, Erwei Song, Wenqi Jiang, Zhiming Li, Yanqi Yang, Yi Xia, Linbin Yang","doi":"10.1038/s43018-025-00988-1","DOIUrl":"https://doi.org/10.1038/s43018-025-00988-1","url":null,"abstract":"<p><p>Cardiotoxicity restricts the clinical use of anthracyclines. Although recent evidence indicates that aberrant activation of the cytosolic DNA-sensing pathway mediates cardiotoxicity, the function of extracellular DNA remains unclear. Here we observe a substantial increase in circulating neutrophil extracellular trap (NET) DNA in individuals with lymphoma experiencing cardiotoxicity after anthracycline-containing treatment. Using mouse models and human organotypic myocardial slices, we demonstrate that doxorubicin induces HMGB1-dependent cardiac NET formation, thereby promoting cardiac remodeling and dysfunction. Mechanistically, extracellular NET DNA is recognized by the transmembrane protein CCDC25 on cardiomyocytes, and their cross-talk generates reactive oxygen species and activates autophagic flux, subsequently impairing cardiac function. Targeting CCDC25 significantly alleviates anthracycline cardiotoxicity and synergizes with the antitumor efficacy of doxorubicin in lymphoma and breast cancer models. Overall, our findings demonstrate a previously unrecognized role of NETs and CCDC25 in anthracycline cardiotoxicity and suggest that targeting CCDC25 could provide a dual therapeutic and cardioprotective advantage.</p>","PeriodicalId":18885,"journal":{"name":"Nature cancer","volume":" ","pages":""},"PeriodicalIF":23.5,"publicationDate":"2025-05-29","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144180267","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}
Nature cancerPub Date : 2025-05-26DOI: 10.1038/s43018-025-00975-6
Young-Mee Kim, Mark A Sanborn, Shaluah Vijeth, Priyanka Gajwani, Xinge Wang, Dahee Jung, Tibor Valyi-Nagy, Sreeparna Chakraborty, Georgina Mancinelli, Peter T Toth, Evan H Phillips, Paul Grippo, Ameen A Salahudeen, Jooman Park, Su Yeon Yeon, Vijayalakshmi Ananthanarayanan, Yuwei Jiang, Steve Seung-Young Lee, Klara Valyi-Nagy, Jalees Rehman
{"title":"Skeletal muscle endothelial dysfunction through the activin A-PGC1α axis drives progression of cancer cachexia.","authors":"Young-Mee Kim, Mark A Sanborn, Shaluah Vijeth, Priyanka Gajwani, Xinge Wang, Dahee Jung, Tibor Valyi-Nagy, Sreeparna Chakraborty, Georgina Mancinelli, Peter T Toth, Evan H Phillips, Paul Grippo, Ameen A Salahudeen, Jooman Park, Su Yeon Yeon, Vijayalakshmi Ananthanarayanan, Yuwei Jiang, Steve Seung-Young Lee, Klara Valyi-Nagy, Jalees Rehman","doi":"10.1038/s43018-025-00975-6","DOIUrl":"https://doi.org/10.1038/s43018-025-00975-6","url":null,"abstract":"<p><p>Cachexia is the wasting of skeletal muscle in cancer and is a major complication that impacts a person's quality of life. We hypothesized that cachexia is mediated by dysfunction of the vascular system, which is essential for maintaining perfusion and tempering inappropriate immune responses. Using transparent tissue topography, we discovered that loss of muscle vascular density precedes muscle wasting in multiple complementary tumor models, including pancreatic adenocarcinoma, colon carcinoma, lung adenocarcinoma and melanoma models. We also observed that persons suffering from cancer cachexia exhibit substantial loss of muscle vascular density. As tumors progress, increased circulating activin A remotely suppresses the expression of peroxisome proliferator-activated receptor-γ coactivator 1α (PGC1α) in the muscle endothelium, thus inducing vascular leakage. Restoring endothelial PGC1α activity preserved vascular density and muscle mass in tumor-bearing mice. Our study suggests that restoring muscle endothelial function could be a valuable therapeutic approach for cancer cachexia.</p>","PeriodicalId":18885,"journal":{"name":"Nature cancer","volume":" ","pages":""},"PeriodicalIF":23.5,"publicationDate":"2025-05-26","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144151133","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}
Nature cancerPub Date : 2025-05-26DOI: 10.1038/s43018-025-00964-9
Alexander Beck, Lisa Gabler-Pamer, Gustavo Alencastro Veiga Cruzeiro, Sander Lambo, Bernhard Englinger, McKenzie L Shaw, Olivia A Hack, Ilon Liu, Rebecca D Haase, Carlos A O de Biagi, Alicia Baumgartner, Andrezza Do Nascimento Silva, Marbod Klenner, Pia S Freidel, Jochen Herms, Louisa von Baumgarten, Joerg C Tonn, Niklas Thon, Katharina Bruckner, Sibylle Madlener, Lisa Mayr, Daniel Senfter, Andreas Peyrl, Irene Slavc, Daniela Lötsch, Christian Dorfer, Rene Geyregger, Nicole Amberg, Christine Haberler, Norman Mack, Benjamin Schwalm, Stefan M Pfister, Andrey Korshunov, Lissa C Baird, Edward Yang, Susan N Chi, Sanda Alexandrescu, Johannes Gojo, Marcel Kool, Volker Hovestadt, Mariella G Filbin
