Nature cancerPub Date : 2025-07-08DOI: 10.1038/s43018-025-01017-x
Ralph J. DeBerardinis
{"title":"An unexpected career in cancer metabolism","authors":"Ralph J. DeBerardinis","doi":"10.1038/s43018-025-01017-x","DOIUrl":"10.1038/s43018-025-01017-x","url":null,"abstract":"Ralph DeBerardinis obtained an MD and PhD from the University of Pennsylvania, then trained in Pediatrics and Medical Genetics at Children’s Hospital of Philadelphia. He moved to the University of Texas Southwestern Medical Center (UTSW) in 2008, serving as Chief of Pediatric Genetics and Metabolism from 2013 to 2024. He became an Investigator in the Howard Hughes Medical Institute in 2018 and was elected to the National Academy of Medicine in 2020. DeBerardinis’s current roles at UTSW include directing the Eugene McDermott Center for Human Growth and Development and the Genetic and Metabolic Disease Program in the Children’s Research Institute.","PeriodicalId":18885,"journal":{"name":"Nature cancer","volume":"6 8","pages":"1297-1298"},"PeriodicalIF":28.5,"publicationDate":"2025-07-08","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144591823","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 : 2025-07-07DOI: 10.1038/s43018-025-01007-z
Giulia Petroni, Claudia Galassi, Kenneth H Gouin, Hsiang-Han Chen, Aitziber Buqué, Norma Bloy, Takahiro Yamazaki, Ai Sato, Manuel Beltrán-Visiedo, Ginevra Campia, Carlos Jiménez-Cortegana, Aagam Shah, Alexander Kirchmair, Chiara Massa, Claudia Wickenhauser, Carlos Eduardo de Andrea, Belén Navarro-Rubio, Irantzu Serrano-Mendioroz, Esther Navarro Manzano, Alexandra M Satty, Brady Rippon, Francesca Finotello, Zlatko Trajanoski, Xi Kathy Zhou, Joseph M Scandura, Elena García-Martínez, Francisco Ayala de la Peña, María Esperanza Rodríguez-Ruiz, Barbara Seliger, Víctor Sánchez-Margalet, Luis de la Cruz-Merino, Reva K Basho, Stephen L Shiao, Heather L McArthur, Silvia C Formenti, Simon R V Knott, Lorenzo Galluzzi
{"title":"IL-17A-secreting γδ T cells promote resistance to CDK4/CDK6 inhibitors in HR<sup>+</sup>HER2<sup>-</sup> breast cancer via CX3CR1<sup>+</sup> macrophages.","authors":"Giulia Petroni, Claudia Galassi, Kenneth H Gouin, Hsiang-Han Chen, Aitziber Buqué, Norma Bloy, Takahiro Yamazaki, Ai Sato, Manuel Beltrán-Visiedo, Ginevra Campia, Carlos Jiménez-Cortegana, Aagam Shah, Alexander Kirchmair, Chiara Massa, Claudia Wickenhauser, Carlos Eduardo de Andrea, Belén Navarro-Rubio, Irantzu Serrano-Mendioroz, Esther Navarro Manzano, Alexandra M Satty, Brady Rippon, Francesca Finotello, Zlatko Trajanoski, Xi Kathy Zhou, Joseph M Scandura, Elena García-Martínez, Francisco Ayala de la Peña, María Esperanza Rodríguez-Ruiz, Barbara Seliger, Víctor Sánchez-Margalet, Luis de la Cruz-Merino, Reva K Basho, Stephen L Shiao, Heather L McArthur, Silvia C Formenti, Simon R V Knott, Lorenzo Galluzzi","doi":"10.1038/s43018-025-01007-z","DOIUrl":"10.1038/s43018-025-01007-z","url":null,"abstract":"<p><p>Resistance to cyclin-dependent kinase 4/6 (CDK4/CDK6) inhibitors leads to treatment failure and disease progression in women with hormone receptor<sup>+</sup>HER2<sup>-</sup> (HR<sup>+</sup>HER2<sup>-</sup>) breast cancer (BC). We delineated a hypoxia-sensitive, CCL2-dependent pathway recruiting interleukin-17A (IL-17A)-secreting γδ T cells to mouse HR<sup>+</sup>HER2<sup>-</sup> BCs following CDK4/CDK6 inhibition, resulting in repolarization of tumor-associated macrophages (TAMs) toward an immunosuppressive CX3CR1<sup>+</sup> phenotype associated with resistance. Increased IL-17A signaling and intratumoral γδ T cell abundance positively correlated with advanced grade and/or reduced survival in two cohorts of individuals with HR<sup>+</sup>HER2<sup>-</sup> BC. Circulating γδ T cells and plasma CCL2 levels negatively correlated with progression in an independent series of individuals with HR<sup>+</sup>HER2<sup>-</sup> BC receiving CDK4/CDK6 inhibitors. Intratumoral γδ T cells were increased in post- versus pretreatment biopsies from individuals with HR<sup>+</sup>HER2<sup>-</sup> BC relapsing on CDK4/CDK6 inhibitors. CX3CR1<sup>+</sup> TAMs had negative prognostic impact in women with HR<sup>+</sup>HER2<sup>-</sup> BC receiving neoadjuvant PD-1 blockage and radiotherapy. Thus, γδ T cells and CX3XR1<sup>+</sup> TAMs may favor resistance to CDK4/CDK6 inhibitors in individuals with HR<sup>+</sup>HER2<sup>-</sup> BC.