Cancer immunology research最新文献

{"title":"A Sampling of Highlights from the Literature.","authors":"","doi":"10.1158/2326-6066.CIR-13-4-WWR","DOIUrl":"https://doi.org/10.1158/2326-6066.CIR-13-4-WWR","url":null,"abstract":"","PeriodicalId":9474,"journal":{"name":"Cancer immunology research","volume":"13 4","pages":"453"},"PeriodicalIF":8.1,"publicationDate":"2025-04-02","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143763037","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":"Endogenous CD4+ T Cells That Recognize ALK and the NPM1::ALK Fusion Protein Can Be Expanded from Human Peripheral Blood.","authors":"Serena Stadler, Rafael B Blasco, Vijay Kumar Singh, Christine Damm-Welk, Amin Ben-Hamza, Carlotta Welters, Leo Hansmann, Roberto Chiarle, Wilhelm Woessmann","doi":"10.1158/2326-6066.CIR-24-0445","DOIUrl":"10.1158/2326-6066.CIR-24-0445","url":null,"abstract":"<p><p>Anaplastic lymphoma kinase (ALK) fusion proteins resulting from chromosomal rearrangements are promising targets for cancer immunotherapy. Although ALK-specific CD8+ T cells and epitopes presented on MHC class I have been identified in patients with ALK-positive malignancies, little is known about ALK-specific CD4+ T cells. We screened peripheral blood of 10 patients with ALK-positive anaplastic large-cell lymphoma in remission and six healthy donors for CD4+ T-cell responses to the whole ALK fusion protein, nucleophosmin 1 (NPM1)::ALK. ALK-specific CD4+ T cells were detected in 15 individuals after stimulation with autologous dendritic cells pulsed with long-overlapping ALK peptide pools. CD4+ T-cell epitopes were predominantly located within three specific regions (p102-188, p257-356, and p593-680) in the ALK portion of the fusion protein. We detected CD4+ T cells in one patient that recognized the NPM1::ALK fusion neoepitope and identified a corresponding T-cell receptor (TCR) by TCRαβ single-cell sequencing. The NPM1::ALK fusion-specific TCR was HLA-DR13-restricted and conferred antigen specificity when expressed in a TCR- reporter cell line (58α-β-). Together, our data provide evidence of ALK-specific CD4+ T cells in human peripheral blood, describe target epitopes in patients, and support the consideration of CD4+ T cells in the development of ALK-specific immunotherapies.</p>","PeriodicalId":9474,"journal":{"name":"Cancer immunology research","volume":" ","pages":"487-495"},"PeriodicalIF":8.1,"publicationDate":"2025-04-02","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11964841/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142945088","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":"There and back again: PD-L1 Positivity as a Biomarker for Immune Checkpoint Blockade in Urothelial Carcinoma.","authors":"Arivarasan Karunamurthy, Diwakar Davar","doi":"10.1158/2326-6066.CIR-25-0202","DOIUrl":"10.1158/2326-6066.CIR-25-0202","url":null,"abstract":"<p><p>Biomarkers of responsiveness to immune checkpoint blockade (ICB) are heavily sought given the breadth and depth of the use of ICB in cancer. PD-L1 expression was among the first biomarkers identified, but multiple factors have precluded more widespread use. In this issue, Galsky and colleagues utilize two separate PD-L1 assays to study urothelial carcinoma specimens and observe that SP142 (relative to 22C3) preferentially stains dendritic cells. These observations may help reconcile the discordant performance of the two PD-L1 assays in ICB-treated urothelial carcinoma while underscoring the role of dendritic cells in orchestrating ICB response. See related article by Galsky et al., p. 476 .