Cancer immunology research最新文献

{"title":"Lenvatinib Combined with PD-1 Blockade Therapy Benefits Gastric Cancers through Immunosuppressive Macrophage Modulation.","authors":"Nina Yi-Tzu Lin, Hirotomo Machiyama, Akihito Kawazoe, Atsuo Sai, Takuma Irie, Takumi Habu, Shota Fukuoka, Atsushi Kumanogoh, Naoya Sakamoto, Genichiro Ishii, Takahiro Kinoshita, Kohei Shitara, Hiroyoshi Nishikawa, Shohei Koyama","doi":"10.1158/2326-6066.CIR-25-0982","DOIUrl":"10.1158/2326-6066.CIR-25-0982","url":null,"abstract":"<p><p>The combination of multikinase inhibitors with PD-1 blockade therapy has emerged as a promising strategy to overcome resistance to PD-1 blockade monotherapy across multiple cancer types, including gastric cancer. In this study, we report that the multikinase inhibitor lenvatinib selectively reduced the number of CD206+CD163+ immunosuppressive macrophages in the tumor microenvironment (TME) and increased antitumor immunity. Longitudinal immunoprofiling was conducted with paired (pre- and posttreatment) tumor samples from patients with advanced gastric cancer who received first- or second-line combination therapy with lenvatinib and pembrolizumab in the EPOC1706 clinical trial. Patients with abundant CD206+CD163+ immunosuppressive macrophage infiltration exhibited favorable responses to combination therapy, accompanied by a significant posttreatment reduction in these cells. Although this immunosuppressive macrophage infiltration was associated with resistance to PD-1 blockade monotherapy, it predicted a response to combination treatment: 8 of the 9 patients with >440 CD206+CD163+ immunosuppressive macrophages/mm2 responded, whereas none of the 8 patients who received monotherapy responded. Mechanistically, lenvatinib inhibited platelet-derived growth factor receptor α (PDGFRα)/fibroblast growth factor receptor (FGFR)-dependent p38 mitogen-activated protein kinase (MAPK) and AKT signaling pathways in F4/80highCD11bint immunosuppressive macrophages, triggering endoplasmic reticulum stress and an unresolved unfolded protein response, resulting in their apoptosis. Furthermore, in multiple animal models, the therapeutic efficacy of the combination was observed in tumors with abundant immunosuppressive macrophages with activated PDGFR/FGFR-AKT/p38 MAPK signaling. Therefore, we propose that the abundance of immunosuppressive macrophages in the TME could serve as a predictive biomarker for patient stratification to guide rational anti-PD-1-based combination therapy in gastric cancer, enabling mechanism-based combination cancer immunotherapy.</p>","PeriodicalId":9474,"journal":{"name":"Cancer immunology research","volume":" ","pages":"1116-1132"},"PeriodicalIF":7.9,"publicationDate":"2026-07-02","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"147763243","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":"An ICAM1-Targeting Chimeric Costimulatory Receptor Mimics the Immune Synapse and Enhances Tumor-Specific T-cell Function.","authors":"Irene M Min, Yanping Yang, Dessislava Stefanova, Yogindra Vedvyas, Diella S Babu, Dong-Hyun Lee, Yago Alcaina, Maria Cristina Riascos, Janusz Puc, Kevin J Chen, Juan Gonzalez-Valdivieso, Jose Thaiparambil, Maneeza Bilal, Bing He, Aidan C Burnett, Rasa Zarnegar, Thomas J Fahey, Moonsoo M Jin","doi":"10.1158/2326-6066.CIR-25-0529","DOIUrl":"10.1158/2326-6066.CIR-25-0529","url":null,"abstract":"<p><p>Engineered T-cell therapies, such as chimeric antigen receptor (CAR)- and T-cell receptor (TCR)-based approaches, have transformed outcomes in hematologic malignancies, yet their efficacy in solid tumors remains limited by tumor antigen escape, immunosuppressive microenvironments, and insufficient activation of CAR or TCR signaling. To overcome these barriers, we developed an intercellular adhesion molecule 1 (ICAM1)-specific chimeric costimulatory receptor (ICCR) engineered for expression in T cells to augment their activation. ICAM1 is broadly expressed across solid tumors and is further