</p>","PeriodicalId":18885,"journal":{"name":"Nature cancer","volume":" ","pages":""},"PeriodicalIF":23.5,"publicationDate":"2025-07-07","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144584367","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 : 2025-07-04DOI: 10.1038/s43018-025-01016-y
David Cibula, Simone Marnitz, Jiří Jarkovský, Roman Kocián, Pavel Dundr, Jaroslav Klát, Ignacio Zapardiel, Octavio Arencibia, Fabio Landoni, Jiri Presl, Francesco Raspagliesi, Michal Zikán, Luc RCW van Lonkhuijzen, Aureli Torne, Jiří Sláma, Lubos Minar, Marcela Ostojich, Radovan Pilka, Almerinda Ferreira Petiz, Anja Petzel, Andrea Burgetová, Daniela Fischerová, Kristyna Nemejcova, Christhardt Köhler
{"title":"Sentinel lymph node biopsy without systematic pelvic lymphadenectomy in females with early-stage cervical cancer: final outcome of the SENTIX prospective, single-arm, noninferiority, international trial","authors":"David Cibula, Simone Marnitz, Jiří Jarkovský, Roman Kocián, Pavel Dundr, Jaroslav Klát, Ignacio Zapardiel, Octavio Arencibia, Fabio Landoni, Jiri Presl, Francesco Raspagliesi, Michal Zikán, Luc RCW van Lonkhuijzen, Aureli Torne, Jiří Sláma, Lubos Minar, Marcela Ostojich, Radovan Pilka, Almerinda Ferreira Petiz, Anja Petzel, Andrea Burgetová, Daniela Fischerová, Kristyna Nemejcova, Christhardt Köhler","doi":"10.1038/s43018-025-01016-y","DOIUrl":"10.1038/s43018-025-01016-y","url":null,"abstract":"Sentinel lymph node (SLN) biopsy with ultrastaging is standard in endometrial and vulvar cancers, whereas systematic pelvic lymphadenectomy (PLND) remains recommended in cervical cancer. The SENTIX trial prospectively evaluated the safety of SLN biopsy without PLND in early-stage cervical cancer. Female patients, International Federation of Gynaecology and Obstetrics 2018 stage IA1/LVSI+ to IB2 disease, were enrolled between 2016 and 2020 across 47 sites in 18 countries. All underwent SLN biopsy followed by hysterectomy/trachelectomy. Patients with undetected, unilateral or intraoperatively metastatic SLNs were excluded from the intention-to-treat cohort. SLNs were assessed by pathological ultrastaging. Of 731 patients enrolled, 594 formed the intention-to-treat cohort. SLN metastases were identified in 82 patients (12%), 56.1% intraoperatively and 43.9% by ultrastaging. At 2 years, the recurrence rate was 6.1% (one-sided 95% CI 7.9%), confirming noninferiority to the 7% reference rate. Two-year disease-free and overall survival rates were 93.3% (95% CI 94.9–91.6) and 97.9% (95% CI 98.9–97.0), respectively. Here we show that SLN biopsy without systematic PLND did not increase the risk of recurrence in patients with early-stage cervical cancer. Pathological ultrastaging of SLNs detected about 44% of N1 cases, which would be missed by a standard lymph node assessment. Trial registration: ClinicalTrials.gov ( NCT02494063 ). Cibula et al. present survival results of the SENTIX trial and demonstrate that SLN biopsy alone does not increase the risk of disease recurrence in patients with early-stage cervical cancer.","PeriodicalId":18885,"journal":{"name":"Nature cancer","volume":"6 9","pages":"1585-1594"},"PeriodicalIF":28.5,"publicationDate":"2025-07-04","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144564970","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 : 2025-07-02DOI: 10.1038/s43018-025-01011-3