</p>","PeriodicalId":9474,"journal":{"name":"Cancer immunology research","volume":" ","pages":"454-455"},"PeriodicalIF":8.1,"publicationDate":"2025-04-02","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143623804","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":"Trabectedin Enhances the Antitumor Effects of IL-12 in Triple-Negative Breast Cancer.","authors":"Emily Schwarz, Himanshu Savardekar, Sara Zelinskas, Abigail Mouse, Gabriella Lapurga, Justin Lyberger, Adithe Rivaldi, Emily M Ringwalt, Katherine E Miller, Lianbo Yu, Gregory K Behbehani, Timothy P Cripe, William E Carson","doi":"10.1158/2326-6066.CIR-24-0775","DOIUrl":"10.1158/2326-6066.CIR-24-0775","url":null,"abstract":"<p><p>IL-12 is a potent NK cell-stimulating cytokine, but the presence of immunosuppressive myeloid cells such as myeloid-derived suppressor cells (MDSC) can inhibit IL-12-induced NK-cell cytotoxicity. Thus, we hypothesized that trabectedin, a myeloid cell-depleting agent, would improve the efficacy of IL-12 in triple-negative breast cancer (TNBC). In vitro treatment of healthy donor NK cells with trabectedin increased expression of the activation marker CD69 and mRNA expression of T-box transcription factor (Tbx21), the cytotoxic ligands TNF-related apoptosis-inducing ligand (TNFSF10), Fas ligand (FASLG), and the dendritic cell (DC)-recruiting chemokine lymphotactin (XCL1). The combination of IL-12 and trabectedin increased NK-cell cytotoxicity and activation and production of IFN-γ, TNF-α, and granzyme B in the presence of human TNBC cells. Treatment of 4T1 and EMT6 tumor-bearing mice with IL-12 and trabectedin led to a significant reduction in tumor burden compared with single-agent controls and the highest levels of plasma IFN-γ, intratumoral CD8+ T cells, and conventional type 1 DC. MDSC and M2-like macrophages were significantly decreased with combination therapy. NK-cell depletion abrogated the effects of combination therapy, as did the elimination of CD8+ T cells. NK-cell depletion led to lower levels of the NK cell-derived chemokine CCL5 and the DC-derived chemokine CXCL10, higher tumor burden, and decreased intratumoral CD8+ T cells. IL-12 and trabectedin also significantly enhanced the response of TNBC to anti-PD-L1 therapy. These data suggest that MDSC depletion augments the ability of IL-12-activated NK cells to drive the infiltration of DC and CD8+ T cells into TNBC for an antitumor effect.</p>","PeriodicalId":9474,"journal":{"name":"Cancer immunology research","volume":" ","pages":"560-576"},"PeriodicalIF":8.1,"publicationDate":"2025-04-02","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11962391/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142945100","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":"Naturally arising memory-phenotype CD4+ T lymphocytes give rise to multiple helper subsets to contribute to tumor immunity while inhibiting GVHD.","authors":"Ziying Yang, Jing Li, Hideaki Watanabe, Feng Gao, Akihisa Kawajiri, Keita Koinuma, Kosuke Sato, Yuko Okuyama, Shunichi Tayama, Yoichiro Iwakura, Naoto Ishii, Takeshi Kawabe","doi":"10.1158/2326-6066.CIR-24-0598","DOIUrl":"https://doi.org/10.1158/2326-6066.CIR-24-0598","url":null,"abstract":"<p><p>Memory-phenotype (MP) CD4+ T lymphocytes spontaneously develop in steady state from peripheral naïve precursors in a manner dependent on self-antigen recognition. While MP cells possess innate type 1 and 3 effector functions that can contribute to host defense and autoimmunity, their immunological functions in tumor immunity and graft-versus-host disease (GVHD), which results from therapeutic bone marrow transplantation (BMT) against hematological malignancies, remain unclear. Here we show that in mixed lymphocyte reactions, MP lymphocytes can generate T helper 1 (Th1), T helper 17 (Th17), and regulatory T (Treg) cell subsets, whereas naïve cells dominantly differentiate to Th1. Consistent with this, naïve lymphocytes mainly induce Th1 responses in the mouse EL4 model of malignant lymphoma and the B16 model of malignant melanoma, whereas MP cells efficiently give rise to Th1, Th17, and Treg subsets to exert mild, IFN--dependent antitumor activities in vivo. Moreover, we demonstrate using a mouse model of BMT that MP cells more efficiently differentiate into Treg cells to partially suppress GVHD as compared to naïve T lymphocytes. Furthermore, our data suggest that when used as donor T lymphocytes in BMT in tumor-bearing mice, MP cells give rise to Th1, Th17, and Treg cells to generate antitumor responses without inducing GVHD. Together these results identify MP cells as a unique T-cell population that has potential to generate multiple T helper subsets including Th1 and Treg cells, thereby contributing to tumor immunity while inhibiting development of BMT-associated GVHD.