Cancer gene therapy最新文献

{"title":"Clinical translation of senescence-related pan-cancer multi-omics: tools for assessment and immunotherapy prediction.","authors":"Xin Gao, Xue-Jian Zhou","doi":"10.1038/s41417-026-01080-1","DOIUrl":"https://doi.org/10.1038/s41417-026-01080-1","url":null,"abstract":"<p><p>Cellular senescence (CS) exerts dual roles in tumorigenesis, yet its pan-cancer molecular characteristics and clinical value remain unclear, hindering its translation to oncology and personalized therapy. To address the lack of specific and universal tools for senescence assessment and immunotherapy response prediction, this study systematically analyzed 1259 CS-related genes from the CellAge database across 31 cancer types by integrating multi-omics data, including bulk RNA-seq, single-cell/spatial transcriptomics, and CRISPR screening. We developed a rank-based algorithm SenScoreR (publicly available at https://gxhub.shinyapps.io/SenScoreR/ ) for senescence quantification, validated with 10 independent datasets, and constructed a machine learning-based predictive model CS.Sig for immunotherapy response. Results showed that tumors had significantly lower Rank-based Senescence Score (RSS) than normal tissues across 31 cancers (average diagnostic AUC = 0.895), with low RSS linked to poor survival; high RSS correlated with reduced genomic instability, enriched CD8⁺ T/NK cell/macrophage infiltration, upregulated PD-L1 expression, and elevated immune cytolytic activity. CS.Sig demonstrated robust performance in predicting ICI response (AUC = 0.716 across 10 cohorts), outperforming 13 existing signatures, while CRISPR screening identified 17 senescence-related targets (e.g., CEP55, PPP1CC) whose knockout enhanced anti-tumor immunity. Our findings clarify CS's role in maintaining tumor genomic stability and shaping immune microenvironments, and the developed SenScoreR, CS.Sig, and identified targets bridge basic CS research with clinical oncology, providing a translational resource and hypothesis basis for future experimental and clinical validation.</p>","PeriodicalId":9577,"journal":{"name":"Cancer gene therapy","volume":" ","pages":""},"PeriodicalIF":6.4,"publicationDate":"2026-09-10","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148929091","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Study on the expression, prognostic value, and molecular mechanisms of TIMP1 in glioma.","authors":"Liubing Hou, Jiayuan Li, Zizhou Zhang, Mengting Zhang, Zihan Chen, Yu Wang, Xiang Zhan, Wei Han, YuXin Han, Xuetao Han, Huandi Zhou, Xiaoying Xue","doi":"10.1038/s41417-026-01077-w","DOIUrl":"https://doi.org/10.1038/s41417-026-01077-w","url":null,"abstract":"<p><p>TIMP1 exerts oncogenic effects in multiple malignant tumors, yet its specific biological functions and molecular mechanisms in glioma remain incompletely elucidated. This study systematically investigated the expression level, clinical prognostic significance and underlying functional mechanisms of TIMP1 in glioma. Pan-cancer analysis verified that TIMP1 is abnormally overexpressed across a wide range of tumor tissues, with particularly prominent upregulation observed in glioma. Its high expression is closely correlated with malignant clinicopathological phenotypes of glioma and serves as an effective indicator of poor overall survival for patients. In vitro functional experiments confirmed that elevated TIMP1 expression accelerates the proliferation, migration and invasion of glioma cells. Mechanistic studies revealed that TIMP1 sustains the malignant progression of glioma by regulating multiple core extracellular matrix genes and activating extracellular matrix signaling pathways. Collectively, TIMP1 facilitates the malignant evolution of glioma via mediating extracellular matrix signaling cascades, and it holds great promise as a novel molecular biomarker for clinical prognostic evaluation and a potential therapeutic target for glioma.</p>","PeriodicalId":9577,"journal":{"name":"Cancer gene therapy","volume":" ","pages":""},"PeriodicalIF":6.4,"publicationDate":"2026-09-03","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148886056","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Hsa_circ_0136682 driving malignancy in breast cancer through the NCL/c-Myc axis.","authors":"Xinyue Gu, Kunhua Huang, Xuanqi Zhang, Ning Leng, Jinzhe Tong, Jifei Li, Yingying Xing","doi":"10.1038/s41417-026-01052-5","DOIUrl":"https://doi.org/10.1038/s41417-026-01052-5","url":null,"abstract":"<p><p>The dysregulated expression of circular RNAs (circRNAs), newly recognized RNA molecules that are widely found across different species, has been implicated in the progression of several cancers, including breast cancer. Our previous research identified a novel