Sarah-Maria Fendt
{"title":"Will it be a turning point?","authors":"Sarah-Maria Fendt","doi":"10.1038/s43018-025-01011-3","DOIUrl":"10.1038/s43018-025-01011-3","url":null,"abstract":"Sarah-Maria Fendt received her doctoral degree from ETH Zurich, Switzerland, and she conducted her postdoctoral research at the Massachusetts Institute of Technology, USA. She is currently a principal investigator at the VIB Center for Cancer Biology and a full professor at KU Leuven, Belgium.","PeriodicalId":18885,"journal":{"name":"Nature cancer","volume":"6 7","pages":"1121-1121"},"PeriodicalIF":28.5,"publicationDate":"2025-07-02","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144554021","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 : 2025-06-30DOI: 10.1038/s43018-025-01004-2
Edith Borcoman, Bastien Cabarrou, Miguel Francisco, Frédéric Bigot, François Ghiringhelli, Damien Vansteene, François Legrand, Maral Halladjian, Célia Dupain, Olivia Le Saux, Clelia Coutzac, Christian Borel, Raphael Chaltiel, Benoit You, Carlos Gomez-Roca, Sophie Cousin, Elodie Coquan, Aurélien Lambert, Esma Saada-Bouzid, Xavier Durando, Mathilde Saint-Ghislain, Gianmaria Frige, Elena Guerini-Rocco, Maria Manuela Tonini, Ivan Bièche, Zahra Castel-Ajgal, Grégoire Marret, Marie-Paule Sablin, Emmanuelle Jeannot, Fabrice Andre, Thomas Filleron, Marta Jimenez, Luca Mazzarella, Nicolas Servant, Maud Kamal, Christophe Le Tourneau
{"title":"Efficacy of pembrolizumab and vorinostat combination in patients with recurrent and/or metastatic squamous cell carcinomas: a phase 2 basket trial","authors":"Edith Borcoman, Bastien Cabarrou, Miguel Francisco, Frédéric Bigot, François Ghiringhelli, Damien Vansteene, François Legrand, Maral Halladjian, Célia Dupain, Olivia Le Saux, Clelia Coutzac, Christian Borel, Raphael Chaltiel, Benoit You, Carlos Gomez-Roca, Sophie Cousin, Elodie Coquan, Aurélien Lambert, Esma Saada-Bouzid, Xavier Durando, Mathilde Saint-Ghislain, Gianmaria Frige, Elena Guerini-Rocco, Maria Manuela Tonini, Ivan Bièche, Zahra Castel-Ajgal, Grégoire Marret, Marie-Paule Sablin, Emmanuelle Jeannot, Fabrice Andre, Thomas Filleron, Marta Jimenez, Luca Mazzarella, Nicolas Servant, Maud Kamal, Christophe Le Tourneau","doi":"10.1038/s43018-025-01004-2","DOIUrl":"10.1038/s43018-025-01004-2","url":null,"abstract":"Immune checkpoint inhibitors improve the treatment of many solid tumors and have shown encouraging results in advanced squamous cell carcinoma (SCC), yet only a minority of patients respond to immune checkpoint inhibitor monotherapy. We conducted the PEVOsq trial, an open-label, nonrandomized, multicenter, basket phase 2 trial to evaluate the combination of pembrolizumab and vorinostat in recurrent/metastatic SCC of various origins. The primary endpoint was the objective response rate (ORR) in each tumor cohort during treatment as per the investigators’ assessment. Secondary endpoints included safety and antitumor activity evaluation in terms of centrally confirmed ORR, progression-free survival, overall survival and duration of response. In the efficacy population (n = 107), the ORR was met in cervical (39%), anal (31%) and vulvar/vaginal (19%) cancer cohorts, but not in head and neck SCC (19%) or penile (18%) cancer cohorts (overall ORR = 26%). Median progression-free survival was 4.0 months (95% confidence interval: 2.6–4.3), and median overall survival was 11.1 months (95% confidence interval: 9.2–17.4). In the safety population, 101 (91%) of 111 patients developed at least one treatment-related adverse event, with 39% and 5.4% of patients experiencing at least one grade 3 and grade 4 treatment-related adverse event, respectively. Vorinostat-related toxicity prompted a dose reduction/interruption in 66% of patients. Whole-exome sequencing analyses revealed several potential predictive biomarkers of response to