Molecular and Cellular Oncology最新文献

{"title":"mRNA vaccines in oncology: personalized cancer immunization and neoantigen targeting.","authors":"Mridula Parganiha, Jaishriram Rathored, Deepika Sai Painkra","doi":"10.1080/23723556.2026.2652613","DOIUrl":"https://doi.org/10.1080/23723556.2026.2652613","url":null,"abstract":"<p><p>Precision oncology is evolving with personalized mRNA neoantigen vaccines, although long-term clinical responses vary. These mRNA-based vaccines have facilitated the development of patient-specific neoantigens. Clinical success is dependent not only on immunogenicity but also on tumor neoantigen clonality, expression, and presentation by the vaccines. Evidence from trials conducted from 2020 to 2025 shows that indicators like minimal residual disease are crucial. The mRNA-4157 (V940) combined with pembrolizumab demonstrated improved recurrence-free survival in resected high-risk melanoma patients (18-month RFS 79% vs 62%; HR 0.56). Similarly, the autogene cevumeran triggered significant neoantigen-specific T cell responses in 8 out of 16 patients with resected pancreatic ductal adenocarcinoma, leading to a delayed recurrence for immune responders (not reached vs 13.4 months; HR 0.08). This highlights a translational model focusing on tumor clonality, antigen quality, and immune accessibility. The review also addresses (i) clonality aware neoantigen selection; (ii) AI-based predictions of antigen presentation and immunogenicity, including issues of false positives; (iii) alternative delivery systems beyond lipid nanoparticles; and (iv) real-world challenges such as turnaround time, batch variability, regulatory frameworks, and operational costs that impact implementation. A structured model for crucial events and validation plans is proposed to bridge the gap between predictions and actual clinical benefits, utilizing techniques like immunopeptidomics and functional T cell assays.</p>","PeriodicalId":37292,"journal":{"name":"Molecular and Cellular Oncology","volume":"13 1","pages":"2652613"},"PeriodicalIF":1.9,"publicationDate":"2026-04-08","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC13064569/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"147677417","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Exploration of the diagnostic and therapeutic potential of the nucleocytoplasmic shuttling protein TMUB1 by inducing G0/G1 cell cycle arrest in ovarian cancer.","authors":"Jiahong Jiang, Jie Li, Shuai Tang, Liping Shu, Yanhong Chen, Jiaxian Qian, Yanzhou Wang, Yin Chen","doi":"10.1080/23723556.2026.2650223","DOIUrl":"https://doi.org/10.1080/23723556.2026.2650223","url":null,"abstract":"<p><strong>Background: </strong>Ovarian cancer is one of the leading causes of gynaecologic malignancies worldwide. This study aimed to explore the diagnostic and therapeutic potential of TMUB1 in ovarian cancer.</p><p><strong>Methods: </strong>To investigate the subcellular localization of TMUB1 under serum deprivation conditions, immunofluorescence staining was performed. The cell cycle distribution was analysed by flow cytometry. TMUB1-interacting proteins were identified through immunoprecipitation followed by mass spectrometry. Kaplan-Meier survival analysis was used to compare overall survival between patients with high and low TMUB1 expression. Stromal and immune scores for tumour tissues in TCGA were calculated to assess the tumour microenvironment.</p><p><strong>Results: </strong>TMUB1 plays a crucial role in regulating the cell cycle by promoting entry into the G0/G1 phase. Survival analysis revealed that TMUB1 expression is positively associated with favourable prognosis in patients with ovarian cancer. Pathway enrichment analysis highlighted several tumour-related pathways, including ECM-receptor interaction, JAK-STAT signalling, p53 signalling and apoptosis. The high TMUB1 expression group presented lower stromal scores. An inverse correlation was observed between TMUB1 expression and the expression of key immune checkpoint proteins.</p><p><strong>Conclusions: </strong>TMUB1 might participate in the regulation of the G0/G1 cell cycle arrest, and it is a potential diagnostic marker and therapeutic target for ovarian cancer.