Cancer CellPub Date : 2025-10-16DOI: 10.1016/j.ccell.2025.09.010
Jorge Luis Galeano Niño, Falk Ponath, Victor A. Ajisafe, Clara R. Becker, Andrew G. Kempchinsky, Martha A. Zepeda-Rivera, Javier A. Gomez, Hanrui Wu, Jessica G. Terrazas, Heather Bouzek, Elizabeth Cromwell, Pritha Chanana, Matthew Wong, Ashish Damania, Michael G. White, Y. Nancy You, Scott Kopetz, Nadim J. Ajami, Jennifer A. Wargo, Christopher D. Johnston, Susan Bullman
{"title":"Tumor-infiltrating bacteria disrupt cancer epithelial cell interactions and induce cell-cycle arrest","authors":"Jorge Luis Galeano Niño, Falk Ponath, Victor A. Ajisafe, Clara R. Becker, Andrew G. Kempchinsky, Martha A. Zepeda-Rivera, Javier A. Gomez, Hanrui Wu, Jessica G. Terrazas, Heather Bouzek, Elizabeth Cromwell, Pritha Chanana, Matthew Wong, Ashish Damania, Michael G. White, Y. Nancy You, Scott Kopetz, Nadim J. Ajami, Jennifer A. Wargo, Christopher D. Johnston, Susan Bullman","doi":"10.1016/j.ccell.2025.09.010","DOIUrl":"https://doi.org/10.1016/j.ccell.2025.09.010","url":null,"abstract":"Tumor-infiltrating bacteria are increasingly recognized as modulators of cancer progression and therapy resistance. We describe a mechanism by which extracellular intratumoral bacteria, including <em>Fusobacterium</em>, modulate cancer epithelial cell behavior. Spatial imaging and single-cell spatial transcriptomics show that these bacteria predominantly localize extracellularly within tumor microniches of colorectal and oral cancers, characterized by reduced cell density, transcriptional activity, and proliferation. <em>In vitro</em>, <em>Fusobacterium nucleatum</em> disrupts epithelial contacts, inducing G0-G1 arrest and transcriptional quiescence. This state confers 5-fluorouracil resistance and remodels the tumor microenvironment. Findings were validated by live-cell imaging, spatial profiling, mouse models, and a 52-patient colorectal cancer cohort. Transcriptomics reveals downregulation of cell cycle, transcription, and antigen presentation genes in bacteria-enriched regions, consistent with a quiescent, immune-evasive phenotype. In an independent rectal cancer cohort, high <em>Fusobacterium</em> burden correlates with reduced therapy response. These results link extracellular bacteria to cancer cell quiescence and chemoresistance, highlighting microbial-tumor interactions as therapeutic targets.","PeriodicalId":9670,"journal":{"name":"Cancer Cell","volume":"58 1","pages":""},"PeriodicalIF":50.3,"publicationDate":"2025-10-16","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145295526","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 : 2025-10-16DOI: 10.1016/j.ccell.2025.09.011
Shelley Herbrich, Mehdi Chaib, Swetha Anandhan, Samuel W. Andrewes, Ashwat Nagarajan, Baoxiang Guan, Nishant Gandhi, Jared Gilliam, Milan Radovich, Padmanee Sharma
{"title":"TET2-mutant clonal hematopoiesis enhances macrophage antigen presentation and improves immune checkpoint therapy in solid tumors","authors":"Shelley Herbrich, Mehdi Chaib, Swetha Anandhan, Samuel W. Andrewes, Ashwat Nagarajan, Baoxiang Guan, Nishant Gandhi, Jared Gilliam, Milan Radovich, Padmanee Sharma","doi":"10.1016/j.ccell.2025.09.011","DOIUrl":"https://doi.org/10.1016/j.ccell.2025.09.011","url":null,"abstract":"Clonal hematopoiesis (CH) is detectable in upwards of 20% of patients with solid tumors and is associated with worsened prognosis; however, its role in tumor immunology and immune checkpoint therapy (ICT) is unknown. Using a bone marrow chimera model of <em>Tet2</em><sup>+/mut</sup> CH in mice with solid tumors, we found the <em>Tet2</em>-mutant myeloid cells are abundant in the tumor microenvironment and contributed to an improved response to