circRNA, hsa_circ_0136682, whose expression pattern and potential function in breast cancer remain to be clarified. This study focuses on uncovering the regulatory impact and specific mechanisms of hsa_circ_0136682 in breast cancer progression. Functionally, we observed a significant upregulation of hsa_circ_0136682 in breast cancer cells, which inhibited cell apoptosis. Gain- and loss-of-function experiments confirmed its ability to promote cell proliferation, migration, and invasiveness in breast cancer, both in vitro and in vivo. Mechanistically, our research demonstrated that hsa_circ_0136682 interacts with nucleolin (NCL) to stabilize c-Myc mRNA and enhance protein expression through post-transcriptional regulation. In summary, our findings suggest that hsa_circ_0136682 drives breast cancer progression via the NCL/c-Myc axis. In breast cancer cells，hsa_circ_0136682 interacts with nucleolin (NCL), NCL protein binding to c-Myc mRNA, forming an RNA-protein ternary complex of hsa_circ_0136682/NCL/c-Myc to stabilize c-Myc mRNA and enhance protein expression. Therefore, hsa_circ_0136682 drives breast cancer progression via the NCL/c-Myc axis.</p>","PeriodicalId":9577,"journal":{"name":"Cancer gene therapy","volume":" ","pages":""},"PeriodicalIF":6.4,"publicationDate":"2026-08-31","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148863743","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"CD73 inhibitor enhances the antitumor activity of selinexor in multiple myeloma by restoring the activation of CD8⁺ T cells.","authors":"Chunli Zhang, Qiuxia Wei, Nigmat Rahim, Gang Bian, Chaoling Wu, Jing Wang, Ping Yang, Jiahui Hua, Mingxia Zhu, Yingtong Chen, Yan Liu, Shuang Gao, Bing Hou, Weilong Zhang, Hongmei Jing","doi":"10.1038/s41417-026-01078-9","DOIUrl":"https://doi.org/10.1038/s41417-026-01078-9","url":null,"abstract":"<p><p>Selinexor, a selective nuclear export inhibitor, blocks exportin-1 and reduces oncoprotein messenger RNA translation, and is approved for the treatment of relapsed/refractory multiple myeloma in combination with proteasome inhibitors, immunomodulators, anti-CD38 antibodies, etc. Nevertheless, selinexor presents limited monotherapy efficacy with an objective response rate of 29% and fails to completely overcome drug resistance. To improve the therapeutic outcome, this study investigated the combined treatment of selinexor and a CD73 inhibitor in a murine tumor model. The expression of CD73 in multiple tumor cell lines following selinexor treatment was first analyzed. In vivo experiments were performed on J558-inoculated BALB/c mice, which were divided into vehicle group, ATG-037 (CD73 inhibitor) monotherapy group, ATG-010 (selinexor) monotherapy group, and combination therapy group. Single-cell RNA sequencing (scRNA-seq) was utilized to characterize immune cell subtypes and tumor-immune crosstalk, and immunofluorescence staining was conducted on histological tumor samples. In addition, a co-culture model of CD8⁺ T cells and multiple myeloma cell lines was established to verify the synergistic anti-tumor effect and underlying mechanism of the combined regimen. The results demonstrated that selinexor treatment upregulated CD73 expression in the majority of tumors. The combination therapy remarkably suppressed tumor growth with an inhibition rate of 62%, which was superior to the monotherapy of ATG-037 (31%) and selinexor (43%). scRNA-seq analysis revealed that the combination treatment synergistically potentiates CD8⁺ T cell activation by enhancing the interaction between CD8⁺ T cells and Enpp1 cells via the CD80-CD28 signaling pathway, and the increased infiltration of CD8⁺ T cells in tumor tissues of the combination group was further validated by immunofluorescence staining. Co-culture experiments further confirmed that CD73 inhibition strengthens selinexor-mediated tumor cell killing by activating CD8⁺ T cells, as evidenced by significantly elevated levels of Granzyme B (P = 0.0252) and IFN-γ (P = 0.0067). In conclusion, CD73 inhibition enhances the anti-myeloma efficacy of selinexor by specifically activating CD8⁺ T cells and ultimately promoting the apoptosis of multiple myeloma cells.