</p>","PeriodicalId":9474,"journal":{"name":"Cancer immunology research","volume":" ","pages":""},"PeriodicalIF":8.1,"publicationDate":"2025-04-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143763027","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":"In situ delivery of Gasdermin E mRNA promotes antitumor immunity via creatine-elicited type Ⅰ interferon signaling in monocytes.","authors":"Hanjun Li, Jing Lu, Shudan Tan, Ting Jiang, Xin He, Wen Qiao, Cegui Hu, Sumiya Dalangood, Jinzhong Lin, Jun Gui","doi":"10.1158/2326-6066.CIR-24-0834","DOIUrl":"https://doi.org/10.1158/2326-6066.CIR-24-0834","url":null,"abstract":"<p><p>Local immunotherapy stimulates immune responses against tumors while avoiding adverse effects associated with systemic administration. However, current strategies for tumor-targeted in situ immunotherapy are still limited. mRNA-based gene therapy represents a promising strategy. Gasdermin E (GSDME)-mediated pyroptosis is reported to exert anti-tumor immunity. Here, we synthetized mRNA encoding GSDME encapsulated by lipid nanoparticles (LNP-Gsdme). In situ delivery of LNP-Gsdme through intratumoral injection suppressed tumor growth, boosted monocyte infiltration and activated CD8+T cells. LNP-Gsdme induced immunogenic cell death (ICD) in tumor cells, releasing creatine as a metabolic damage-associated molecular pattern. Creatine elicited cGAMP-STING-type I interferon signaling pathway in monocytes and reprogrammed intratumoral monocytes toward an immunostimulatory phenotype, consequently potentiating CD8+T cell-mediated anti-tumor immune responses. Furthermore, creatine supplementation enhanced the antitumor efficacy of LNP-Gsdme. Our study uncovers creatine as an important metabolic biomarker of pyroptosis-induced ICD in tumors, providing new insights and a promising therapeutic approach for in vivo mRNA-based immunotherapies for cancer.</p>","PeriodicalId":9474,"journal":{"name":"Cancer immunology research","volume":" ","pages":""},"PeriodicalIF":8.1,"publicationDate":"2025-04-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143762940","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":"Memory-like natural killer cell and CD19-antibody based immunotherapy in combination with tyrosine-kinase inhibition has antitumor effects against Ph(-like) acute lymphoblastic leukemia.","authors":"Zoya Eskandarian, Richard Hauch, Sabrina Schuster, Dorothee Winterberg, Hjördis Grabellus, Carlotta Imelmann, Anna-Lena Heitmann, Marlene Goos, Khadija Rudloff, Julia Strauss, Gerrit Wolters-Eisfeld, Peter Nollau, Katja Klausz, Ulrich Schüller, Matthias Peipp, Michael Spohn, Martin A Horstmann","doi":"10.1158/2326-6066.CIR-24-0746","DOIUrl":"https://doi.org/10.1158/2326-6066.CIR-24-0746","url":null,"abstract":"<p><p>Philadelphia-like acute lymphoblastic leukemia (Ph-like ALL) is a molecularly distinct tyrosine kinase-driven cancer that has a high relapse rate and poor response toward combinatorial chemotherapy. Tyrosine kinase inhibitors (TKI) in the clinic improve the survival of patients with Ph-like ALL. Engineered antibody and cell-based immunotherapies can advance treatment for this genetic subtype of ALL. Allogeneic memory-like natural killer (ML-NK) cells have been used to treat leukemia and have shown a low risk of graft-versus-host reaction, which may be combined with leukemia epitope-targeting antibodies. However, mutation or pathway-directed TKI of Ph-like ALL can interfere with memory-function and antibody-dependent NK cell-mediated cytotoxicity (ADCC). Here, we explored the potential of ML-NK cells and Fc-enhanced CD19-ADCC in combination with TKI directed against kinase-driven leukemia models, including patient-derived xenografted Ph-like ALL. We demonstrate that receptor crosslinking in coculture with K562 feeder cells generated a robust memory-like state of NK cells than coactivation with soluble interleukins (ILs) 12, 15, and 18, as determined by genomic and functional studies. After