upregulated by IFNγ released during early T-cell engagement, creating a feed-forward loop that reinforces tumor recognition. ICCR engagement with ICAM1 triggered NF-κB signaling independently of TCR-peptide (p)/MHC engagement; however, full T-cell activation and cytotoxic function remained dependent on intact TCR signaling. In primary T cells, ICCR increased proliferation, cytokine production, and cytotoxicity, resulting in improved tumor control in two anaplastic thyroid cancer xenograft models treated with allogeneic or autologous ICCR-T cells. Mechanistically, ICCR strengthened tumor cell engagement, promoted selection and expansion of tumor-specific TCR clonotypes, and amplified downstream signaling pathways. These findings identify ICCR as a strategy that leverages an immune synapse-mimetic mechanism to enhance the function of low-activity tumor-specific TCRs and improve T-cell responses in solid tumor microenvironments.</p>","PeriodicalId":9474,"journal":{"name":"Cancer immunology research","volume":" ","pages":"1133-1149"},"PeriodicalIF":7.9,"publicationDate":"2026-07-02","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC13357678/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"147763169","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}

{"title":"Tumor-Derived Complement C3 Overexpression in STK11-Mutant Lung Adenocarcinoma Drives Tumor Growth and Immune Checkpoint Inhibitor Resistance.","authors":"Sora Suzuki, Bojidar Kandar, Catrina Ting, Peter Deraska, Te-An Chen, Thejaswini Giridharan, Anm Nazmul H Khan, Kristopher Attwood, Han Yu, Kayla Catalfamo, Prashant K Singh, Ryan T Bushey, Elizabeth B Gottlin, Michael J Campa, Edward F Patz, Daniel Ajona, Ruben Pio, Brahm H Segal, Edwin H Yau","doi":"10.1158/2326-6066.CIR-25-0534","DOIUrl":"10.1158/2326-6066.CIR-25-0534","url":null,"abstract":"<p><p>Loss-of-function STK11 mutations occur in 15% to 20% of lung adenocarcinomas (LUAD) and correlate with immunotherapy failure and worse survival. By integrating analysis of human tumor samples, a human LUAD cell line panel, and Cancer Cell Line Encyclopedia and The Cancer Genome Atlas datasets, we found that C3 production was increased in human STK11-mutant versus STK11-wildtype (WT) LUAD, modulated by LKB1 loss, whereas high C3 expression in STK11-mutant LUAD was associated with worse survival. STK11 knockout (STK11-KO) in syngeneic murine LUAD tumors resulted in increased neutrophil and reduced T-cell infiltration and anti-PD-1 resistance. STK11-KO tumor growth was similar in C3-/- versus WT mice. In contrast, C3 deletion in STK11-KO tumors resulted in dramatic inhibition of tumor growth and enhanced sensitivity to anti-PD-1 in immunocompetent mice but had no significant effect in CD8-depleted WT mice or nude mice, pointing to tumor-derived C3 promoting immune evasion. Mechanistically, STK11 loss drove tumor-derived C3 production and downstream CXCL2 and complement factor H production that promoted immune evasion and impaired anti-PD-1 efficacy. Our results show a C3-driven signaling axis for STK11-mutant LUAD promoting immune evasion and identify therapeutic targets to render these tumors sensitive to anti-PD-1.</p>","PeriodicalId":9474,"journal":{"name":"Cancer immunology research","volume":" ","pages":"1172-1185"},"PeriodicalIF":7.9,"publicationDate":"2026-07-02","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC13348722/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"147763181","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}