</p>","PeriodicalId":9577,"journal":{"name":"Cancer gene therapy","volume":" ","pages":""},"PeriodicalIF":6.4,"publicationDate":"2026-08-27","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148839196","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Calcium dysregulation in breast cancer progression: mechanisms of calcicoptosis and therapeutic implications","authors":"Yu-Ting He,&nbsp;Jun-Hui Yin,&nbsp;Zhuo-Ling Li,&nbsp;Wen-Jing Zhang,&nbsp;Zi-Hao Gu,&nbsp;Na-Min Yang,&nbsp;Kang Li,&nbsp;Yi Zhou,&nbsp;Liang Ji","doi":"10.1038/s41417-026-01076-x","DOIUrl":"10.1038/s41417-026-01076-x","url":null,"abstract":"Disruption of calcium ion (Ca2+) homeostasis represents a critical mechanism in breast cancer (BC) progression, with aberrant Ca2+ transport through store-operated Ca2+ entry pathways, plasma membrane channels, and membrane contact sites (MCSs) playing a significant role in malignant transformation, metastasis, and therapeutic resistance. This dysregulation involves complex interactions among endoplasmic reticulum Ca2+ storage systems, Ca2+-dependent signaling cascades, and specialized MCSs that facilitate abnormal Ca2+ transfer between cellular organelles. Of particular therapeutic relevance, calcicoptosis—a novel form of Ca2+ overload-induced cell death—exhibits remarkable selectivity for BC cells over normal tissues, offering promising avenues for therapy, particularly in aggressive subtypes with limited treatment options. The distinct Ca2+ handling properties of BC cells present opportunities for targeted interventions that exploit these vulnerabilities through pharmacological modulation of Ca2+ transport mechanisms. This review synthesizes current understanding of Ca2+-mediated pathways in BC and outlines a framework for developing precision medicine approaches that leverage Ca2+ dysregulation as both a biomarker and a therapeutic target, with the potential to transform treatment strategies for patients with treatment-resistant disease.","PeriodicalId":9577,"journal":{"name":"Cancer gene therapy","volume":"33 10","pages":"1141-1149"},"PeriodicalIF":6.4,"publicationDate":"2026-08-25","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148817546","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"E-cadherin-driven interleukin-6 expression promotes autophagy-mediated platinum resistance in ovarian clear cell carcinoma","authors":"Chiao-Yun Lin,&nbsp;An-Shine Chao,&nbsp;Shih-Ming Jung,&nbsp;Ren-Chin Wu,&nbsp;Ting-Chang Chang,&nbsp;Yun-Shien Lee,&nbsp;Yun-Hsin Tang,&nbsp;Shih-Sin Huang,&nbsp;Angel Chao,&nbsp;Chyong-Huey Lai","doi":"10.1038/s41417-026-01074-z","DOIUrl":"10.1038/s41417-026-01074-z","url":null,"abstract":"Ovarian clear cell carcinoma (OCCC) is a distinct histological subtype of epithelial ovarian cancer that frequently exhibits chemotherapy resistance and poor outcomes. We investigated the regulatory role of E-cadherin signaling in driving interleukin-6 (IL-6) expression and promoting autophagy-dependent cisplatin resistance. In epithelial-like OCCC cell lines, elevated E-cadherin expression enhanced cisplatin resistance through β-catenin-mediated IL-6 transcription. Proteomic analysis of matched primary and recurrent OCCC specimens revealed upregulation of autophagy signaling in recurrent tumors. Immunoprecipitation confirmed direct interaction between IL-6 and sequestosome-1 (SQSTM1/p62) via its PB1 domain. In cisplatin-refractory patient-derived xenografts, IL-6 blockade significantly inhibited tumor growth. Clinically, in a cohort of 70 OCCC patients, increased serum IL-6 levels correlated with elevated CA125 (p &lt; 0.001), recurrence (p &lt; 0.001), advanced tumor stage (p = 0.014), and worse survival outcomes. High serum IL-6 was independently associated with shorter progression-free survival (p = 0.005). Collectively, these findings identify the E-cadherin/IL-6/autophagy axis as a key mediator of platinum resistance.","PeriodicalId":9577,"journal":{"name":"Cancer gene therapy","volume":"33 10","pages":"1099-1112"},"PeriodicalIF":6.4,"publicationDate":"2026-08-22","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148788519","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"NAT10 promotes prostate cancer progression by acetylating mRNA of MARK2 and activating mTOR/HIF-1α/C-Myc pathway to enhance glycolytic reprogramming.","authors":"Yiming Zhang, Jian Wang, Ganping Wang, Bingkun Li, Binshen Chen","doi":"10.1038/s41417-026-01075-y","DOIUrl":"https://doi.org/10.1038/s41417-026-01075-y","url":null,"abstract":"<p><p>The dysregulation of mRNA modifications, particularly acetylation of cytidine (ac4C), has emerged as a pivotal mechanism in the context of tumor biology, including prostate cancer (PCa), where its exact role mediated by NAT10 remains ill-defined. This study aimed to elucidate the clinical significance of NAT10 in PCa. Our results indicated a pronounced overexpression of NAT10 in PCa tissues and cell lines, which correlated with enhanced cellular proliferation, migration, invasion, and overall tumor growth. Furthermore, acetylated RNA immunoprecipitation sequencing (acRIP-seq) revealed that NAT10 facilitates ac4C modification of MARK2 mRNA, which was consequentially linked to a decrease in mRNA stability and translational efficiency upon NAT10 knockdown, as validated through western blot analysis. Mechanistic investigations demonstrated that NAT10 elevates MARK2 expression, activating the mTOR/HIF-1α/C-Myc signaling cascade, thereby promoting aerobic glycolysis in PCa cells. Consequently, these findings underscore the crucial role of ac4C mRNA modifications in the progression of PCa and position MARK2 as a significant mediator of metabolic reprogramming, suggesting that targeting ac4C mRNA modifications may provide a novel therapeutic strategy for managing prostate cancer.