</p>","PeriodicalId":37292,"journal":{"name":"Molecular and Cellular Oncology","volume":"13 1","pages":"2650223"},"PeriodicalIF":1.9,"publicationDate":"2026-03-30","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC13037437/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"147595294","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"The LNK adaptor protein: a dual regulator of proliferation and migration in solid tumors.","authors":"Jessica C Mantilla-Ollarves, Laura Velazquez, Leticia Rocha-Zavaleta","doi":"10.1080/23723556.2026.2644701","DOIUrl":"https://doi.org/10.1080/23723556.2026.2644701","url":null,"abstract":"<p><p>Cancer is a significant public health problem. Alterations in critical cellular responses, such as proliferation, survival, and migration, are hallmarks of cancer. Deregulation of the JAK/STAT, MAPK, and PI3K/AKT signaling pathways has been implicated in the development of most solid cancers; therefore, their strict control is a primary research focus. The LNK adaptor protein is a key negative regulator of these pathways in normal cells and in certain hematological malignancies, where it regulates the proliferation, migration, and inflammatory response of different cell types. However, the function of LNK in solid tumors is less clear. Recent evidence suggests that LNK inhibits proliferation and migration in some types of solid tumors but activates these same processes in others. In this review, we provide an overview of the essential functions of LNK in healthy tissues, compare these functions with LNK's reported activities in solid tumors, and discuss the potential mechanisms involved in the dual actions of the LNK protein.</p>","PeriodicalId":37292,"journal":{"name":"Molecular and Cellular Oncology","volume":"13 1","pages":"2644701"},"PeriodicalIF":1.9,"publicationDate":"2026-03-16","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12997970/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"147487792","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Lactylation-related genes signature panel in hepatocellular carcinoma reveals the prognostic and therapeutic optimization.","authors":"Ting Xiao, Xianqun Xu, Ziwu Zhao, Han Xue, Shuang Guo, Xinghua Long","doi":"10.1080/23723556.2026.2621475","DOIUrl":"https://doi.org/10.1080/23723556.2026.2621475","url":null,"abstract":"<p><p>Lactylation-related genes (LRGs) exert a significant influence on tumor progression and are critically involved in modulating responses to immune checkpoint inhibitors (ICIs). Leveraging a curated set of 332 LRGs derived from the literature, we identified prognosis-specific hepatocellular carcinoma (HCC) clusters through consensus clustering analysis. Using an integrated bioinformatics approach, we systematically evaluated differences in immune microenvironment infiltration, somatic mutations, copy number variations, and epigenetic modifications between the two tumor subtypes. We subsequently developed a lactylation-related genes signature (LRGS) and independently validated its prognostic efficacy in the TCGA cohort. Notably, the high-LRGS group exhibited significantly reduced overall survival(OS) and diminished response to ICIs. Conversely, the high-LRGS group demonstrated heightened sensitivity to several antitumor agents, including AZD5153, cediranib, foretinib, and vorinostat, relative to the low-LRGS group. Our findings establish a robust LRGS model, offering a clinically actionable tool for prognostic assessment and precision therapy in HCC.</p>","PeriodicalId":37292,"journal":{"name":"Molecular and Cellular Oncology","volume":"13 1","pages":"2621475"},"PeriodicalIF":1.9,"publicationDate":"2026-02-22","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12928659/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"147285474","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"SNX1 inhibits human ovarian cancer progression via regulation of the cell cycle, apoptosis and migration.","authors":"Pin Li, Xiaoyan Yu, Kailing Wen, Lei Wang, Jingran Yu, Ping Chen","doi":"10.1080/23723556.2025.2604899","DOIUrl":"10.1080/23723556.2025.2604899","url":null,"abstract":"<p><p>Sorting nexin 1 (SNX1), a member of the sorting nexin family, has been implicated in various cellular processes, yet its