{"title":"Refining the 8th edition TNM classification for EBV related nasopharyngeal carcinoma.","authors":"Xiao-Jing Du, Gao-Yuan Wang, Xiao-Dong Zhu, Ya-Qian Han, Feng Lei, Liang-Fang Shen, Kun-Yu Yang, Lei Chen, Yan-Ping Mao, Ling-Long Tang, Ling Li, Zheng Wu, Gui-Qiong Xu, Qin Zhou, Jing Huang, Rui Guo, Yuan Zhang, Xu Liu, Guan-Qun Zhou, Wen-Fei Li, Cheng Xu, Li Lin, Yu-Pei Chen, Fo-Ping Chen, Xiao-Yu Liang, Si-Yuan Chen, Shu-Qi Li, Chun-Yan Cui, Ji-Bin Li, Jian Ren, Ming-Yuan Chen, Li-Zhi Liu, Ying Sun, Jun Ma","doi":"10.1016/j.ccell.2023.12.020","DOIUrl":"10.1016/j.ccell.2023.12.020","url":null,"abstract":"<p><p>The AJCC/UICC TNM classification describes anatomic extent of tumor progression and guides treatment decisions. Our comprehensive analysis of 8,834 newly diagnosed patients with non-metastatic Epstein-Barr virus related nasopharyngeal carcinoma (NPC) from six Chinese centers indicates certain limitations in the current staging system. The 8th edition of the AJCC/UICC TNM classification inadequately differentiates patient outcomes, particularly between T2 and T3 categories and within the N classification. We propose reclassifying cases of T3 NPC with early skull-base invasion as T2, and elevating N1-N2 cases with grade 3 image-identified extranodal extension (ENE) to N3. Additionally, we suggest combining T2N0 with T1N0 into a single stage IA. For de novo metastatic (M1) NPC, we propose subdivisions of M1a, defined by 1-3 metastatic lesions without liver involvement, and M1b, characterized by >3 metastatic lesions or liver involvement. This proposal better reflects responses of NPC patients to the up-to-date treatments and their evolving risk profiles.</p>","PeriodicalId":9670,"journal":{"name":"Cancer Cell","volume":" ","pages":"464-473.e3"},"PeriodicalIF":50.3,"publicationDate":"2024-03-11","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"139502207","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 : 2024-03-11Epub Date: 2024-01-18DOI: 10.1016/j.ccell.2023.12.018
Leire Bejarano, Annamaria Kauzlaric, Eleni Lamprou, Joao Lourenco, Nadine Fournier, Michelle Ballabio, Roberto Colotti, Roeltje Maas, Sabine Galland, Matteo Massara, Klara Soukup, Johanna Lilja, Jean-Philippe Brouland, Andreas F Hottinger, Roy T Daniel, Monika E Hegi, Johanna A Joyce
{"title":"Interrogation of endothelial and mural cells in brain metastasis reveals key immune-regulatory mechanisms.","authors":"Leire Bejarano, Annamaria Kauzlaric, Eleni Lamprou, Joao Lourenco, Nadine Fournier, Michelle Ballabio, Roberto Colotti, Roeltje Maas, Sabine Galland, Matteo Massara, Klara Soukup, Johanna Lilja, Jean-Philippe Brouland, Andreas F Hottinger, Roy T Daniel, Monika E Hegi, Johanna A Joyce","doi":"10.1016/j.ccell.2023.12.018","DOIUrl":"10.1016/j.ccell.2023.12.018","url":null,"abstract":"<p><p>Brain metastasis (BrM) is a common malignancy, predominantly originating from lung, melanoma, and breast cancers. The vasculature is a key component of the BrM tumor microenvironment with critical roles in regulating metastatic seeding and progression. However, the heterogeneity of the major BrM vascular components, namely endothelial and mural cells, is still poorly understood. We perform single-cell and bulk RNA-sequencing of sorted vascular cell types and detect multiple subtypes enriched specifically in BrM compared to non-tumor brain, including previously unrecognized immune regulatory subtypes. We integrate the human data with mouse models, creating a platform to interrogate vascular targets for the treatment of BrM. We find that the CD276 immune checkpoint molecule is significantly upregulated in the BrM vasculature, and anti-CD276 blocking antibodies prolonged survival in preclinical trials. This study provides important insights into the complex interactions between the vasculature, immune cells, and cancer cells, with translational relevance for designing therapeutic interventions.</p>","PeriodicalId":9670,"journal":{"name":"Cancer Cell","volume":" ","pages":"378-395.e10"},"PeriodicalIF":50.3,"publicationDate":"2024-03-11","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"139502195","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 : 2024-01-11DOI: 10.1016/j.ccell.2023.12.019