treatment. Further studies in a larger number of patients are required to validate these findings. ClinicalTrials.gov identifier: NCT04357873 . Borcoman and colleagues present the efficacy and safety results of the phase 2 PEVOsq basket trial investigating the combination of pembrolizumab with the epidrug vorinostat in patients with recurrent and/or metastatic squamous cell carcinoma.","PeriodicalId":18885,"journal":{"name":"Nature cancer","volume":"6 8","pages":"1370-1383"},"PeriodicalIF":28.5,"publicationDate":"2025-06-30","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12380617/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144528987","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}
Nature cancerPub Date : 2025-06-30DOI: 10.1038/s43018-025-01003-3
Laura Antonucci, Na Li, Angeles Duran, Isidoro Cobo, Chiara Nicoletti, Kosuke Watari, Shuvro Prokash Nandi, Feng Zhu, Yongmei Zhao, Irene Riahi, Motoyuki Tsuda, Vidhi M. Shah, Terry Morgan, Trent Waugh, Luca Caputo, Yuan Liu, Alexandra Rundberg Nilsson, Hongxu Xian, Jelena Todoric, Li Gu, Elsa Sanchez-Lopez, Guido Eibl, Emily A. Vucic, Michal Krawczyk, Qianlan Xu, Andrew M. Lowy, Georgia Hatzivassiliou, Merone Roose-Girma, Dorota Skowronska-Krawczyk, David A. Scott, Dafna Bar-Sagi, Pablo Tamayo, Ying Wu, Rosalie C. Sears, Christopher K. Glass, Ludmil B. Alexandrov, Pier Lorenzo Puri, David W. Dawson, Yinling Hu, Maria T. Diaz-Meco, Jorge Moscat, Michael Karin
{"title":"Self-amplifying NRF2–EZH2 epigenetic loop converts KRAS-initiated progenitors to invasive pancreatic cancer","authors":"Laura Antonucci, Na Li, Angeles Duran, Isidoro Cobo, Chiara Nicoletti, Kosuke Watari, Shuvro Prokash Nandi, Feng Zhu, Yongmei Zhao, Irene Riahi, Motoyuki Tsuda, Vidhi M. Shah, Terry Morgan, Trent Waugh, Luca Caputo, Yuan Liu, Alexandra Rundberg Nilsson, Hongxu Xian, Jelena Todoric, Li Gu, Elsa Sanchez-Lopez, Guido Eibl, Emily A. Vucic, Michal Krawczyk, Qianlan Xu, Andrew M. Lowy, Georgia Hatzivassiliou, Merone Roose-Girma, Dorota Skowronska-Krawczyk, David A. Scott, Dafna Bar-Sagi, Pablo Tamayo, Ying Wu, Rosalie C. Sears, Christopher K. Glass, Ludmil B. Alexandrov, Pier Lorenzo Puri, David W. Dawson, Yinling Hu, Maria T. Diaz-Meco, Jorge Moscat, Michael Karin","doi":"10.1038/s43018-025-01003-3","DOIUrl":"10.1038/s43018-025-01003-3","url":null,"abstract":"Pancreatic ductal adenocarcinoma (PDAC) emerges from mutant KRAS-harboring but dormant low-grade pancreatic intraepithelial neoplasia (PanIN). To examine the role of oxidative stress, a putative PDAC risk factor, we established an organoid-based transformation system. Although the prototypic oxidant H2O2 induced organoid transformation, its effect was nonmutational and was mediated by the oxidant-responsive transcription factor NRF2, which induced the histone methyltransferase EZH2. Congruently, nonoxidizing NRF2 activators triggered organoid malignant conversion through NRF2 and EZH2, establishing a hitherto unknown epigenetic mechanism underlying PanIN-to-PDAC progression. While NRF2 induced EZH2 gene transcription in mouse and human PDAC, EZH2, a general repressor, coactivated transcription of NRF2-encoding NFE2L2 and interacted with other transcription factors to induce genes that sustain PDAC metabolic demands. The self-amplifying NRF2–EZH2 epigenetic loop also accounted for inflammation-driven PanIN-to-PDAC progression in vivo and was upregulated in established human PDAC, whose malignancy was maintained by NRF2 binding to the EZH2 promoter. Using pancreatic organoids and genetic mouse models, Antonucci et al. show that cellular stress activates an NRF2–EZH2 epigenetic axis leading to metabolic reprogramming and subsequent malignant transformation of KRAS-mutant benign lesions.","PeriodicalId":18885,"journal":{"name":"Nature cancer","volume":"6 7","pages":"1263-1282"},"PeriodicalIF":28.5,"publicationDate":"2025-06-30","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144528988","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 : 2025-06-27DOI: 10.1038/s43018-025-00980-9