role in ovarian cancer (OV) remains poorly characterized. In this study, we systematically investigated the expression pattern, prognostic relevance and functional impact of SNX1 in OV. Bioinformatics analysis revealed that SNX1 is significantly downregulated in OV tissues, and its low expression is associated with poor overall and progression-free survival. Gene set enrichment analysis indicated that SNX1 downregulation is linked to activation of cancer-related pathways, including p53 signaling, PI3K/AKT signaling, and cell cycle-associated programs such as E2F targets and G2/M checkpoint. Functionally, SNX1 overexpression inhibited OV cell proliferation, blocked G1/S transition (with downregulation of E2F1, CDK2, CDK6, and cyclin D1), promoted apoptosis, and suppressed cell migration by modulating EMT markers (upregulating E-cadherin; downregulating <i>N</i>-cadherin, vimentin, Snail1, and <i>β</i>-catenin). Drug sensitivity analysis demonstrated a synergistic anti-tumor effect between SNX1 overexpression and paclitaxel treatment. Collectively, our findings identify SNX1 as a tumor suppressor and potential therapeutic target in OV, functioning through regulation of cell cycle, apoptosis and migration.</p>","PeriodicalId":37292,"journal":{"name":"Molecular and Cellular Oncology","volume":"13 1","pages":"2604899"},"PeriodicalIF":1.9,"publicationDate":"2025-12-31","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12758353/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145901344","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Inactivation of Acetyl-CoA Acyltransferase 1 enhances the proliferation and motility of nasopharyngeal carcinoma cells.","authors":"Wanqi Wei, Limei Li, Weilin Zhao, Shixing Zheng, Xiaoying Zhou, Haili Liang, Wen Wang, Feng He, Yushan Liang, Guangwu Huang, Zhe Zhang, Xue Xiao","doi":"10.1080/23723556.2025.2583342","DOIUrl":"10.1080/23723556.2025.2583342","url":null,"abstract":"<p><p>Acetyl-CoA acyltransferase 1 (ACAA1), encoding the peroxisomal 3-ketoacyl-CoA thiolase (POT1), plays a pivotal role in the fatty acid beta-oxidation pathway. Accumulating evidence has linked this enzyme to the onset and development of diverse human malignancies. Here, we observed a marked downregulation of ACAA1 in nasopharyngeal carcinoma (NPC), which displayed an inverse correlation with the expression genes coded by Epstein-Barr virus (EBV). Receiver operating characteristic (ROC) curve and Kaplan-Meier survival analysis highlighted the potential of ACAA1 as a valuable diagnostic and prognostic biomarker for NPC. Next, gain-of- function experiments were conducted, and the results vividly illustrated that overexpression of ACAA1 potently impeded the proliferation, migration, and invasion of NPC cells. The inhibitory effect was further verified by the reduced Ki-67 staining intensity and the altered distribution pattern of actin filaments, which are crucial indicators of cell proliferation and motility. Gene ontology (GO) and Kyoto Encyclopedia of Genes and Genomes (KEGG) analyses revealed significant enrichment of immune-related pathways in NPC cells with elevated ACAA1 expression. Moreover, comprehensive xCell, ESTIMATE, and Immunophenoscore analyses underscored the positive association between ACAA1 and immune cell infiltration and the tumor immune effective microenvironment in NPC. Especially, a positive correlation between ACAA1 expression in tumor cells and six immune checkpoint-related genes, namely CD27, PDCD1, CD86, BTLA, TIGIT, and CD28, on immune cells within the tumor microenvironment. Collectively, our findings highlight the potential of ACAA1 as a tumor - suppressor gene and suggest its possible involvement in the immune evasion mechanisms of NPC. This study may provide novel insights into the molecular pathogenesis of NPC and offer new therapeutic targets for this malignancy.