James D. Phelan, Sebastian Scheich, Jaewoo Choi, George W. Wright, Björn Häupl, Ryan M. Young, Sara A. Rieke, Martine Pape, Yanlong Ji, Henning Urlaub, Arnold Bolomsky, Carmen Doebele, Alena Zindel, Tanja Wotapek, Monica Kasbekar, Brett Collinge, Da Wei Huang, Zana A. Coulibaly, Vivian M. Morris, Xiaoxuan Zhuang, Thomas Oellerich
{"title":"Response to Bruton’s tyrosine kinase inhibitors in aggressive lymphomas linked to chronic selective autophagy","authors":"James D. Phelan, Sebastian Scheich, Jaewoo Choi, George W. Wright, Björn Häupl, Ryan M. Young, Sara A. Rieke, Martine Pape, Yanlong Ji, Henning Urlaub, Arnold Bolomsky, Carmen Doebele, Alena Zindel, Tanja Wotapek, Monica Kasbekar, Brett Collinge, Da Wei Huang, Zana A. Coulibaly, Vivian M. Morris, Xiaoxuan Zhuang, Thomas Oellerich","doi":"10.1016/j.ccell.2023.12.019","DOIUrl":"https://doi.org/10.1016/j.ccell.2023.12.019","url":null,"abstract":"<p><span>Diffuse large B cell lymphoma<span><span> (DLBCL) is an aggressive, profoundly heterogeneous cancer, presenting a challenge for precision medicine. Bruton’s tyrosine kinase (BTK) inhibitors block B cell receptor (BCR) signaling and are particularly effective in certain molecular subtypes of DLBCL that rely on chronic active BCR signaling to promote oncogenic NF-κB. The MCD </span>genetic subtype, which often acquires mutations in the BCR subunit, CD79B, and in the innate immune adapter, MYD88</span></span><sup>L265P</sup><span>, typically resists chemotherapy but responds exceptionally to BTK inhibitors. However, the underlying mechanisms of response to BTK inhibitors are poorly understood. Herein, we find a non-canonical form of chronic selective autophagy in MCD DLBCL that targets ubiquitinated MYD88</span><sup>L265P</sup><span> for degradation in a TBK1-dependent manner. MCD tumors acquire genetic and epigenetic alterations that attenuate this autophagic tumor suppressive pathway. In contrast, BTK inhibitors promote autophagic degradation of MYD88</span><sup>L265P</sup>, thus explaining their exceptional clinical benefit in MCD DLBCL.</p>","PeriodicalId":9670,"journal":{"name":"Cancer Cell","volume":"20 1","pages":""},"PeriodicalIF":50.3,"publicationDate":"2024-01-11","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"139420281","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 : 2024-01-11DOI: 10.1016/j.ccell.2023.12.013
Danish Memon, Adam J. Schoenfeld, Darwin Ye, George Fromm, Hira Rizvi, Xiang Zhang, Mohamed Reda Keddar, Divij Mathew, Kyung Jin Yoo, Jingya Qiu, Jayon Lihm, Jayalaksmi Miriyala, Jennifer L. Sauter, Jia Luo, Andrew Chow, Umesh K. Bhanot, Caroline McCarthy, Chad M. Vanderbilt, Cailian Liu, Mohsen Abu-Akeel, Matthew D. Hellmann
{"title":"Clinical and molecular features of acquired resistance to immunotherapy in non-small cell lung cancer","authors":"Danish Memon, Adam J. Schoenfeld, Darwin Ye, George Fromm, Hira Rizvi, Xiang Zhang, Mohamed Reda Keddar, Divij Mathew, Kyung Jin Yoo, Jingya Qiu, Jayon Lihm, Jayalaksmi Miriyala, Jennifer L. Sauter, Jia Luo, Andrew Chow, Umesh K. Bhanot, Caroline McCarthy, Chad M. Vanderbilt, Cailian Liu, Mohsen Abu-Akeel, Matthew D. Hellmann","doi":"10.1016/j.ccell.2023.12.013","DOIUrl":"https://doi.org/10.1016/j.ccell.2023.12.013","url":null,"abstract":"<p>Although immunotherapy with PD-(L)1 blockade is routine for lung cancer, little is known about acquired resistance. Among 1,201 patients with non-small cell lung