ICT. Mechanistically, <em>Tet2</em><sup>+/mut</sup> macrophages inside the tumor act as immunogenic antigen-presenting cells that more effectively cross-prime naive CD8<sup>+</sup> T cells in response to IFNγ. In human cohorts of 35,971 non-small cell lung cancer patients and 25,064 colorectal adenocarcinoma patients<em>, TET2-</em>mutant CH is associated with improved outcome specifically with ICT. This study proposes a role for <em>Tet2</em><sup>+/mut</sup> antigen presenting macrophages in shaping antitumor immunity and identifies <em>TET2-</em>mutant CH as a potential biomarker for improved response to ICT in patients with solid tumors.","PeriodicalId":9670,"journal":{"name":"Cancer Cell","volume":"13 1","pages":""},"PeriodicalIF":50.3,"publicationDate":"2025-10-16","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145295525","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 : 2025-10-09DOI: 10.1016/j.ccell.2025.09.008
Pashtoon Murtaza Kasi
{"title":"Hidden spark: From cold to hot in BRAF colorectal cancer","authors":"Pashtoon Murtaza Kasi","doi":"10.1016/j.ccell.2025.09.008","DOIUrl":"https://doi.org/10.1016/j.ccell.2025.09.008","url":null,"abstract":"Immunotherapy as single-agent PD-1 blockade does not work for patients with microsatellite stable (MSS) colorectal cancer. In this issue of <em>Cancer Cell</em>, Morris et al. demonstrate that targeting the mitogen-activated protein kinase (MAPK) pathway in combination with immunotherapy can reprogram BRAF-V600E mutant MSS colorectal cancers toward immune responsiveness.","PeriodicalId":9670,"journal":{"name":"Cancer Cell","volume":"85 1","pages":""},"PeriodicalIF":50.3,"publicationDate":"2025-10-09","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145247550","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 : 2025-10-09DOI: 10.1016/j.ccell.2025.09.009
Xueli Bai, Xiang Li, Yiwen Chen, Guoliang Qiao, Qi Zhang, Tao Ma, Shunliang Gao, Min Zhang, Yan Shen, Jian Wu, Jun Yu, Risheng Que, Xiaochen Zhang, Ke Sun, Wenbo Xiao, Tian’an Jiang, Tingbo Liang
{"title":"Neoadjuvant nab-paclitaxel plus gemcitabine followed by modified FOLFIRINOX for resectable pancreatic cancer: A randomized phase 3 trial","authors":"Xueli Bai, Xiang Li, Yiwen Chen, Guoliang Qiao, Qi Zhang, Tao Ma, Shunliang Gao, Min Zhang, Yan Shen, Jian Wu, Jun Yu, Risheng Que, Xiaochen Zhang, Ke Sun, Wenbo Xiao, Tian’an Jiang, Tingbo Liang","doi":"10.1016/j.ccell.2025.09.009","DOIUrl":"https://doi.org/10.1016/j.ccell.2025.09.009","url":null,"abstract":"This single-center, randomized phase 3 trial (NCT03750669) evaluated sequential neoadjuvant nab-paclitaxel plus gemcitabine followed by modified FOLFIRINOX versus upfront surgery in 324 patients with resectable pancreatic cancer. Patients in the neoadjuvant group received nab-paclitaxel plus gemcitabine followed by modified FOLFIRINOX before surgery and then four cycles of adjuvant therapy (preferably gemcitabine plus capecitabine), while those in the upfront surgery group underwent immediate resection followed by six cycles of adjuvant therapy. The primary endpoint was event-free survival. Notably, 50% of patients had tumors in the pancreatic body or tail. Median event-free survival was 15.3 months (95% confidence interval [CI], 12.6–19.3) versus 10.9 months (95% CI, 9.1–13.5; hazard ratio [HR], 0.71; 95% CI, 0.54–0.93; <em>p</em> = 0.0136). Median overall survival was 35.4 months versus 27.2 months (HR, 0.73; 95% CI, 0.53–1.00; nominal <em>p</em> = 0.0477). Grade ≥3 adverse events occurred in 47.6% versus 30.7% of patients. This neoadjuvant regimen improves event-free survival with manageable safety.","PeriodicalId":9670,"journal":{"name":"Cancer Cell","volume":"68 1","pages":""},"PeriodicalIF":50.3,"publicationDate":"2025-10-09","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145247551","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 : 2025-10-09DOI: 10.1016/j.ccell.2025.09.007