{"title":"Tumor-Infiltrating Platelets Recruit Neutrophils to Promote Tumor Growth through the 5-HIAA-GPR35-ERK1/2 Axis in Hepatocellular Carcinoma.","authors":"Ning Li, Peng-Cheng Wang, Jing-Yue Pan, Ye Xu, Yu-Hang Ye, Rong-Qi Sun, Si-Yuan Pan, Ya-Ya Ji, Jian Zhou, Jia Fan, Rong-Xin Chen, Shao-Lai Zhou, Zheng-Jun Zhou","doi":"10.1158/2326-6066.CIR-25-0498","DOIUrl":"10.1158/2326-6066.CIR-25-0498","url":null,"abstract":"<p><p>Tumor-associated neutrophils (TAN) promote tumor growth and metastasis in hepatocellular carcinoma (HCC). Platelets can activate neutrophils and contribute to inflammation and organ damage; however, the relationship between TANs and platelets in HCC remains unclear. We performed multiplex immunohistochemistry and found that tumor-infiltrating platelets and TANs exhibited similar spatial distributions in patient-derived HCC samples. Then, a transwell migration assay demonstrated that supernatants from platelets cocultured with HCC cells enhanced neutrophil migration in vitro compared with supernatants from platelets or HCC cells cultured alone. Subsequent metabolomics analysis and in vitro and in vivo validation revealed that platelet-derived 5-hydroxyindole acetic acid (5-HIAA) promoted neutrophil migration via G protein-coupled receptor 35 (GPR35). Furthermore, in Hepa1-6 mouse models of HCC, GPR35+ neutrophils were found to facilitate HCC growth. Analysis of human HCC single-cell RNA sequencing (RNA-seq) data and mouse neutrophil bulk RNA-seq data revealed significant upregulation of the MAPK signaling pathway and pathways associated with neutrophil migration and cytokine production in GPR35+ neutrophils. Finally, in vitro experiments demonstrated that 5-HIAA activated the ERK1/2 pathway, enhanced protumor cytokine production, and promoted HCC cell growth via GPR35, all of which were suppressed by the GPR35 inhibitor CID2745687. Together, these data indicate that tumor-infiltrating platelets recruit neutrophils to promote tumor growth through the 5-HIAA-GPR35-ERK1/2 axis in HCC.</p>","PeriodicalId":9474,"journal":{"name":"Cancer immunology research","volume":" ","pages":"1186-1201"},"PeriodicalIF":7.9,"publicationDate":"2026-07-02","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"147653781","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":"UBA2-High Osteosarcoma Suppresses Immune Infiltration by Autophagy-Mediated MHC-I Degradation.","authors":"Lingfeng Yu, Mengpan Li, Tongtong Liu, Jiangpeng Wu, Huanliang Meng, Wenyuan Xu, Weisong Zhao, Hao Zhu, Zhen Wang, Shibing Guo, Zhuoying Wang, Mengxiong Sun, Tao Zhang, Yafei Jiang, Jing Han, Xiaojun Ma, Wei Sun, Yingqi Hua, Zhengdong Cai","doi":"10.1158/2326-6066.CIR-25-1321","DOIUrl":"10.1158/2326-6066.CIR-25-1321","url":null,"abstract":"<p><p>Osteosarcoma responds poorly to immune-checkpoint blockade (ICB), and the molecular drivers of its immune-cold state remain unclear. Using multi-omics analyses, we identified an immune-cold osteosarcoma subtype characterized by enrichment of protein SUMOylation and found the SUMO E1 subunit UBA2 as a key driver. UBA2 was anomalously upregulated in osteosarcoma cohorts and linked to worse outcomes. Functionally, UBA2 promoted autophagy, thereby exerting noncanonical protumor and immunosuppressive effects. Mechanistically, UBA2 catalyzed SUMO2-dependent SUMOylation of SESN2, enhancing autophagic flux. At the immune interface, UBA2 did not alter the expression of immune checkpoint molecules but reduced surface MHC-I through NBR1-mediated autophagy-lysosomal degradation, thereby limiting CD8+ T-cell infiltration. In vivo, pharmacologic UBA2 inhibition with ML-792 slowed tumor growth and sensitized tumors to ICB therapy. Together, these findings show that UBA2 links SUMOylation to autophagy-driven loss of antigen presentation and immune exclusion, highlighting the UBA2-autophagy-MHC-I axis as a therapeutic target and potential biomarker in osteosarcoma.