receptor crosslinking and subsequent ILs-preactivation, the optimized ML-NK cells showed enhanced antileukemic effector functions which could compensate for exhausted B cell precursor leukemia-infiltrating primary NK cells. TKI differentially affected multiple features of NK cell biology including viability, expansion, metabolism, receptor repertoire and cytotoxicity. ADCC was maintained upon exposure to specific ABL or JAK-inhibitors, in contrast to the multi-target TKI dasatinib impeding SYK-dependent ADCC. In conclusion, optimized ML-NK cell and CD19 antibody-based immunotherapy combined with carefully selected TKI demonstrates significant in vitro treatment efficacy in kinase-driven leukemia.</p>","PeriodicalId":9474,"journal":{"name":"Cancer immunology research","volume":" ","pages":""},"PeriodicalIF":8.1,"publicationDate":"2025-04-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143762947","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":"Anti-CTLA4 therapy leads to early expansion of a peripheral Th17 population and induction of Th1 cytokines.","authors":"Mari Nakazawa, Soren Charmsaz, Elsa Hallab, Mike Fang, Chester Kao, Madelena Brancati, Kabeer Munjal, Howard L Li, James M Leatherman, Ervin Griffin, Christopher J Thoburn, Evan J Lipson, Yasser Ged, Jean Hoffman-Censits, Marina Baretti, Laura Tang, Sanjay Bansal, Rachel Garonce-Hediger, Aditi Guha, G Scott Chandler, Rajat Mohindra, Elizabeth M Jaffee, Won Jin Ho, Mark Yarchoan","doi":"10.1158/2326-6066.CIR-24-1055","DOIUrl":"https://doi.org/10.1158/2326-6066.CIR-24-1055","url":null,"abstract":"<p><p>The systemic immunological effects of combining anti-CTLA4 therapy with PD-(L)1 blockade remain incompletely characterized, despite the widespread use of this combination in treating various solid tumors across multiple stages of disease. Herein, we investigated the additive impact of anti-CTLA4 on peripheral immune signatures in patients undergoing PD-(L)1 blockade, using blood samples from a cohort of patients receiving checkpoint inhibitor therapy for advanced solid tumors. We performed in-parallel analysis of peripheral blood mononuclear cells (PBMC) using Cytometry by Time-of-Flight (CyTOF) and plasma cytokines using Luminex immunoassay. Our study cohort included 104 patients, 54 who received anti-PD(L)1 alone and 50 who received anti-PD(L)1 in combination with anti-CTLA4. As compared to single-agent anti-PD(L)1, combination therapy was associated with a greater expansion of CD4+ T helper cell subsets, including Th17 (adjusted p=0.04) and regulatory T cells (Treg) (adjusted p=0.02), after multivariable and multiple testing adjustment. In patients receiving anti-CTLA4, examination of functional marker expression within the Th17 subset revealed an increase in expression of the Th1-related transcription factor TBET (p=0.003). Assessment of the peripheral cytokine signatures showed an increase in Th1-associated cytokines (p=0.002) in recipients of combination anti-PD(L)1 and anti-CTLA4, particularly the IFN-inducible cytokines MIG (adjusted p=0.05) and IP-10 (adjusted p=0.05). Our results confirm prior reports that anti-CTLA4 therapy is associated with augmentation of Th17 cell subsets, and they also show that anti-CTLA4 may reshape CD4+ T-cell responses through Th17-to-Th1 plasticity, revealing a potential mechanism for enhanced antitumor immunity with broader implications immune modulation in immunotherapy.</p>","PeriodicalId":9474,"journal":{"name":"Cancer immunology research","volume":" ","pages":""},"PeriodicalIF":8.1,"publicationDate":"2025-03-27","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143718112","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":"Eph receptors activate myeloid checkpoint receptor LILRB5 to support tumor development.","authors":"Yubo He, Chengcheng Zhang, Lingxiao Tan, Mi Deng, Xiaoye Liu, Ryan Huang, Xing Yang, Jingjing Xie, Qi Lou, Meng Fang, Caroline Smith, Samuel John, Wei Xiong, Xin Li, Cheryl Lewis, Jade Homsi, Ankit Gupta, Ningyan Zhang, Zhiqiang An, Chengcheng Zhang","doi":"10.1158/2326-6066.CIR-24-0737","DOIUrl":"https://doi.org/10.1158/2326-6066.CIR-24-0737","url":null,"abstract":"<p><p>Immunosuppressive