Cancer immunology research最新文献

{"title":"Artificial Intelligence Can Predict Personalized Immunotherapy Outcomes in Cancer.","authors":"Ling Huang, Xuewei Wu, Jingjing You, Zhe Jin, Wenle He, Jie Sun, Hui Shen, Xin Liu, Xin Yue, Wenli Cai, Shuixing Zhang, Bin Zhang","doi":"10.1158/2326-6066.CIR-24-1270","DOIUrl":"10.1158/2326-6066.CIR-24-1270","url":null,"abstract":"<p><p>The rapid advancement of artificial intelligence (AI) technologies has opened new avenues for advancing personalized immunotherapy in cancer treatment. This review highlights current research progress in applying AI to optimize the use of immunotherapy for patients with cancer. Recent studies demonstrate that AI models can accurately diagnose cancers and discover biomarkers by integrating multi-omics and imaging data, establish predictive models to estimate treatment responses and adverse reactions, formulate personalized treatment plans integrating multiple modalities by considering various factors, and achieve precise patient stratification and clinical trial matching, thereby addressing specific obstacles throughout processes from diagnosis to treatment in personalized immunotherapy. Furthermore, this review also discusses the challenges and limitations faced by AI in clinical applications, such as difficulties in data acquisition, low quality of data, poor interpretability of models, and insufficient generalization ability. Finally, we outline future research directions, including optimizing data management, developing explainable AI, and improving the generalization ability of models. These efforts aim to optimize the role of AI in personalized immunotherapy and promote the development of precision medicine. To ensure the clinical applicability of these AI models, large-scale studies, multi-omics integration, and prospective clinical trials are necessary.</p>","PeriodicalId":9474,"journal":{"name":"Cancer immunology research","volume":" ","pages":"964-977"},"PeriodicalIF":8.1,"publicationDate":"2025-07-02","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144274255","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":"Identification of the Distinct Immune Microenvironment Features Associated with Progression Following High-Dose Melphalan and Autologous Stem Cell Transplant in Multiple Myeloma.","authors":"Parvathi Sudha, Travis S Johnson, Habib Hamidi, Ke Yang, Enze Liu, Brent Smith, Vivek Chopra, Michael Nixon, Faiza Zafar, Sherif S Farag, Gareth J Morgan, Ola Landgren, Kelvin Lee, Attaya Suvannasankha, Magdalena Czader, Rafat Abonour, Mohammad Abu Zaid, Brian A Walker","doi":"10.1158/2326-6066.CIR-25-0019","DOIUrl":"10.1158/2326-6066.CIR-25-0019","url":null,"abstract":"<p><p>A key treatment for patients with multiple myeloma is high-dose melphalan followed by autologous stem cell transplant (ASCT). It can provide a deep response with long-term remission. However, some patients progress quickly, and it is not clear why. In this study, we performed single-cell RNA and T-cell receptor sequencing of the immune microenvironment of 40 patients before and after ASCT to determine if differences in the immune composition could define those who would progress. Clear differences in cell populations were identified in progressors, including increased T-cell infiltration, decreased T-cell receptor diversity, and decreased frequency of monocytes and CD56bright NK cells. We identified cell interactions that predicted progression, including increased frequency of CD8+ exhausted T cells and stromal cells and decreased frequency of CD56bright NK cells and plasmacytoid dendritic cells. We propose and validate a model of progression that can also be determined by flow cytometry. Together, these data highlight the importance of the immune microenvironment in understanding responses to ASCT.