Cancer CellPub Date : 2026-07-13Epub Date: 2026-06-18DOI: 10.1016/j.ccell.2026.05.019
Motohiro Izumi, Susumu S Kobayashi, Balazs Halmos
{"title":"Targeting drug-tolerant persister cells: Let's bring on the TROPs!","authors":"Motohiro Izumi, Susumu S Kobayashi, Balazs Halmos","doi":"10.1016/j.ccell.2026.05.019","DOIUrl":"10.1016/j.ccell.2026.05.019","url":null,"abstract":"<p><p>In this issue of Cancer Cell, Liao et al. identify TROP2 as an EGFR tyrosine kinase inhibitor-induced vulnerability in drug-tolerant persister lung cancer cells. They show that anti-TROP2 antibody-drug conjugates target this residual population, supporting an \"induce-target-kill\" strategy to delay resistance and extend the benefit of EGFR tyrosine kinase inhibition.</p>","PeriodicalId":9670,"journal":{"name":"Cancer Cell","volume":" ","pages":"1333-1335"},"PeriodicalIF":56.1,"publicationDate":"2026-07-13","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148276204","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":"Targeting TROP2 in drug-tolerant persister cells delays EGFR tyrosine kinase inhibitor resistance in non-small-cell lung cancer.","authors":"Jun Liao, Wenxiu Yao, Yan Yu, Anlin Li, Jie Huang, Xingya Li, Longhua Sun, Yongchang Zhang, Yongsheng Wang, Xiujuan Qu, Jun Zhao, Haiyong Wang, Weitao Zhuang, Liyang Hu, Xueyuan Chen, Lanlan Pang, Mengjuan Yang, Zexin Chen, Yaxiong Zhang, Ting Li, Wenyan Yu, Yiming Zeng, Jing Li, Ritesh Kataria, Gideon Blumenthal, Omobolaji Akala, Yanjun Liu, Yuping Shen, Junyou Ge, Shaodong Hong, Yunpeng Yang, Li Zhang, Wenfeng Fang","doi":"10.1016/j.ccell.2026.05.020","DOIUrl":"10.1016/j.ccell.2026.05.020","url":null,"abstract":"<p><p>Drug-tolerant persister (DTP) cells play a key role in the development of resistance to EGFR tyrosine kinase inhibitors (TKIs) in EGFR-mutant non-small-cell lung cancer (NSCLC). Through comprehensive analyses, we identify that TROP2 is dynamically upregulated during TKI-induced DTP formation and functionally contributes to DTP maintenance. Mechanistically, c-Myc acts as a transcriptional repressor of TROP2, and TKI-mediated MAPK pathway inhibition reduces c-Myc levels, leading to TROP2 upregulation. Importantly, combining the TROP2-targeting antibody-drug conjugate (ADC) sacituzumab tirumotecan (sac-TMT) with osimertinib effectively suppresses DTP emergence and delays tumor relapse in preclinical models. An ongoing phase 2 trial evaluating first-line sac-TMT plus osimertinib combination therapy in patients with advanced EGFR-mutant NSCLC shows preliminary efficacy. Together, our findings establish TROP2 as a therapeutically actionable vulnerability in DTP cells and support the clinical development of TROP2-ADC combined with EGFR-TKI as a first-line strategy to delay TKI resistance and improve outcomes in EGFR-mutant NSCLC.</p>","PeriodicalId":9670,"journal":{"name":"Cancer Cell","volume":" ","pages":"1401-1417.e9"},"PeriodicalIF":56.1,"publicationDate":"2026-07-13","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148276229","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}
Cancer CellPub Date : 2026-07-13Epub Date: 2026-06-25DOI: 10.1016/j.ccell.2026.05.015
Ziv Shulman
{"title":"Intratumoral B cells under stress.","authors":"Ziv Shulman","doi":"10.1016/j.ccell.2026.05.015","DOIUrl":"10.1016/j.ccell.2026.05.015","url":null,"abstract":"<p><p>In this issue of Cancer Cell, Bashir et al. show that stress-induced corticosterone suppresses germinal center B cell responses and impairs anti-tumor immunity. Their study identifies gut microbiota-derived phage DNA as a key trigger of TLR9 activation and corticosterone secretion by cancer-associated fibroblasts, revealing an intricate bacteria-driven immune-suppression mechanism.</p>","PeriodicalId":9670,"journal":{"name":"Cancer Cell","volume":" ","pages":"1339-1340"},"PeriodicalIF":56.1,"publicationDate":"2026-07-13","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148327092","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}