myeloid cells are critical obstacles to T cell-centered immune checkpoint blockade therapies, which have been successful in treating a fraction of cancer patients. How tumor cells interact with myeloid cells to regulate immune responses and tumor development is unclear. Here, we report that certain membrane tyrosine kinase Eph receptors, including EphA7 and EphB1, specifically bind the immune inhibitory receptors leukocyte immunoglobin like receptor family B 5 (LILRB5) and leukocyte immunoglobin like receptor family B 2 (LILRB2). These Eph receptors induce LILRB5-mediated signaling activation, and LILRB5 also activates Eph receptor signaling. Activation of LILRB5 promoted immunosuppressive marker expression and inhibited activating marker expression on myeloid cells from cancer patients in vitro. Upon myeloid cell-specific expression of LILRB5 in transgenic mice, the interaction between the Eph receptor on tumor cells and LILRB5 on myeloid cells led to increased tumor growth, increased immunosuppressive myeloid cells, and decreased frequencies of functional T cells compared to control mice. Eph-induced LILRB5 signaling and functions were reversed by LILRB5 blockade. In sum, certain Eph receptors functionally interact with the myeloid checkpoint receptor LILRB5 resulting in bi-directional signaling, and LILRB5 plays an important role in supporting immunosuppressive myeloid cells and sustaining tumor development.</p>","PeriodicalId":9474,"journal":{"name":"Cancer immunology research","volume":" ","pages":""},"PeriodicalIF":8.1,"publicationDate":"2025-03-27","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143718114","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":"Mesenchymal stem cells and fibroblasts contribute to microvascular proliferation in glioblastoma and are correlated with immunosuppression and poor outcome.","authors":"Candice C Poon, Shelley M Herbrich, Yulong Chen, Anwar Hossain, Gregory N Fuller, Sonali Jindal, Sreyashi Basu, Daniel Ledbetter, Marc Macaluso, Lynette M Phillips, Joy Gumin, Zhong He, Brittany C Parker Kerrigan, Sanjay K Singh, Pratishtha Singh, Mohammad Fayyad Zaman, Derek Ng Tang, Sangeeta Goswami, Frederick F Lang, Padmanee Sharma","doi":"10.1158/2326-6066.CIR-24-0743","DOIUrl":"https://doi.org/10.1158/2326-6066.CIR-24-0743","url":null,"abstract":"<p><p>Microvascular proliferation (MVP) is a disease-defining hallmark of glioblastoma (GBM) and other World Health Organization (WHO) grade 4 gliomas. MVP also serves as a poor prognostic marker in various solid tumors. Despite its clinical significance, the mechanisms and biological consequences of MVP are controversial and remain unclear. In this study, we performed single cell RNA-sequencing (scRNA-seq) on paired CD45-CD105+ vascular/perivascular stromal cells (PVSCs) and CD45+CD105± immune cells from 16 primary glioma patient samples, both with and without MVP. This analysis revealed the presence of developmentally-related mesenchymal stem cells (MSCs) alongside cancer-associated fibroblasts (CAFs), pericytes, fibromyocytes, and smooth muscle cells within the CD45-CD105+ compartment. RNA velocity analysis identified PDGFRB as a putative driver gene guiding MSCs toward more mature PVSCs in the context of MVP. Signaling network analysis and digital spatial profiling uncovered interactions between PDGFRB+ PVSCs and immunosuppressive myeloid cell subsets enriched in the perivascular niche, suggesting targetable receptor-ligand interactions. Additionally, a gene signature of MVP-associated PVSCs from gliomas predicted worse prognosis in multiple other solid tumors. This study provides a transcriptomic cell atlas of PVSCs and immune cells in glioma, helping to refine the biological model of MVP which has traditionally focused on endothelial cells.</p>","PeriodicalId":9474,"journal":{"name":"Cancer immunology research","volume":" ","pages":""},"PeriodicalIF":8.1,"publicationDate":"2025-03-25","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143699791","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}