cancer (NSCLC) treated with PD-(L)1 blockade, acquired resistance is common, occurring in >60% of initial responders. Acquired resistance shows differential expression of inflammation and interferon (IFN) signaling. Relapsed tumors can be separated by upregulated or stable expression of IFNγ response genes. Upregulation of IFNγ response genes is associated with putative routes of resistance characterized by signatures of persistent IFN signaling, immune dysfunction, and mutations in antigen presentation genes which can be recapitulated in multiple murine models of acquired resistance to PD-(L)1 blockade after <em>in vitro</em> IFNγ treatment. Acquired resistance to PD-(L)1 blockade in NSCLC is associated with an ongoing, but altered IFN response. The persistently inflamed, rather than excluded or deserted, tumor microenvironment of acquired resistance may inform therapeutic strategies to effectively reprogram and reverse acquired resistance.</p>","PeriodicalId":9670,"journal":{"name":"Cancer Cell","volume":"51 1","pages":""},"PeriodicalIF":50.3,"publicationDate":"2024-01-11","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"139420317","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 : 2024-01-08DOI: 10.1016/j.ccell.2023.12.010
Mirjam E. Hoekstra, Maarten Slagter, Jos Urbanus, Mireille Toebes, Nadine Slingerland, Iris de Rink, Roelof J.C. Kluin, Marja Nieuwland, Ron Kerkhoven, Lodewyk F.A. Wessels, Ton N. Schumacher
{"title":"Distinct spatiotemporal dynamics of CD8+ T cell-derived cytokines in the tumor microenvironment","authors":"Mirjam E. Hoekstra, Maarten Slagter, Jos Urbanus, Mireille Toebes, Nadine Slingerland, Iris de Rink, Roelof J.C. Kluin, Marja Nieuwland, Ron Kerkhoven, Lodewyk F.A. Wessels, Ton N. Schumacher","doi":"10.1016/j.ccell.2023.12.010","DOIUrl":"https://doi.org/10.1016/j.ccell.2023.12.010","url":null,"abstract":"<p>Cells in the tumor microenvironment (TME) influence each other through secretion and sensing of soluble mediators, such as cytokines and chemokines. While signaling of interferon γ (IFNγ) and tumor necrosis factor α (TNFα) is integral to anti-tumor immune responses, our understanding of the spatiotemporal behavior of these cytokines is limited. Here, we describe a single cell transcriptome-based approach to infer which signal(s) an individual cell has received. We demonstrate that, contrary to expectations, CD8<sup>+</sup> T cell-derived IFNγ is the dominant modifier of the TME relative to TNFα. Furthermore, we demonstrate that cell pools that show abundant IFNγ sensing are characterized by decreased expression of transforming growth factor β (TGFβ)-induced genes, consistent with IFNγ-mediated TME remodeling. Collectively, these data provide evidence that CD8<sup>+</sup> T cell-secreted cytokines should be categorized into local and global tissue modifiers, and describe a broadly applicable approach to dissect cytokine and chemokine modulation of the TME.</p>","PeriodicalId":9670,"journal":{"name":"Cancer Cell","volume":"9 1","pages":""},"PeriodicalIF":50.3,"publicationDate":"2024-01-08","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"139379756","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 : 2024-01-08Epub Date: 2023-12-28DOI: 10.1016/j.ccell.2023.12.006
Vidhi Chandra, Le Li, Olivereen Le Roux, Yu Zhang, Rian M Howell, Dhwani N Rupani, Seyda Baydogan, Haiyan D Miller, Erick Riquelme, Joseph Petrosino, Michael P Kim, Krishna P L Bhat, James R White, Jay K Kolls, Yuliya Pylayeva-Gupta, Florencia McAllister