</p>","PeriodicalId":9474,"journal":{"name":"Cancer immunology research","volume":" ","pages":"1070-1079"},"PeriodicalIF":8.1,"publicationDate":"2025-07-02","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12214876/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143974034","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":"Somatic Mutations in HLA Class Genes and Antigen-Presenting Molecules in Malignant Glioma.","authors":"Sara C Schulte, Wolfgang Peter, Georg Rosenberger, Moritz Schäfer, Cecile L Maire, Alessandra Rünger, Alice Ryba, Kristoffer Riecken, Krystian D Fita, Jakob Matschke, Nuray Akyüz, Judith Dierlamm, Gunnar W Klau, Franz L Ricklefs, Jens Gempt, Manfred Westphal, Katrin Lamszus, Alexander Dilthey, Malte Mohme","doi":"10.1158/2326-6066.CIR-24-0419","DOIUrl":"10.1158/2326-6066.CIR-24-0419","url":null,"abstract":"<p><p>Immune evasion is a hallmark of gliomas, yet the genetic mechanisms by which tumors escape immune surveillance remain incompletely understood. In this study, we systematically examined the presence of somatic mutations in HLA genes and genes encoding proteins involved in antigen presentation across isocitrate dehydrogenase wild-type and mutant gliomas using targeted next-generation sequencing. To address the challenges associated with detecting somatic mutations in these highly polymorphic and complex regions of the genome, we applied a combination of short-read and long-read sequencing techniques, extended the genetic region of interest (exons and introns), and applied a tailored bioinformatics analysis pipeline, which enabled an accurate evaluation of comprehensive sequencing data. Our analysis identified mutations in HLA class II and nonclassic HLA genes as well as genes associated with antigen presentation, such as TAP1/2 and B2M. Three-dimensional modeling of individual mutations simulated the potential impact of somatic mutations in TAP1 and B2M on the encoded protein configuration. The presence of somatic mutations supports the role of antigen-presenting genes in the pathophysiology and potential immune escape of gliomas. Our data demonstrated an increased frequency of such mutations in recurrent glioblastoma, potentially resulting from a positive selection or mutagenic enrichment of tumor cells during tumor progression. Taken together, this research generates new insights and hypotheses for the functional analysis and optimization of immunotherapy strategies for gliomas, which may guide personalized treatment paradigms.</p>","PeriodicalId":9474,"journal":{"name":"Cancer immunology research","volume":" ","pages":"1111-1123"},"PeriodicalIF":8.1,"publicationDate":"2025-07-02","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143954635","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":"METTL3 Inhibition Restores PD-L1 Expression and CD8+ T-cell Cytotoxic Function in Immunotherapy-Treated Gastric Cancer.","authors":"Ming Fang, Yaling Li, Peng Wang, Yanan Wang, Xiaoqian Wang, Xiaoxia Wa, Yu Zhang, Zhenyu He, Jiawei Li, Ling Li, Yun Su, Huinian Zhou, Jianzheng He, Yongqi Liu","doi":"10.1158/2326-6066.CIR-24-1179","DOIUrl":"10.1158/2326-6066.CIR-24-1179","url":null,"abstract":"<p><p>The efficacy of immunotherapy targeting PD-1/PD-L1 in gastric cancer depends on PD-L1 expression levels and the infiltration of immune cells within the tumor microenvironment (TME). Although methyltransferase-like 3 (METTL3) plays a role in the development and progression of gastric cancer, its mechanism of regulating the TME in gastric cancer remains unclear. In this study, we demonstrated that the expression of PD-L1 is regulated by METTL3. We found that METTL3 mediated N6-methyladenosine (m6A) modification of PDL1 mRNA in the 3' untranslated region and induced mRNA degradation through an m6A/YTHDF2-dependent pathway in human gastric cancer cells. METTL3 knockdown or inhibition in gastric cancer cells significantly enhanced Jurkat cell migration and cytotoxic activity. In clinical gastric cancer tissue, a negative correlation was observed between the expression levels of PD-L1 and those of METTL3 or YTHDF2. In vivo, combination treatment with the METTL3 inhibitor STM2457 and PD-1 mAb resulted in a significant reduction in tumor growth, enhanced PD-L1 expression, and increased infiltration of CD8+ T cells. Finally, lower METTL3 expression in tumors correlated with improved sensitivity to anti-PD-1 immunotherapy in patients. Our findings revealed that METTL3-mediated m6A modification of PDL1 mRNA levels represents an epigenetic mechanism regulating antitumor immunity in gastric cancer, and inhibiting METTL3 during PD-1 mAb treatment reshaped the TME, thereby establishing a promising treatment approach for enhancing immunotherapy efficacy in patients with gastric cancer.