Allison L. Boyd, Mickie Bhatia
{"title":"Charting human hematopoiesis to understand B cell leukemia","authors":"Allison L. Boyd, Mickie Bhatia","doi":"10.1038/s43018-025-00980-9","DOIUrl":"10.1038/s43018-025-00980-9","url":null,"abstract":"B cell leukemias are heterogeneous cancers believed to develop from pro-B lymphoid progenitors. Single-cell transcriptomics of patients and donors now reveal a map of B cell leukemia cell states and suggest that the cell of origin may be more dedifferentiated than previously assumed, thus influencing our understanding of the disease.","PeriodicalId":18885,"journal":{"name":"Nature cancer","volume":"6 7","pages":"1126-1128"},"PeriodicalIF":28.5,"publicationDate":"2025-06-27","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144512212","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 : 2025-06-27DOI: 10.1038/s43018-025-01001-5
Bing Song, Kaiwen Wang, Saiyang Na, Jia Yao, Farjana J. Fattah, Alexandra L. Martin, Mitchell S. von Itzstein, Donghan M. Yang, Jialiang Liu, Yaming Xue, Chaoying Liang, Yuzhi Guo, Indu Raman, Chengsong Zhu, Jonathan E. Dowell, Jade Homsi, Sawsan Rashdan, Shengjie Yang, Mary E. Gwin, Tuoqi Wu, David Hsiehchen, Yvonne Gloria-McCutchen, Catherine Pei-ju Lu, Prithvi Raj, Xiao-chen Bai, Jun Wang, Jose Conejo-Garcia, Yang Xie, Junzhou Huang, David E. Gerber, Tao Wang
{"title":"Profiling antigen-binding affinity of B cell repertoires in tumors by deep learning predicts immune-checkpoint inhibitor treatment outcomes","authors":"Bing Song, Kaiwen Wang, Saiyang Na, Jia Yao, Farjana J. Fattah, Alexandra L. Martin, Mitchell S. von Itzstein, Donghan M. Yang, Jialiang Liu, Yaming Xue, Chaoying Liang, Yuzhi Guo, Indu Raman, Chengsong Zhu, Jonathan E. Dowell, Jade Homsi, Sawsan Rashdan, Shengjie Yang, Mary E. Gwin, Tuoqi Wu, David Hsiehchen, Yvonne Gloria-McCutchen, Catherine Pei-ju Lu, Prithvi Raj, Xiao-chen Bai, Jun Wang, Jose Conejo-Garcia, Yang Xie, Junzhou Huang, David E. Gerber, Tao Wang","doi":"10.1038/s43018-025-01001-5","DOIUrl":"10.1038/s43018-025-01001-5","url":null,"abstract":"The capability to profile the landscape of antigen-binding affinities of a vast number of antibodies (B cell receptors, BCRs) will provide a powerful tool to reveal biological insights. However, experimental approaches for detecting antibody–antigen interactions are costly and time-consuming and can only achieve low-to-mid throughput. In this work, we developed Cmai (contrastive modeling for antigen–antibody interactions) to address the prediction of binding between antibodies and antigens that can be scaled to high-throughput sequencing data. We devised a biomarker based on the output from Cmai to map the antigen-binding affinities of BCR repertoires. We found that the abundance of tumor antigen-targeting antibodies is predictive of immune-checkpoint inhibitor (ICI) treatment response. We also found that, during immune-related adverse events (irAEs) caused by ICI, humoral immunity is preferentially responsive to intracellular antigens from the organs affected by the irAEs. We used Cmai to construct a BCR-based irAE risk score, which predicted the timing of the occurrence of irAEs. Song et al. developed a computational tool to profile binding pairs between tumor-derived antigens and antibodies from high-throughput B cell receptor sequencing data, predicting response to immune-checkpoint inhibitor therapy and risk of adverse events.","PeriodicalId":18885,"journal":{"name":"Nature cancer","volume":"6 9","pages":"1570-1584"},"PeriodicalIF":28.5,"publicationDate":"2025-06-27","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144512216","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}