{"title":"Gut epithelial Interleukin-17 receptor A signaling can modulate distant tumors growth through microbial regulation.","authors":"Vidhi Chandra, Le Li, Olivereen Le Roux, Yu Zhang, Rian M Howell, Dhwani N Rupani, Seyda Baydogan, Haiyan D Miller, Erick Riquelme, Joseph Petrosino, Michael P Kim, Krishna P L Bhat, James R White, Jay K Kolls, Yuliya Pylayeva-Gupta, Florencia McAllister","doi":"10.1016/j.ccell.2023.12.006","DOIUrl":"10.1016/j.ccell.2023.12.006","url":null,"abstract":"<p><p>Microbes influence cancer initiation, progression and therapy responsiveness. IL-17 signaling contributes to gut barrier immunity by regulating microbes but also drives tumor growth. A knowledge gap remains regarding the influence of enteric IL-17-IL-17RA signaling and their microbial regulation on the behavior of distant tumors. We demonstrate that gut dysbiosis induced by systemic or gut epithelial deletion of IL-17RA induces growth of pancreatic and brain tumors due to excessive development of Th17, primary source of IL-17 in human and mouse pancreatic ductal adenocarcinoma, as well as B cells that circulate to distant tumors. Microbial dependent IL-17 signaling increases DUOX2 signaling in tumor cells. Inefficacy of pharmacological inhibition of IL-17RA is overcome with targeted microbial ablation that blocks the compensatory loop. These findings demonstrate the complexities of IL-17-IL-17RA signaling in different compartments and the relevance for accounting for its homeostatic host defense function during cancer therapy.</p>","PeriodicalId":9670,"journal":{"name":"Cancer Cell","volume":" ","pages":"85-100.e6"},"PeriodicalIF":48.8,"publicationDate":"2024-01-08","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11238637/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"139073440","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 : 2024-01-08DOI: 10.1016/j.ccell.2023.12.009
Simona F Shaitelman, Wendy A Woodward
{"title":"Neoadjuvant radioimmunotherapy synergy in triple-negative breast cancer: Is microenvironment-guided patient selection on the horizon?","authors":"Simona F Shaitelman, Wendy A Woodward","doi":"10.1016/j.ccell.2023.12.009","DOIUrl":"10.1016/j.ccell.2023.12.009","url":null,"abstract":"<p><p>Neoadjuvant chemotherapy plus immunotherapy for triple-negative breast cancer (TNBC) is associated with improved but incomplete response. In this issue of Cancer Cell, Shiao et al. characterize longitudinal biopsies from a window of opportunity study with single-cell RNA sequencing (scRNA-seq) and spatial proteomic profiling and elucidate synergy between radiotherapy (RT) and pembrolizumab.</p>","PeriodicalId":9670,"journal":{"name":"Cancer Cell","volume":"42 1","pages":"10-12"},"PeriodicalIF":50.3,"publicationDate":"2024-01-08","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"139402025","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 : 2024-01-04DOI: 10.1016/j.ccell.2023.12.007
Jessica A. Lavery, Paul C. Boutros, Daniel Knight, Tuomas Tammela, Chaya S. Moskowitz, Lee W. Jones
{"title":"Association of exercise with pan-cancer incidence and overall survival","authors":"Jessica A. Lavery, Paul C. Boutros, Daniel Knight, Tuomas Tammela, Chaya S. Moskowitz, Lee W. Jones","doi":"10.1016/j.ccell.2023.12.007","DOIUrl":"https://doi.org/10.1016/j.ccell.2023.12.007","url":null,"abstract":"Abstract not available","PeriodicalId":9670,"journal":{"name":"Cancer Cell","volume":"35 1","pages":""},"PeriodicalIF":50.3,"publicationDate":"2024-01-04","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"139091978","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":"A global phase 3 study of serplulimab plus chemotherapy as first-line treatment for advanced squamous non-small-cell lung cancer (ASTRUM-004)","authors":"Caicun Zhou, Yanping Hu, Ekaterine Arkania, Saadettin Kilickap, Kejing Ying, Fei Xu, Lin Wu, Xiang Wang, Maksym Viguro, Tamta Makharadze, Hongmei Sun, Feng Luo, Jianhua Shi, Aimin Zang, Yueyin Pan, Zhendong Chen, Zhongyao Jia, Vladimer Kuchava, Ping Lu, Ling Zhang, Jun Zhu","doi":"10.1016/j.ccell.2023.12.004","DOIUrl":"https://doi.org/10.1016/j.ccell.2023.12.004","url":null,"abstract":"<p><span>Combining immunotherapy with chemotherapy can provide improved survival in advanced squamous non-small-cell lung cancer (NSCLC) patients without targetable gene alterations. 