</p>","PeriodicalId":9474,"journal":{"name":"Cancer immunology research","volume":" ","pages":"1037-1052"},"PeriodicalIF":8.1,"publicationDate":"2025-07-02","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143972842","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":"NEDDylation Regulates CD8+ T-cell Metabolism and Antitumor Immunity.","authors":"Borja Jiménez-Lasheras, Paloma Velasco-Beltrán, Leire Egia-Mendikute, Lorena Pérez-Gutiérrez, So Young Lee, Ander de Blas, Ana García-Del Río, Samanta Romina Zanetti, Asier Antoñana-Vildosola, Adrián Barreira-Manrique, Alexandre Bosch, Jone Etxaniz-Díaz de Durana, Endika Prieto-Fernández, Marina Serrano-Maciá, Naroa Goikoetxea-Usandizaga, Mikel Azkargorta, Félix Elortza, Thomas Gruber, Sebastian Peer, Gottfried Baier, Ashwin Woodhoo, María Luz Martínez-Chantar, Asis Palazon","doi":"10.1158/2326-6066.CIR-24-0127","DOIUrl":"10.1158/2326-6066.CIR-24-0127","url":null,"abstract":"<p><p>NEDDylation is a posttranslational modification whereby the ubiquitin-like molecule NEDD8 is attached to protein substrates in a process dependent on NEDD8-activating enzyme regulatory subunit (NAE1). NEDDylation is emerging as a regulator of cancer biology, but its precise role in antitumor immunity has not been thoroughly characterized. In this study, we examine the impact of NEDDylation in CD8+ T cell-mediated antitumor responses. Analysis of publicly available single-cell RNA sequencing databases revealed that CD8+ tumor-infiltrating lymphocytes showed increased expression of NEDD8 during their differentiation into effector memory cells. In vitro activation of mouse and human CD8+ T cells drove the upregulation of the NEDDylation enzymatic pathway, resulting in an enrichment of NEDDylated proteins. In vivo tumor challenge assays demonstrated that CD8+ T cells lacking NAE1 exhibited reduced antitumor capability and a less activated phenotype with compromised differentiation into effector cells. Upregulating NEDDylation by knocking out deNEDDylase sentrin-specific protease 8 increased the in vitro cytotoxic capability of CD8+ CAR T cells. In addition, LC MS/MS proteomic analyses of NAE1-deficient CD8+ T cells and CD8+ T cells treated with the NEDDylation inhibitor MLN4924 showed a pronounced impairment in metabolic pathways, including glycolysis and oxidative phosphorylation. In this context, we validated lactate dehydrogenase A, α-enolase, and hexokinase 1, which are relevant glycolytic enzymes, as NEDD8 targets. In line with this, NEDDylation-deficient CD8+ T cells demonstrated reduced transcription, protein expression, and enzymatic activity of lactate dehydrogenase. In summary, we uncover NEDDylation as a critical regulator of CD8+ T cell-mediated antitumor immunity.</p>","PeriodicalId":9474,"journal":{"name":"Cancer immunology research","volume":" ","pages":"1004-1021"},"PeriodicalIF":8.1,"publicationDate":"2025-07-02","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12214884/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143989945","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":"A Sampling of Highlights from the Literature: Article Recommendations from Our Deputy and Senior Editors.","authors":"","doi":"10.1158/2326-6066.CIR-13-7-WWR","DOIUrl":"https://doi.org/10.1158/2326-6066.CIR-13-7-WWR","url":null,"abstract":"","PeriodicalId":9474,"journal":{"name":"Cancer immunology research","volume":"13 7","pages":"963"},"PeriodicalIF":8.1,"publicationDate":"2025-07-02","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144539071","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":"First-in-Human Clinical Trial of Vaccination with WDVAX, a Dendritic Cell-Activating Scaffold Incorporating Autologous Tumor Cell Lysate, in Patients with Metastatic Melanoma.","authors":"F Stephen Hodi, Anita Giobbie-Hurder, Kwasi Adu-Berchie, Srin Ranasinghe, Ana Lako, Mariano Severgnini, Emily M Thrash, Jason L Weirather, Joanna Baginska, Michael P Manos, Edward J Doherty, Alexander Stafford, Heather Daley, Jerome Ritz, Patrick A Ott, Kathleen L Pfaff, Scott J Rodig, Charles H Yoon, Glenn Dranoff, David J