Francesco Di Meo, Francesca Albano, Annamaria Cesarano, Yunfei Wang, Brandon Kale, Kenneth Shain, Ariosto Silva, Noriyoshi Kurihara, Hirofumi Tenshin, David Jellyman, Xiaofei Song, Sasan Ghaffari, Hector Mesa, Ben Creelan, Ciara Freeman, Xiaohong Zhao, Mark B. Meads, Paulo C. Rodriguez, Silvia Marino, Frederick Locke, Fabiana Perna
{"title":"Developing SEMA4A-directed CAR T cells to overcome low BCMA antigen density in multiple myeloma","authors":"Francesco Di Meo, Francesca Albano, Annamaria Cesarano, Yunfei Wang, Brandon Kale, Kenneth Shain, Ariosto Silva, Noriyoshi Kurihara, Hirofumi Tenshin, David Jellyman, Xiaofei Song, Sasan Ghaffari, Hector Mesa, Ben Creelan, Ciara Freeman, Xiaohong Zhao, Mark B. Meads, Paulo C. Rodriguez, Silvia Marino, Frederick Locke, Fabiana Perna","doi":"10.1016/j.ccell.2025.09.007","DOIUrl":"https://doi.org/10.1016/j.ccell.2025.09.007","url":null,"abstract":"Chimeric antigen receptor (CAR) T cell therapy targeting B cell maturation antigen (BCMA) for multiple myeloma (MM) is effective, but relapses associated with low-to-negative BCMA expression are common, indicating the need for additional targets. We quantitatively profile antigen density in a cohort of patients relapsed after BCMA CAR T therapy, showing high number of SEMA4A molecules/cell where BCMA density is low. SEMA4A deletion limits MM cell growth, migration, tissue infiltration, and osteoclast formation, while extending mouse survival. We generate monoclonal antibodies targeting SEMA4A-extracellular domain for CAR construction, screen engineered T cells for expansion, cytokine release, and cytotoxicity against MM cells. Lead constructs lack reactivity against normal non-hematopoietic tissues. SEMA4A CAR T cells show superior efficacy than BCMA CAR T cells eliminating patient-derived BCMA<sup>low</sup> tumors and MM cells progressing under suboptimal doses of BCMA CAR T cells. This study prepares for a phase 1 clinical trial with SEMA4A-directed CAR T cells for MM.","PeriodicalId":9670,"journal":{"name":"Cancer Cell","volume":"24 1","pages":""},"PeriodicalIF":50.3,"publicationDate":"2025-10-09","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145247580","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 : 2025-10-02DOI: 10.1016/j.ccell.2025.09.005
Julie F. Cheung, Brian G. Hunt, Shudipto Wahed, Elaine Cheng, Kelli A. Connolly, Srividhya Venkatesan, Jennifer L. Loza, Ishan Bansal, Eric Fagerberg, Emily A. Kessler, Clémence Riffard, Jessica Buck, John Attanasio, Emily R. Borr, Wei Wei, Ivana William, Brittany Fitzgerald, Nikhil S. Joshi
{"title":"Distinct T cell functions enable efficient immunoediting and prevent tumor emergence of developing sarcomas","authors":"Julie F. Cheung, Brian G. Hunt, Shudipto Wahed, Elaine Cheng, Kelli A. Connolly, Srividhya Venkatesan, Jennifer L. Loza, Ishan Bansal, Eric Fagerberg, Emily A. Kessler, Clémence Riffard, Jessica Buck, John Attanasio, Emily R. Borr, Wei Wei, Ivana William, Brittany Fitzgerald, Nikhil S. Joshi","doi":"10.1016/j.ccell.2025.09.005","DOIUrl":"https://doi.org/10.1016/j.ccell.2025.09.005","url":null,"abstract":"T cells edit tumors by eliminating neoantigen-expressing tumor cells. Yet, how and when this is achieved remains uncertain. Using a murine sarcoma model with fluorescent neoantigens, we found that tumors developed later and in fewer T cell-sufficient mice (∼53% penetrance) than T cell-deficient mice (∼100%). With T cells, all emergent tumor cells had silenced neoantigens, but