{"title":"Cellular hierarchies of embryonal tumors with multilayered rosettes are shaped by oncogenic microRNAs and receptor-ligand interactions.","authors":"Alexander Beck, Lisa Gabler-Pamer, Gustavo Alencastro Veiga Cruzeiro, Sander Lambo, Bernhard Englinger, McKenzie L Shaw, Olivia A Hack, Ilon Liu, Rebecca D Haase, Carlos A O de Biagi, Alicia Baumgartner, Andrezza Do Nascimento Silva, Marbod Klenner, Pia S Freidel, Jochen Herms, Louisa von Baumgarten, Joerg C Tonn, Niklas Thon, Katharina Bruckner, Sibylle Madlener, Lisa Mayr, Daniel Senfter, Andreas Peyrl, Irene Slavc, Daniela Lötsch, Christian Dorfer, Rene Geyregger, Nicole Amberg, Christine Haberler, Norman Mack, Benjamin Schwalm, Stefan M Pfister, Andrey Korshunov, Lissa C Baird, Edward Yang, Susan N Chi, Sanda Alexandrescu, Johannes Gojo, Marcel Kool, Volker Hovestadt, Mariella G Filbin","doi":"10.1038/s43018-025-00964-9","DOIUrl":"https://doi.org/10.1038/s43018-025-00964-9","url":null,"abstract":"<p><p>Embryonal tumor with multilayered rosettes (ETMR) is a pediatric brain tumor with dismal prognosis. Characteristic alterations of the chromosome 19 microRNA cluster (C19MC) are observed in most ETMR; however, the ramifications of C19MC activation and the complex cellular architecture of ETMR remain understudied. Here we analyze 11 ETMR samples from patients using single-cell transcriptomics and multiplexed spatial imaging. We reveal a spatially distinct cellular hierarchy that spans highly proliferative neural stem-like cells and more differentiated neuron-like cells. C19MC is predominantly expressed in stem-like cells and controls a transcriptional network governing stemness and lineage commitment, as resolved by genome-wide analysis of microRNA-mRNA binding. Systematic analysis of receptor-ligand interactions between malignant cell types reveals fibroblast growth factor receptor and Notch signaling as oncogenic pathways that can be successfully targeted in preclinical models and in one patient with ETMR. Our study provides fundamental insights into ETMR pathobiology and a powerful rationale for more effective targeted therapies.</p>","PeriodicalId":18885,"journal":{"name":"Nature cancer","volume":" ","pages":""},"PeriodicalIF":23.5,"publicationDate":"2025-05-26","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144151120","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}
Nature cancerPub Date : 2025-05-22DOI: 10.1038/s43018-025-00956-9
{"title":"Curating a single-cell data atlas for a deeper understanding of intra-tumor heterogeneity.","authors":"","doi":"10.1038/s43018-025-00956-9","DOIUrl":"https://doi.org/10.1038/s43018-025-00956-9","url":null,"abstract":"","PeriodicalId":18885,"journal":{"name":"Nature cancer","volume":" ","pages":""},"PeriodicalIF":23.5,"publicationDate":"2025-05-22","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144128212","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}
Nature cancerPub Date : 2025-05-22DOI: 10.1038/s43018-025-00979-2
Anca Apavaloaei, Qingchuan Zhao, Leslie Hesnard, Maxime Cahuzac, Chantal Durette, Jean-David Larouche, Marie-Pierre Hardy, Krystel Vincent, Sylvie Brochu, Jean-Philippe Laverdure, Joël Lanoix, Mathieu Courcelles, Patrick Gendron, Mathieu Lajoie, Maria Virginia Ruiz Cuevas, Eralda Kina, Julie Perrault, Juliette Humeau, Grégory Ehx, Sébastien Lemieux, Ian R Watson, Daniel E Speiser, Michal Bassani-Sternberg, Pierre Thibault, Claude Perreault
{"title":"Tumor antigens preferentially derive from unmutated genomic sequences in melanoma and non-small cell lung cancer.","authors":"Anca Apavaloaei, Qingchuan Zhao, Leslie Hesnard, Maxime Cahuzac, Chantal Durette, Jean-David Larouche, Marie-Pierre Hardy, Krystel Vincent, Sylvie Brochu, Jean-Philippe Laverdure, Joël Lanoix, Mathieu Courcelles, Patrick Gendron, Mathieu Lajoie, Maria Virginia Ruiz Cuevas, Eralda Kina, Julie Perrault, Juliette Humeau, Grégory Ehx, Sébastien Lemieux, Ian R Watson, Daniel E Speiser, Michal Bassani-Sternberg, Pierre Thibault, Claude Perreault","doi":"10.1038/s43018-025-00979-2","DOIUrl":"https://doi.org/10.1038/s43018-025-00979-2","url":null,"abstract":"<p><p>Melanoma and non-small cell lung cancer (NSCLC) display exceptionally high mutational burdens. Hence, immune targeting in these cancers has primarily focused on tumor antigens (TAs) predicted to derive from nonsynonymous mutations. Using comprehensive proteogenomic analyses, we identified 589 TAs in cutaneous melanoma (n = 505) and NSCLC (n = 90). Of these, only 1% were derived from mutated sequences, which was explained by a low RNA expression of most nonsynonymous mutations and their localization outside genomic regions proficient for major histocompatibility complex (MHC) class I-associated peptide generation. By contrast, 99% of TAs originated from unmutated genomic sequences specific to cancer (aberrantly expressed tumor-specific antigens (aeTSAs), n = 220), overexpressed in cancer (tumor-associated antigens (TAAs), n = 165) or specific to the cell lineage of origin (lineage-specific antigens (LSAs), n = 198). Expression of aeTSAs was epigenetically regulated, and most were encoded by noncanonical genomic sequences. aeTSAs were shared among tumor samples, were immunogenic and could contribute to the response to immune checkpoint blockade observed in previous studies, supporting their immune targeting across cancers.</p>","PeriodicalId":18885,"journal":{"name":"Nature cancer","volume":" ","pages":""},"PeriodicalIF":23.5,"publicationDate":"2025-05-22","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144128216","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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