Mooney","doi":"10.1158/2326-6066.CIR-24-0333","DOIUrl":"10.1158/2326-6066.CIR-24-0333","url":null,"abstract":"<p><p>The optimal means to prime for effective antitumor immunity in a patient with cancer remain elusive in the current era of checkpoint blockade. Crafting a strategy to amplify the number and function of CD8+ T cells while blocking regulatory cells should increase immunotherapy efficacy. Biomaterial carriers have been demonstrated in preclinical studies to amplify the effects of immunomodulatory agents, synergistically integrate the effects of different agents, and concentrate and manipulate immune cells in vivo. Herein, we report data from a phase I trial in patients with metastatic melanoma who received the cytokine GM-CSF and the innate Toll-like receptor 9 agonist CpG oligonucleotide admixed with autologous tumor lysate onto a microporous poly-lactide-co-glycolide matrix polymer scaffold that achieves precise control over the spatial and temporal release of immunostimulatory agents in vivo. This materials system (WDVAX) served as a physical antigen-presenting structure to which dendritic cells and other immune-stimulating cells are recruited and activated. In this first clinical trial of a macroscale biomaterial-based vaccine, WDVAX treatment was found to be feasible and to induce immune activation in patients with melanoma.</p>","PeriodicalId":9474,"journal":{"name":"Cancer immunology research","volume":" ","pages":"978-989"},"PeriodicalIF":8.1,"publicationDate":"2025-07-02","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143983395","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":"Adaptive NK Cells Exhibit Tumor-Specific Immune Memory and Cytotoxicity in Ovarian Cancer.","authors":"Yizhe Sun, Andrea Rodgers Furones, Okan Gultekin, Shruti Khare, Shi Yong Neo, Wenyang Shi, Lidia Moyano-Galceran, Kong-Peng Lam, Ramanuj Dasgupta, Jonas Fuxe, Sahar Salehi, Kaisa Lehti, Dhifaf Sarhan","doi":"10.1158/2326-6066.CIR-24-0852","DOIUrl":"10.1158/2326-6066.CIR-24-0852","url":null,"abstract":"<p><p>Adaptive NK (aNK) cells have emerged as a subset of NK cells with memory-like properties and specific cytotoxicity, offering promising therapeutic potential in cancer immunotherapy. In this study, we explored the role of aNK cells in high-grade serous ovarian cancer, focusing on their ability to establish tumor-specific immune memory and effectively target autologous tumors. Through a combination of in silico, in vitro, and ex vivo approaches, we demonstrated that aNK cells, in contrast to conventional NK cells, exhibit recall responses, specific cytotoxicity, and preferential infiltration into the tumor microenvironment. Our data revealed that aNK cells interact with dendritic cells within the tumor microenvironment via the HLA-E/NKG2C axis and CXCR2 signaling, contributing to their memory formation and tumor-targeting capabilities. These findings suggest that aNK cells could serve as potent agents in NK cell-based immunotherapies, particularly in solid tumors such as high-grade serous ovarian cancer, in which they resist immunosuppressive signals and maintain robust antitumor activity. This study provides new insights into the adaptive-like properties of aNK cells, underscoring their potential for advancing cancer immunotherapy strategies.</p>","PeriodicalId":9474,"journal":{"name":"Cancer immunology research","volume":" ","pages":"1080-1097"},"PeriodicalIF":8.1,"publicationDate":"2025-07-02","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143978841","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":"Deep Immune Phenotyping Reveals Distinct Immunopathogenesis in Checkpoint Inhibitor-Induced Colitis Compared with Ulcerative Colitis.","authors":"Giulia Pesch, Ignazio Piseddu, Jan Gaertig, Nora Kramer, Rafaela Kramer, Thomas U Schulz, Maximilian Zwiebel, Stephan Ledderose, Jimmy Retzlaff, Markus Eckstein, Georg Schett, Claudia Kammerbauer, Christina Schmitt, Joerg Kumbrink, Michael Erdmann, Wolfgang Kruis, Michael Dougan, Julia Mayerle, Lars E French, Julio Vera, Thierry M Nordmann, Matthias Mann, Frederick Klauschen, David Anz, Lucie Heinzerling","doi":"10.1158/2326-6066.CIR-24-0387","DOIUrl":"10.1158/2326-6066.CIR-24-0387","url":null,"abstract":"<p><p>Although