Cancer CellPub Date : 2026-07-13Epub Date: 2026-05-07DOI: 10.1016/j.ccell.2026.04.007
Pierre Foidart, Zheqi Li, Xinran Cai, Marco Seehawer, Daniel D Brown, Amatullah Tawawalla, Pilar Baldominos, Salma Parvin, Jun Nishida, Ernesto Rojas-Jimenez, Triet M Bui, Benedetto Diciaccio, Rahul Kumar, Brent T Schlegel, Marie-Anne Goyette, TashJae Scales, Pengze Yan, Xintao Qiu, Rong Li, Yijia Jiang, Yingtian Xie, Mahmoud Aarabi, Xiao-Yun Huang, Laura E Stevens, Paloma Cejas, Lise Mangiante, Cristina Irene Sotomayor Vivas, Kathleen E Houlahan, Christina Curtis, Steffi Oesterreich, Isaac S Harris, Anthony G Letai, Adrian V Lee, Henry W Long, Judith Agudo, Kornelia Polyak
{"title":"Whole-genome doubling drives immune evasion by silencing antigen presentation.","authors":"Pierre Foidart, Zheqi Li, Xinran Cai, Marco Seehawer, Daniel D Brown, Amatullah Tawawalla, Pilar Baldominos, Salma Parvin, Jun Nishida, Ernesto Rojas-Jimenez, Triet M Bui, Benedetto Diciaccio, Rahul Kumar, Brent T Schlegel, Marie-Anne Goyette, TashJae Scales, Pengze Yan, Xintao Qiu, Rong Li, Yijia Jiang, Yingtian Xie, Mahmoud Aarabi, Xiao-Yun Huang, Laura E Stevens, Paloma Cejas, Lise Mangiante, Cristina Irene Sotomayor Vivas, Kathleen E Houlahan, Christina Curtis, Steffi Oesterreich, Isaac S Harris, Anthony G Letai, Adrian V Lee, Henry W Long, Judith Agudo, Kornelia Polyak","doi":"10.1016/j.ccell.2026.04.007","DOIUrl":"10.1016/j.ccell.2026.04.007","url":null,"abstract":"<p><p>Whole-genome doubling (WGD) is a common yet poorly understood event associated with poor clinical outcomes. Here, we characterize mechanisms by which WGD drives tumor evolution, utilizing mouse mammary tumor models of WGD established through cell fusion. We find that WGD increases transcriptomic and epigenetic heterogeneity and identify the YM155 BIRC5 inhibitor as a compound specifically suppressing WGD+ tumors. WGD triggers immune evasion by escaping CD8<sup>+</sup> T cell responses, rendering WGD+ tumors more sensitive to anti-PD-L1. Through single-cell profiling, we discover that WGD+ cancer cells exhibit reduced antigen presentation and response to IFNγ, attributed to the epigenetic silencing of MHCI transcriptional regulators via elevated histone H3 lysine 27 trimethylation. Further investigations reveal decreased KDM6 activity and increased succinate levels in WGD+ tumors. PRC2 inhibition preferentially suppresses WGD+ tumor growth, enhances antigen presentation, and CD8<sup>+</sup> T cell infiltration. Our results underscore metabolic and epigenetic alterations as critical drivers of WGD-associated immune escape.</p>","PeriodicalId":9670,"journal":{"name":"Cancer Cell","volume":" ","pages":"1418-1436.e12"},"PeriodicalIF":56.1,"publicationDate":"2026-07-13","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC13160227/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"147855948","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}
Cancer CellPub Date : 2026-07-13Epub Date: 2026-06-18DOI: 10.1016/j.ccell.2026.05.016
Alexander Birbrair, David J Simon, Sebastien Talbot, Shengtao Zhou