neoantigen-negative tumor cells were also present in every T cell-deficient mouse. This suggested silencing was necessary but not sufficient for outgrowth. Genetic removal of neoantigens restored tumor penetrance if implemented on day 5 post-tumor initiation, but not day 10, because CD8<sup>+</sup> and CD4<sup>+</sup> T cells infiltrated the tissue and eliminated most neoantigen-positive and -negative tumor cells within 8 days. Single-cell analyses on day-7 tumors showed oncogenic changes including increased proliferation and T cell-dependent upregulation of the IFNγ-response gene <em>Cd274</em> (PD-L1). T cell-depletion rescued both neoantigen-positive and -negative cells, while IFNγ blockade rescued only negative cells. This shows that T cells efficiently edit sarcomas of neoantigens and prevent early tumors via IFNγ-independent and IFNγ-dependent (bystander) mechanisms.","PeriodicalId":9670,"journal":{"name":"Cancer Cell","volume":"2 1","pages":""},"PeriodicalIF":50.3,"publicationDate":"2025-10-02","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145204007","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 : 2025-10-02DOI: 10.1016/j.ccell.2025.08.010
Giovanni Randon, Isacco Montroni, Filippo Pietrantonio
{"title":"Bringing immunotherapy to clinical practice in dMMR/MSI-high colon cancer","authors":"Giovanni Randon, Isacco Montroni, Filippo Pietrantonio","doi":"10.1016/j.ccell.2025.08.010","DOIUrl":"https://doi.org/10.1016/j.ccell.2025.08.010","url":null,"abstract":"Upfront resection is the standard treatment for localized dMMR/MSI-high colon cancer. In this issue of <em>Cancer Cell</em>, Wang et al. showed that dual anti-CTLA-4/PD-1 IBI310/sintilimab for 6 weeks improved pathological complete response over sintilimab in patients with cT4/N+ tumors. This combination represents a referral regimen for neoadjuvant or organ-preserving strategies.","PeriodicalId":9670,"journal":{"name":"Cancer Cell","volume":"113 1","pages":""},"PeriodicalIF":50.3,"publicationDate":"2025-10-02","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145204004","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":"Neoadjuvant treatment of IBI310 plus sintilimab in locally advanced MSI-H/dMMR colon cancer: A randomized phase 1b study","authors":"Feng Wang, Gong Chen, Meng Qiu, Jinfeng Ma, Xianwei Mo, Haiyi Liu, Yongqiang Li, Peirong Ding, Xiangbin Wan, Yingbin Hu, Xiwen Huang, Weiqin Jiang, Xiaojun Wu, Jia Luo, Yanbing Zhou, Leping Li, Yanlai Sun, Quan Wang, Nanya Wang, Wu Jiang, Rui-Hua Xu","doi":"10.1016/j.ccell.2025.09.004","DOIUrl":"https://doi.org/10.1016/j.ccell.2025.09.004","url":null,"abstract":"Although neoadjuvant immunotherapy showed promising efficacy in locally advanced microsatellite instability-high or mismatch repair-deficient (MSI-H/dMMR) colon cancer, whether dual immune checkpoint inhibition provides additional benefit over anti-PD-1 monotherapy remains unclear. This randomized phase 1b trial (<span><span>NCT05890742</span><svg aria-label=\"Opens in new window\" focusable=\"false\" height=\"20\" viewbox=\"0 0 8 8\"><path d=\"M1.12949 2.1072V1H7V6.85795H5.89111V2.90281L0.784057 8L0 7.21635L5.11902 2.1072H1.12949Z\"></path></svg></span>) evaluated a neoadjuvant regimen of IBI310 (anti-cytotoxic T lymphocyte-associated antigen 4 [CTLA-4]) plus sintilimab (<em>n</em> = 52) versus sintilimab monotherapy (<em>n</em> = 49). Surgery was performed in 51 and 45 patients, respectively. The primary endpoint, pathological complete response (pCR) rate, was significantly higher in the combination compared to the monotherapy arm within the modified intent-to-treat (mITT) population (78.4% versus 46.7%, <em>p</em> = 0.0015), with consistent results in the intent-to-treat (ITT) population (76.9% versus 42.9%). Safety in both arms was comparable and manageable without new safety signals. After a median follow-up of 21.4 months, no disease recurrences occurred. One death occurred in each arm due to postoperative complication and adverse events. These findings demonstrate the added benefit of neoadjuvant IBI310 plus sintilimab over sintilimab monotherapy for locally advanced MSI-H/dMMR colon cancer.","PeriodicalId":9670,"journal":{"name":"Cancer Cell","volume":"10 1","pages":""},"PeriodicalIF":50.3,"publicationDate":"2025-10-02","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145204008","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 : 2025-10-02DOI: 10.1016/j.ccell.2025.09.006
W.H. Adrian Tsui, Peiyong Jiang, Y.M. Dennis Lo
{"title":"Cell-free DNA fragmentomics in cancer","authors":"W.H. Adrian Tsui, Peiyong Jiang, Y.M. Dennis Lo","doi":"10.1016/j.ccell.2025.09.006","DOIUrl":"https://doi.org/10.1016/j.ccell.2025.09.006","url":null,"abstract":"The analysis of cell-free DNA (cfDNA) fragmentation patterns, known as “fragmentomics,” has opened new opportunities in noninvasive cancer diagnostics. Due to its close relationships with genomic organization and cell death, cfDNA fragmentomics lies at the intersection of many aspects of cancer biology, including epigenetic dysregulation, transcriptomic alterations, and aberrant cellular turnover patterns. Recent advances in library preparation, sequencing technologies, and integrative epigenomic-fragmentomic analyses have uncovered novel fragmentomic features that reveal specific cellular dysfunctions in cancer. Additionally, cutting-edge artificial intelligence algorithms now harness high-dimensional fragmentomic features, boosting the precision and power of cancer detection. Promising results from recent clinical trials evaluating the utility of fragmentomic analyses in real-world settings support its potential. In this review, we explore the exciting frontiers of cfDNA fragmentomics, discuss critical unanswered questions, and highlight future directions to unlock the promise of fragmentomics-based liquid biopsies in cancer care.","PeriodicalId":9670,"journal":{"name":"Cancer Cell","volume":"19 1","pages":""},"PeriodicalIF":50.3,"publicationDate":"2025-10-02","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145204005","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 : 2025-09-28DOI: 10.1016/j.ccell.2025.08.005
Johannes Haybaeck, Nicolas Zeller, Monika Julia Wolf, Achim Weber, Ulrich Wagner, Michael Odo Kurrer, Juliane Bremer, Giandomenica Iezzi, Rolf Graf, Pierre-Alain Clavien, Robert Thimme, Hubert Blum, Sergei A. Nedospasov, Kurt Zatloukal, Muhammad Ramzan, Sandra Ciesek, Thomas Pietschmann, Patrice N. Marche, Michael Karin, Manfred Kopf, Mathias Heikenwalder
{"title":"A Lymphotoxin-Driven Pathway to Hepatocellular Carcinoma","authors":"Johannes Haybaeck, Nicolas Zeller, Monika Julia Wolf, Achim Weber, Ulrich Wagner, Michael Odo Kurrer, Juliane Bremer, Giandomenica Iezzi, Rolf Graf, Pierre-Alain Clavien, Robert Thimme, Hubert Blum, Sergei A. Nedospasov, Kurt Zatloukal, Muhammad Ramzan, Sandra Ciesek, Thomas Pietschmann, Patrice N. Marche, Michael Karin, Manfred Kopf, Mathias Heikenwalder","doi":"10.1016/j.ccell.2025.08.005","DOIUrl":"https://doi.org/10.1016/j.ccell.2025.08.005","url":null,"abstract":"(Cancer Cell <em>16</em>, 295–308; October 6, 2009)","PeriodicalId":9670,"journal":{"name":"Cancer Cell","volume":"28 1","pages":""},"PeriodicalIF":50.3,"publicationDate":"2025-09-28","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145182868","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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