</p>","PeriodicalId":9474,"journal":{"name":"Cancer immunology research","volume":" ","pages":"1080-1099"},"PeriodicalIF":7.9,"publicationDate":"2026-07-02","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"147833840","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 Sampling of Highlights from the Literature: Article Recommendations from Our Deputy and Senior Editors.","authors":"","doi":"10.1158/2326-6066.CIR-14-7-WWR","DOIUrl":"https://doi.org/10.1158/2326-6066.CIR-14-7-WWR","url":null,"abstract":"","PeriodicalId":9474,"journal":{"name":"Cancer immunology research","volume":"14 7","pages":"1051"},"PeriodicalIF":7.9,"publicationDate":"2026-07-02","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148367189","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":"Low Inflammation Correlates with Protumor Tim4+TREM1+ Resident Macrophage Expansion and Limited Monocyte-Derived Macrophage Differentiation during Peritoneal Colorectal Cancer.","authors":"Margarita Ferriz, Natalia Álvarez-Ladrón, Alejandra Gutiérrez-González, Marta H Fernández-Sesma, Adrián Vega-Pérez, Juan Carlos Oliveros, Ana Cayuela López, Eduard Batlle, Daniele V Tauriello, Alejandro Prados, Carlos Ardavín","doi":"10.1158/2326-6066.CIR-25-0388","DOIUrl":"10.1158/2326-6066.CIR-25-0388","url":null,"abstract":"<p><p>Accumulating evidence indicates that peritoneal macrophages, comprising resident peritoneal macrophages (resMØ) and monocyte-derived nonresident macrophages (moMØ), contribute to peritoneal tumor progression by promoting tumor cell proliferation and migration and driving immunosuppression. However, the mechanisms governing the expansion of resMØs and moMØs, as well as their differential contributions to the peritoneal macrophage pool in tumor-bearing mice and to tumor growth, remain to be elucidated. Using a mouse model of colorectal cancer peritoneal metastasis, induced by intraperitoneal injection of tumor organoids derived from primary tumors in genetically engineered mice carrying Apc, Kras, Tgfbr2, and Trp53 mutations, and recapitulating human-like metastatic colorectal cancer, we investigated the origin, expansion, and function of peritoneal macrophages during metastatic tumor growth. Our data support that the low inflammatory status of the peritoneal cavity during colorectal cancer peritoneal tumor growth restrains monocyte recruitment and the differentiation of Tim4- resMØs and moMØs while enabling a marked, proliferation-driven expansion of Tim4+ resMØs. Tumor-induced Tim4+ resMØs displayed a migratory and protumor transcriptomic signature characterized by the activation of genes encoding key protumorigenic molecules and potential immunotherapeutic targets, including Adora2a/Adora2b, Arg1, Ido2, Acod1, Mmp12, Cd274, Pdcd1lg2, Spp1, Trem1, and Vegfa. Correspondingly, during peritoneal colorectal cancer tumor growth, Tim4+TREM1+ resMØs migrated to the omentum, the principal peritoneal target organ for metastasis, and promoted colorectal cancer peritoneal tumor progression. These findings may help lead to the development of immunotherapies for colorectal cancer peritoneal metastasis that target tumor-associated peritoneal macrophages.</p>","PeriodicalId":9474,"journal":{"name":"Cancer immunology research","volume":" ","pages":"1100-1115"},"PeriodicalIF":7.9,"publicationDate":"2026-07-02","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"147763214","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":"Help! Male Hormones Dampen CD4+ T-cell Help in Cancer.","authors":"Juyeun Lee, Justin D Lathia","doi":"10.1158/2326-6066.CIR-26-0513","DOIUrl":"10.1158/2326-6066.CIR-26-0513","url":null,"abstract":"<p><p>Sex differences in antitumor immunity contribute to disparities in cancer outcomes, yet the role of CD4+ T helper cells in this context remains poorly understood. In this issue, Hunt and colleagues show that sex hormones restrain CD4+ T-cell help in males, weakening antitumor immune responses and promoting tumor progression. This work identifies CD4+ T-cell help as a previously underappreciated driver of sex-biased cancer immunity, with potential implications for sex-informed immunotherapy strategies. See related article by Hunt et al., p. 1068.