{"title":"Context dependency in cancer neuroscience.","authors":"Alexander Birbrair, David J Simon, Sebastien Talbot, Shengtao Zhou","doi":"10.1016/j.ccell.2026.05.016","DOIUrl":"10.1016/j.ccell.2026.05.016","url":null,"abstract":"<p><p>Neural signaling shapes tumor progression, but it is not intrinsically tumor-promoting or tumor-restrictive. We argue that neural directionality is context-dependent and governed by tumor kinetics, tissue architecture, neural state, receptor and target-cell topology, immune-host biology, and treatment history. We propose a mechanistically interpretable and clinically actionable reporting framework for precision neuromodulatory oncology.</p>","PeriodicalId":9670,"journal":{"name":"Cancer Cell","volume":" ","pages":"1321-1324"},"PeriodicalIF":56.1,"publicationDate":"2026-07-13","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148276208","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}
Cancer CellPub Date : 2026-07-13DOI: 10.1016/j.ccell.2026.06.005
Luigi Perelli, Giannicola Genovese, Nizar M Tannir
{"title":"Starved of oxygen and fueled by macrophages: Path to progression in RCC.","authors":"Luigi Perelli, Giannicola Genovese, Nizar M Tannir","doi":"10.1016/j.ccell.2026.06.005","DOIUrl":"10.1016/j.ccell.2026.06.005","url":null,"abstract":"<p><p>In this issue of Cancer Cell, Vuong et al. perform a cross-species functional and molecular analysis of the mechanisms of response and adaptation to VEGFR kinase inhibitors and immunotherapy, identifying SPP1<sup>+</sup> tumor-associated macrophages as key players of response to therapy. They further demonstrate that chronic treatment promotes metastatic spread.</p>","PeriodicalId":9670,"journal":{"name":"Cancer Cell","volume":"44 7","pages":"1330-1332"},"PeriodicalIF":56.1,"publicationDate":"2026-07-13","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148435236","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}
Cancer CellPub Date : 2026-07-13Epub Date: 2026-06-04DOI: 10.1016/j.ccell.2026.05.008
Julius C Enssle, Björn Häupl, Arber Qoku, Boya Wang, George W Wright, Sharon Barrans, Yulai Zhou, Matthew A Care, Cathy Burton, Caitlin Gribbin, Jennifer Ziello, Jason Weirather, Yibo Dai, Atish Kizhakeyil, Xubin Li, James D Phelan, Smriti Kanangat, Stephan Eckert, Sebastian Scheich, Sebastian Wolf, Da Wei Huang, Josefine Jakob, Sebastian P Perner, Andrea Di Fonzo, Martine Pape, Marion Bodach, Dominique Jahn, Uwe Plessmann, Annette M Staiger, German Ott, Philipp Berning, Georg Lenz, Daniel J Hodson, Bernhard Kuster, Roland Schmitz, Henning Urlaub, Michael R Green, Ari M Melnick, Reuben Tooze, Coraline Mlynarczyk, Giorgio Inghirami, Florian Buettner, Louis M Staudt, Thomas Oellerich
{"title":"Pathogenesis of diffuse large B cell lymphoma proteogenotypes.","authors":"Julius C Enssle, Björn Häupl, Arber Qoku, Boya Wang, George W Wright, Sharon Barrans, Yulai Zhou, Matthew A Care, Cathy Burton, Caitlin Gribbin, Jennifer Ziello, Jason Weirather, Yibo Dai, Atish Kizhakeyil, Xubin Li, James D Phelan, Smriti Kanangat, Stephan Eckert, Sebastian Scheich, Sebastian Wolf, Da Wei Huang, Josefine Jakob, Sebastian P Perner, Andrea Di Fonzo, Martine Pape, Marion Bodach, Dominique Jahn, Uwe Plessmann, Annette M Staiger, German Ott, Philipp Berning, Georg Lenz, Daniel J Hodson, Bernhard Kuster, Roland Schmitz, Henning Urlaub, Michael R Green, Ari M Melnick, Reuben Tooze, Coraline Mlynarczyk, Giorgio Inghirami, Florian Buettner, Louis M Staudt, Thomas Oellerich","doi":"10.1016/j.ccell.2026.05.008","DOIUrl":"10.1016/j.ccell.2026.05.008","url":null,"abstract":"<p><p>The clinical and molecular heterogeneity of diffuse large B cell lymphoma (DLBCL) is incompletely understood. By integrating proteomic, transcriptomic, and genomic data from 