537 previously untreated patients with stage IIIB/IIIC or IV squamous NSCLC without targetable gene alterations were enrolled and randomized (2:1) to receive serplulimab 4.5 mg/kg or placebo, both in combination with nab-paclitaxel and </span>carboplatin, intravenously in 3-week cycles. The primary endpoint of progression-free survival (PFS) was met at the first interim analysis. At the second interim analysis, PFS benefit was maintained in serplulimab-chemotherapy group (hazard ratio [HR] 0.53, 95% confidence interval [CI] 0.42–0.67). At the final analysis, serplulimab-chemotherapy significantly improved median OS compared to placebo-chemotherapy (HR 0.73, 95% CI 0.58–0.93; p = 0.010). Grade ≥3 serplulimab or placebo-related adverse events occurred in 126 (35.2%) and 58 (32.4%) patients, respectively. Our results demonstrate that adding serplulimab to chemotherapy significantly improves survival in advanced squamous NSCLC patients, with manageable safety.</p>","PeriodicalId":9670,"journal":{"name":"Cancer Cell","volume":"18 1","pages":""},"PeriodicalIF":50.3,"publicationDate":"2024-01-04","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"139092035","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 : 2024-01-04DOI: 10.1016/j.ccell.2023.12.005
Madeleine Benguigui, Tim J. Cooper, Prajakta Kalkar, Sagie Schif-Zuck, Ruth Halaban, Antonella Bacchiocchi, Iris Kamer, Abhilash Deo, Bar Manobla, Rotem Menachem, Jozafina Haj-Shomaly, Avital Vorontsova, Ziv Raviv, Chen Buxbaum, Petros Christopoulos, Jair Bar, Michal Lotem, Mario Sznol, Amiram Ariel, Shai S. Shen-Orr, Yuval Shaked
{"title":"Interferon-stimulated neutrophils as a predictor of immunotherapy response","authors":"Madeleine Benguigui, Tim J. Cooper, Prajakta Kalkar, Sagie Schif-Zuck, Ruth Halaban, Antonella Bacchiocchi, Iris Kamer, Abhilash Deo, Bar Manobla, Rotem Menachem, Jozafina Haj-Shomaly, Avital Vorontsova, Ziv Raviv, Chen Buxbaum, Petros Christopoulos, Jair Bar, Michal Lotem, Mario Sznol, Amiram Ariel, Shai S. Shen-Orr, Yuval Shaked","doi":"10.1016/j.ccell.2023.12.005","DOIUrl":"https://doi.org/10.1016/j.ccell.2023.12.005","url":null,"abstract":"<p>Despite the remarkable success of anti-cancer immunotherapy, its effectiveness remains confined to a subset of patients—emphasizing the importance of predictive biomarkers in clinical decision-making and further mechanistic understanding of treatment response. Current biomarkers, however, lack the power required to accurately stratify patients. Here, we identify interferon-stimulated, Ly6E<sup>hi</sup> neutrophils as a blood-borne biomarker of anti-PD1 response in mice at baseline. Ly6E<sup>hi</sup> neutrophils are induced by tumor-intrinsic activation of the STING (stimulator of interferon genes) signaling pathway and possess the ability to directly sensitize otherwise non-responsive tumors to anti-PD1 therapy, in part through IL12b-dependent activation of cytotoxic T cells. By translating our pre-clinical findings to a cohort of patients with non-small cell lung cancer and melanoma (n = 109), and to public data (n = 1440), we demonstrate the ability of Ly6E<sup>hi</sup> neutrophils to predict immunotherapy response in humans with high accuracy (average AUC ≈ 0.9). Overall, our study identifies a functionally active biomarker for use in both mice and humans.</p>","PeriodicalId":9670,"journal":{"name":"Cancer Cell","volume":"55 1","pages":""},"PeriodicalIF":50.3,"publicationDate":"2024-01-04","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"139091941","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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