</p>","PeriodicalId":9474,"journal":{"name":"Cancer immunology research","volume":" ","pages":"1052-1053"},"PeriodicalIF":7.9,"publicationDate":"2026-07-02","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"147980558","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":"ATF7ip Inhibits the Tumor Immune Response by Promoting Terminal CD8+ T-cell Exhaustion.","authors":"Sujit Kashyap, Jun Hyung Sin, Sophia M Guldberg, Jacqueline L Yee, Maya Lopez-Ichikawa, Sloan H Phillips, Matthew H Spitzer, Michael Waterfield","doi":"10.1158/2326-6066.CIR-25-0816","DOIUrl":"10.1158/2326-6066.CIR-25-0816","url":null,"abstract":"<p><p>CD8+ T-cell exhaustion limits the immune response to tumors because of ineffective T-cell effector functions. Thus, therapies that inhibit T-cell exhaustion are critical for optimizing cancer treatment. Recent studies have implicated epigenetic proteins in T-cell exhaustion. In this study, we identified activating transcription factor 7-interacting protein (ATF7ip) as an epigenetic protein critical for inducing T-cell exhaustion. Loss of Atf7ip in CD8+ T cells resulted in decreased terminal exhaustion and increased numbers of progenitor-exhausted cells in both chronic viral infections and cancer. Given the decreased T-cell terminal exhaustion observed with Atf7ip deficiency in CD8+ T cells, this may be one mechanism that leads to decreased tumor burden. Mechanistically, ATF7ip functions to stimulate the deposition of repressive H3K9me3 at critical immune-effector gene loci, such as Il7r and Il2, leading to enhanced exhaustion. Our data suggest that ATF7ip may be a rational target for deletion in adoptive T-cell therapies to reduce CD8+ T-cell exhaustion.</p>","PeriodicalId":9474,"journal":{"name":"Cancer immunology research","volume":" ","pages":"1054-1067"},"PeriodicalIF":7.9,"publicationDate":"2026-07-02","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC13459102/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"147670517","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}

{"title":"NMB+CXCL13+CD4+ T Cell-Derived Neuromedin B Promotes Neuropeptide S Receptor 1-Positive Malignant Cell Senescence and Malignancy.","authors":"Mingke Yu, Lianhui Duan, Yulin Huang, Yixin Cheng, Yuting Wang, Guanyin Huang, Jingrui Lian, Siqi Chen, Feiqiu Wen, Ling Guo, Xin Hong, Sangyu Shen, Guiping Chen, Yuanhong Gao, Chun Wu, Xuefei Liu","doi":"10.1158/2326-6066.CIR-25-1081","DOIUrl":"10.1158/2326-6066.CIR-25-1081","url":null,"abstract":"<p><p>Colorectal cancer with liver metastases remains a clinical challenge. CXCL13 is widely recognized as a biomarker of immunotherapy response. However, the functional heterogeneity (protumor vs. antitumor) of CXCL13+CD4+ T-cell subsets has long been controversial. Through integrated analysis of single-cell RNA sequencing data from colorectal cancer clinical samples and pan-cancer datasets, combined with experimental validations, we first identified a prometastatic neuromedin B+ (NMB+)CXCL13+CD4+ T-cell subset and uncovered a mechanism by which this subset regulates tumor cell \"senescence-malignant transition,\" the NMB-NPSR1 axis. These NMB+CXCL13+CD4+ T cells induced senescence in NPSR1+ malignant cells via NMB secretion, leading to enhanced invasiveness and migration despite reduced proliferation. Activation of NPSR1 triggered the Wnt signaling pathway and epithelial-mesenchymal transition, thereby enhancing cellular malignancy. This NPSR1+ senescent subpopulation also recruited endothelial cells and disrupted tight junction integrity, fostering a prometastatic microenvironment. As a proof-of-principle study, the combination of the NPSR1 inhibitor SHA68 and anti-PD-1 demonstrated remarkable antitumor effects using mouse models of colorectal cancer metastasis. Overall, this study uncovered the role of NMB+CXCL13+CD4+ T cells in promoting tumor cell senescence while influencing tumor metastasis, offering potential clinical implications for the diagnosis and treatment of metastatic colorectal cancer.</p>","PeriodicalId":9474,"journal":{"name":"Cancer immunology research","volume":" ","pages":"1150-1171"},"PeriodicalIF":7.9,"publicationDate":"2026-07-02","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"147763252","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}