478 DLBCL tumors, we identify seven DLBCL proteogenotypes (PGs) reflecting specific pathophysiological features that span known molecular subtypes. PG4 is associated with poor outcome independent of established risk factors such as cell-of-origin, international prognostic index, or genetic features. PG4 contains activated B cell-like and germinal center B cell-like tumors and genetically unclassified cases. It shares a dark-zone-related B cell phenotype and shows enrichment for BTG1 mutations that can activate MYC. Single-cell sequencing and spatial transcriptomics reveal enhanced MYC and TCF3/4 transcriptional activity irrespective of MYC translocations. The PG4 tumor microenvironment is characterized by exhausted CD8<sup>+</sup> T cells. Our study identifies common oncogenic themes underlying high-risk DLBCL tumors and provides a proteogenomic framework for future diagnostic and therapeutic approaches.</p>","PeriodicalId":9670,"journal":{"name":"Cancer Cell","volume":" ","pages":"1437-1457.e14"},"PeriodicalIF":56.1,"publicationDate":"2026-07-13","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148161985","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}
Cancer CellPub Date : 2026-07-13Epub Date: 2026-05-07DOI: 10.1016/j.ccell.2026.04.005
Courtney T S Kureshi, Michael J Walsh, Rakeeb Kureshi, Victoire Cardot-Ruffino, Dennis A Agardy, Lestat R Ali, James M Dougan, Li Qiang, Jiao Shen, Chong Zuo, Patrick J Lenehan, S Jennifer Wang, Eugena Chang, Joshua Remland, Lauren Brais, Thomas E Clancy, James M Cleary, Jason L Hornick, Brandon M Huffman, Joseph D Mancias, George Molina, Mark Fairweather, Jonathan A Nowak, Kimberly J Perez, Douglas A Rubinson, Sarah Slater, Ritchell van Dams, Jiping Wang, Brian M Wolpin, Lei Zhao, Katharine Barrientos, Ruslan Novosiadly, Miranda Broz, Harshabad Singh, Michael Dougan, Stephanie K Dougan
{"title":"Dendritic cell redundancy enables priming of anti-tumor CD4<sup>+</sup> T cells in pancreatic cancer.","authors":"Courtney T S Kureshi, Michael J Walsh, Rakeeb Kureshi, Victoire Cardot-Ruffino, Dennis A Agardy, Lestat R Ali, James M Dougan, Li Qiang, Jiao Shen, Chong Zuo, Patrick J Lenehan, S Jennifer Wang, Eugena Chang, Joshua Remland, Lauren Brais, Thomas E Clancy, James M Cleary, Jason L Hornick, Brandon M Huffman, Joseph D Mancias, George Molina, Mark Fairweather, Jonathan A Nowak, Kimberly J Perez, Douglas A Rubinson, Sarah Slater, Ritchell van Dams, Jiping Wang, Brian M Wolpin, Lei Zhao, Katharine Barrientos, Ruslan Novosiadly, Miranda Broz, Harshabad Singh, Michael Dougan, Stephanie K Dougan","doi":"10.1016/j.ccell.2026.04.005","DOIUrl":"10.1016/j.ccell.2026.04.005","url":null,"abstract":"<p><p>Pancreatic ductal adenocarcinoma (PDAC) is resistant to current immunotherapies and lacks effective anti-tumor CD8<sup>+</sup> T cells, which is potentially due to insufficient cross-presentation by cDC1s. Here, we combine a STING agonist with anti-CTLA-4 and anti-PD-1 to achieve durable remissions and immunologic memory in multiple mouse models of poorly immunogenic PDAC. We find that tumor control does not depend on CD8<sup>+</sup> T cells or tumor cell MHC expression but instead requires IFNγ-producing CD4<sup>+</sup> T cells (Th1s) that are primed by dendritic cells in lymph nodes. The triple combination immunotherapy induces an accumulation of activated cDC2s carrying tumor antigen into tumor-draining lymph nodes; cDC2s are required for orthotopic tumor clearance. Intratumoral CD4<sup>+</sup> T cells and cDC2s remain present in treatment-naive and chemotherapy-exposed human PDAC. In chemotherapy-exposed patients' blood, cDC2s outnumber cDC1s by 10-fold. Therefore, therapeutic targeting of the cDC2-CD4<sup>+</sup> T cell-IFNγ axis could be efficacious in PDAC.</p>","PeriodicalId":9670,"journal":{"name":"Cancer Cell","volume":" ","pages":"1381-1400.e9"},"PeriodicalIF":56.1,"publicationDate":"2026-07-13","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC13430408/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"147855946","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}