initially assumed to be similar, immune checkpoint inhibitor (ICI)-induced autoimmunity can differ from spontaneous autoimmune disease in regard to clinical presentation, pathogenesis, and therapy. Despite limited pathogenetic understanding, ICI-induced colitis (irColitis), a common adverse event during ICI therapy, is treated analogously to its autoimmune counterpart, ulcerative colitis (UC). Thus, there is a tremendous need to characterize immunophenotypes in both forms of colonic inflammation to ultimately identify specific therapeutic strategies. In a multicenter study, local and systemic immunophenotypes of patients with irColitis were compared with those of patients with UC. Colonic mucosa, patient serum, and peripheral blood mononuclear cells (PBMC) of 20 patients with irColitis, 15 patients with UC, and 25 patients receiving ICI without toxicity were investigated. Immunophenotyping was performed using gene expression analyses of mucosal samples and PBMC, serum proteomics, and flow cytometry-based PBMC analysis. Mucosal gene expression analysis revealed higher expression of B cell- and TNF signaling-related genes in UC, whereas irColitis mucosa showed an upregulation of genes associated with effector T-cell responses and IFN signaling. Immunophenotyping of PBMC demonstrated increased activation and differentiation of T cells and higher expression of exhaustion markers in irColitis compared with UC. In contrast, dendritic cells and B cells demonstrated increased markers of activation in patients with UC. Taken together, irColitis is characterized by T cell-associated immunity, whereas B cell- and dendritic cell-mediated immune responses and TNF signaling are more important for UC immunopathogenesis. These observations could help identify more specific and efficient treatment strategies for irColitis.</p>","PeriodicalId":9474,"journal":{"name":"Cancer immunology research","volume":" ","pages":"1053-1069"},"PeriodicalIF":8.2,"publicationDate":"2025-07-02","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143978983","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":"The TRIB2-DNMT1 Pathway Generates an Immune-Cold Microenvironment in Glioblastoma, and Its Inhibition Promotes Immunotherapy.","authors":"Berta Segura-Collar, Blanca Cómitre-Mariano, Denisse Alcivar López, Lucia Modejar-Ruescas, Marta Caamaño-Moreno, Elena Tovar Ambel, Javier Gutierrez-Martin, Marina Garín, Oscar Toldos, Aurelio Hernández-Laín, Ricardo Gargini, Juan M Sepúlveda","doi":"10.1158/2326-6066.CIR-24-0807","DOIUrl":"10.1158/2326-6066.CIR-24-0807","url":null,"abstract":"<p><p>The lack of response of glioblastoma (GBM) to immunotherapy is closely related to the limited number of T cells in the tumor microenvironment. However, it is still not known why GBM is characterized by an immune-cold tumor microenvironment with reduced CD8+ T-cell infiltration when there is substantial myeloid cell infiltration and a substantial alteration of the blood-brain barrier. The aim of this study was to identify regulators of low CD8+ T-cell infiltration in GBM. Using transcriptomic screening, we found that tribbles homolog 2 (TRIB2) is a regulator of the immune-cold microenvironment characteristic of GBM. Further analysis of a cohort of 114 brain tumors with IHC, RNA sequencing, and qRT-PCR showed that TRIB2 inhibited the transcription of genes involved in antigen presentation by the tumor cells and those involved in T-cell recruitment by modulating the expression of methylation regulators, in particular DNA methyltransferase 1. Further, we observed 75% survival after TRIB2 inhibition in murine glioma models and showed transcriptomic reprogramming by decitabine of genes involved in the processes described above. In our patient-derived tumor fragments assay, we observed a consistent, generalized response to decitabine, suggesting that DNA methyltransferase 1 inhibition (DNMT1) could be a promising therapeutic strategy for GBM.</p>","PeriodicalId":9474,"journal":{"name":"Cancer immunology research","volume":" ","pages":"1022-1036"},"PeriodicalIF":8.1,"publicationDate":"2025-07-02","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143964322","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}