</p>","PeriodicalId":37292,"journal":{"name":"Molecular and Cellular Oncology","volume":"12 1","pages":"2583342"},"PeriodicalIF":1.9,"publicationDate":"2025-11-17","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12631977/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145589244","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Loss of Schwann cell's normal rhythmic core clock gene expression and gain of rhythmic expression of oncogenic driver genes in malignant NF1-associated peripheral nerve sheath tumor.","authors":"Sandra Leisz, Antonio Pelligrino, Saskia Fritzsche, Merle Wiegers, Markus Wösle, Christian Linke, Swanhild Lohse, Daniel Tippner, Christian Scheller, Christian Strauss, Eva Ehrentreich-Förster, Faramarz Dehghani, Stanislav Sys, Erik Maronde, Anja Harder","doi":"10.1080/23723556.2025.2561292","DOIUrl":"10.1080/23723556.2025.2561292","url":null,"abstract":"<p><p>Neurofibromatosis type 1 (NF1) is an autosomal dominant tumor syndrome caused by pathogenic variants in the <i>NF1</i> gene. Beside tumor formation, patients often have sleep disturbances, suggesting circadian involvement. Previous NF1 studies have implicated MAPK pathway, cAMP-PKA, calcium signaling, and ALK in circadian regulation, and shown disrupted rhythms in murine astrocytes lacking <i>NF1</i>. However, whether human Schwann cells show rhythmic gene expression remains unknown, although impaired rhythms may contribute to tumorigenesis. In this study, we analyzed normal human Schwann cells and NF1-derived malignant peripheral nerve sheath tumors (MPNST) for rhythmic gene expression. Cultured cells were synchronized via serum shock, and mRNA levels of core clock and associated genes (e.g. <i>ARNTL</i>, <i>JUN, TGFA, CLOCK, VEGFA, MYC</i>) were quantified at defined intervals. We observed rhythmic core clock gene expression in normal Schwann cells, demonstrating intrinsic circadian oscillations in peripheral glia. In contrast, MPNST lacked rhythmicity in core clock genes, instead showing de novo rhythmic expression of oncogenes and growth factors like <i>MYC</i> and <i>VEGFA</i>. Thus, loss of clock gene rhythmicity (desynchronization) and emergence of rhythmic oncogene expression (synchronization) in NF1-associated MPNST further our understanding of peripheral glial physiology and tumorigenesis. These insights suggest that chronotherapeutic strategies may be beneficial for NF1-associated MPNST.</p>","PeriodicalId":37292,"journal":{"name":"Molecular and Cellular Oncology","volume":"12 1","pages":"2561292"},"PeriodicalIF":1.9,"publicationDate":"2025-09-23","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12459363/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145151321","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Cytokeratin expression in breast cancer: from mechanisms, progression, diagnosis, and prognosis to therapeutic implications.","authors":"Ensiyeh Bahadoran, Sahar Moghbelinejad, Ghazaleh Mohammadi, Hamid Shahbazmohammadi, Zohreh Abdolvahabi, Manijeh Jalilvand, Isareza Zare, Masood Alaei, Sanaz Keshavarz Shahbaz","doi":"10.1080/23723556.2025.2526230","DOIUrl":"10.1080/23723556.2025.2526230","url":null,"abstract":"<p><strong>Background and aim: </strong>Cytokeratins (CKs) are structural proteins vital to epithelial integrity and play key roles in breast cancer progression. This review explores their expression, functions, and therapeutic potential.</p><p><strong>Methods: </strong>A systematic review was performed using PubMed, Scopus, and Google Scholar. We focused on in vivo, in vitro, and human studies - as well as review articles - published through 1982 that included keywords such as KRT5/13/16/17/18/19/23/80, Cytokeratin 5/13/16/17/18/19/23/80, Keratin 5/13/16/17/18/19/23/80, CK5/13/16/17/18/19/23/80, Cancer, Tumor, Breast cancer, Triple-negative breast cancer, and TNBC. Following title, abstract, and full-text screening of extracted studies, irrelevant articles and duplicates were excluded.</p><p><strong>Results: </strong>CK5 and CK17 are strongly associated with aggressive breast cancer subtypes, particularly triple-negative breast cancer (TNBC), influencing tumor invasiveness and drug resistance. CK18 and CK19 play key roles in estrogen receptor signaling and epithelial stability. Newly identified CKs, CK23 and CK80, show strong correlations with metastasis and poor prognosis. CK-driven pathways, such as the Wnt/β-catenin and EMT pathways, contribute to tumor progression and therapy resistance.</p><p><strong>Conclusion: </strong>CKs are key biomarkers for breast cancer classification, prognosis, and therapy response. Their roles in tumor biology suggest potential for targeted treatment and personalized care to improve outcomes.