Cancer CellPub Date : 2026-07-13Epub Date: 2026-06-11DOI: 10.1016/j.ccell.2026.05.010
Mark White, Andrew D Campbell, Owen J Sansom
{"title":"The cartography of KRAS inhibitor resistance in colorectal cancer.","authors":"Mark White, Andrew D Campbell, Owen J Sansom","doi":"10.1016/j.ccell.2026.05.010","DOIUrl":"10.1016/j.ccell.2026.05.010","url":null,"abstract":"<p><p>In this issue of Cancer Cell, Alonso et al. demonstrate that in patients with advanced colorectal cancer, there are regionally distinct genomic and transcriptomic adaptive responses to KRAS G12C inhibition, including epithelial cell state changes and pro-inflammatory pathway enrichment, and provide insights into key resistance mechanisms to KRAS G12C inhibition.</p>","PeriodicalId":9670,"journal":{"name":"Cancer Cell","volume":" ","pages":"1336-1338"},"PeriodicalIF":56.1,"publicationDate":"2026-07-13","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148223446","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}
Cancer CellPub Date : 2026-07-13Epub Date: 2026-05-21DOI: 10.1016/j.ccell.2026.04.009
Salvador Alonso, Kevan Chu, Elizabeth Granowsky, Valeria Saraiba Rabanales, Marie J Parsons, Himari Gunasinghe, Jinru Shia, Rona Yaeger, Lukas E Dow
{"title":"Concurrent genetic and non-genetic resistance mechanisms to KRAS inhibition in colorectal cancer.","authors":"Salvador Alonso, Kevan Chu, Elizabeth Granowsky, Valeria Saraiba Rabanales, Marie J Parsons, Himari Gunasinghe, Jinru Shia, Rona Yaeger, Lukas E Dow","doi":"10.1016/j.ccell.2026.04.009","DOIUrl":"10.1016/j.ccell.2026.04.009","url":null,"abstract":"<p><p>KRAS is mutationally activated in 45%-50% of colorectal cancer (CRC) cases, and while KRAS-targeted therapies have shown clinical promise, drug resistance limits their efficacy. To explore the mechanisms underlying KRAS inhibitor resistance, we use targeted exome sequencing and spatial transcriptomics on patient-matched CRC biopsies following combined treatment with KRAS<sup>G12C</sup> and EGFR inhibitors. We show that acquired genetic events are identified in most patients at progression but are often subclonal and coexist with transcriptional adaptive states. Mesenchymal, YAP, and fetal-like transcriptional signatures predominate in resistant tumors, while inflammatory programs are induced early on treatment. Single-cell spatial analysis reveals intratumoral heterogeneity, with diverse adaptive states in different zones of individual tumors. Using human and murine organoid models, we show that drug-induced inflammatory programs are, at least in part, cancer-cell autonomous, and precede the emergence of drug resistance. We identify TBK1 as a target to abrogate the inflammatory adaptive phase and enhance responses to KRAS inhibition.</p>","PeriodicalId":9670,"journal":{"name":"Cancer Cell","volume":" ","pages":"1368-1380.e8"},"PeriodicalIF":56.1,"publicationDate":"2026-07-13","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC13417870/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"147986587","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}
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