</p>","PeriodicalId":37292,"journal":{"name":"Molecular and Cellular Oncology","volume":"12 1","pages":"2526230"},"PeriodicalIF":2.6,"publicationDate":"2025-07-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12218508/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144555202","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Single-cell analysis reveals XCL1+ CD8+ T cells as a therapeutic target in hepatocellular carcinoma.","authors":"Guowei Li, Fan Yang, Zechao Li, Zhicheng Chen, Geng Luo, Hongtao Yuan, Chaoxian Zhao","doi":"10.1080/23723556.2025.2523085","DOIUrl":"10.1080/23723556.2025.2523085","url":null,"abstract":"<p><p>XCL1 (lymphotactin), a C-chemokine primarily produced by activated CD8+ T cells, remains poorly characterized in the context of immunotherapy. Here, we conducted comprehensive analyses based on multiple scRNA-seq datasets to identify the presence of XCL1+ CD8+ T cells in hepatocellular carcinoma (HCC) tumor microenvironment. Multiplex Immunohistochemistry and clinical data revealed that the infiltration of this cell population correlated with favorable outcomes. Cell-cell communication demonstrated interactions between XCL1+ CD8+ T cells and NK cells or myeloid cells via CD99 and MIF signaling pathways, respectively. These findings were further supported by spatial transcriptomic data. Using two independent bulk RNA-seq datasets, we found the mean of expression of XCL1 and CD8A could be an independent factor for prognosis of HCC, and next built a prediction score with five marker genes involved in XCL1+ CD8+ T cell population. Our findings proposed that XCL1 may play a key role in anti-tumor immunity and XCL1+ CD8+ T cell population could be a potential target to improve responses for immunotherapy in HCC.</p>","PeriodicalId":37292,"journal":{"name":"Molecular and Cellular Oncology","volume":"12 1","pages":"2523085"},"PeriodicalIF":1.9,"publicationDate":"2025-06-23","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12716029/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145805819","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"TRIM22 promotes glioblastoma development by ubiquitinating Bcl-2.","authors":"Jiahao Zhang, Yuning Chen, Gaosong Wang, Hui Huang, Yuankun Liu, Jin Huang, Junfei Shao, Jiantong Jiao, Chao Cheng","doi":"10.1080/23723556.2025.2518679","DOIUrl":"10.1080/23723556.2025.2518679","url":null,"abstract":"<p><p>Glioblastoma (GBM) exhibits elevated TRIM22 expression correlated with tumor progression, as validated in TCGA/GEO databases. The effects of TRIM22 knockdown and overexpression on GBM proliferation were evaluated with cellular assays. TRIM22 was identified as a potential Bcl-2 activator via a ubiquitination microarray. Flow cytometry (FCM) was utilized to investigate cell apoptosis. Additionally, the expression levels of Bcl-2 and proteins associated with Bcl-2 were evaluated using Western blot analysis. The interaction and ubiquitination of TRIM22 and Bcl-2 were analyzed via immunoprecipitation (IP). TRIM22 overexpression is correlated with glioma progression, and TRIM22 deficiency inhibits GBM cell proliferation. FCM revealed that TRIM22 knockdown promotes GBM cell apoptosis. A TRIM22-overexpressing ubiquitination microarray identified TRIM22 as a potential activator of Bcl-2. Western blot analysis revealed that TRIM22 increases the protein expression levels of Bcl-2. Ubiquitination assays revealed that TRIM22 promotes the stability of Bcl-2 via nondegradative ubiquitination. IP experiments indicated that TRIM22 binds to Bcl-2. TRIM22 may significantly impact glioma progression by modulating Bcl-2. Previous studies have shown that knockdown of TRIM22 can enhance the sensitivity of temozolomide treatment, so TRIM22 is expected to become a new target for glioma immunotherapy.</p>","PeriodicalId":37292,"journal":{"name":"Molecular and Cellular Oncology","volume":"12 1","pages":"2518679"},"PeriodicalIF":2.6,"publicationDate":"2025-06-18","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12184166/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144477148","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}