</p>","PeriodicalId":9577,"journal":{"name":"Cancer gene therapy","volume":" ","pages":""},"PeriodicalIF":6.4,"publicationDate":"2026-08-21","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148788506","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Investigating the role of costimulatory domains in enhancing CAR-T cell persistence in TNBC.","authors":"Hany E Marei, Giacomo Pozzoli, Carlo Cenciarelli","doi":"10.1038/s41417-026-01073-0","DOIUrl":"https://doi.org/10.1038/s41417-026-01073-0","url":null,"abstract":"<p><p>This work summarizes how costimulatory domains can mediate the persistence, function, and therapeutic potential of CAR-T cells in triple-negative breast cancer (TNBC), a highly aggressive malignancy with limited treatment options and an immunosuppressive tumor microenvironment. Although CAR-T cell therapy has produced remarkable results in hematologic malignancies, its translation to TNBC remains limited by poor T cell persistence, metabolic dysfunction, and rapid exhaustion. Current evidence identifies canonical costimulatory domains (CD28 and 4-1BB) as having differential effects on intracellular signaling, metabolic programming, and T cell differentiation; CD28-based CAR-T cells promote rapid activation and glycolytic metabolism but are commonly associated with terminal differentiation and decreased durability, whereas 4-1BB signaling supports mitochondrial fitness, oxidative phosphorylation, and the development of memory-like T cells that support longer-lasting persistence. The functional differences in CAR-T cells are context-dependent and influenced by antigen density, hypoxia, and other immunosuppressive signals within the TNBC tumor microenvironment. Newer costimulatory domains, such as HVEM and TNFRSF9, have added an additional layer of complexity to T cell signaling by modulating activating and inhibitory pathways, and their incorporation into CAR designs offers new ways to optimally regulate T cell responses; however, their functions are not fully defined in TNBC models. Additionally, dual costimulation strategies and combination therapies (metabolic reprogramming of T cells, epigenetic modulation, and immune checkpoint blockade) have shown promise in preclinical studies, but their translational value remains to be validated. An important message arising from this review is that while persistence may be improved through enhanced costimulatory signaling, the ideal performance of CAR T therapy occurs with the establishment of an ideal balance of stimulating signals that promote the sustained function of effector T cells while inhibiting the exhaustion of T cells and avoiding the deleterious effects of tonic activation. Furthermore, it is critical to evaluate data from TNBC models compared to other solid tumors to inform rational CAR T design strategies in TNBC.</p>","PeriodicalId":9577,"journal":{"name":"Cancer gene therapy","volume":" ","pages":""},"PeriodicalIF":6.4,"publicationDate":"2026-08-21","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148788510","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Targeting VPS35 increases chemotherapy sensitivity in gastric cancer cells via regulation of the NF-κB signaling pathway","authors":"Zhigang Zhang,&nbsp;Wanrui Gao,&nbsp;Ke Liu,&nbsp;Mingliang Fan,&nbsp;Qingqing Zhou,&nbsp;Xiaoxiao Zuo","doi":"10.1038/s41417-026-01069-w","DOIUrl":"10.1038/s41417-026-01069-w","url":null,"abstract":"Vacuolar protein sorting-associated protein 35 (VPS35), a core component of the retromer complex, recognizes cytosolic retrieval signals in cargo proteins and mediates intracellular protein transport. Although previous studies have demonstrated that VPS35 promotes the growth and invasion of gastric cancer (GC), its role and mechanisms in GC chemoresistance remain largely uncharacterized. Here, VPS35 is identified as a potential predictive biomarker for chemotherapy response in GC. Clinically relevant chemotherapeutic agents, including 5-fluorouracil and cisplatin, significantly upregulate VPS35 expression, which is inversely associated with chemosensitivity. Functional assays demonstrate that VPS35 overexpression induces chemoresistance in GC cells, whereas VPS35 knockdown enhances tumor sensitivity to drug-induced cytotoxicity. Mechanistically, VPS35 contributes to chemoresistance by facilitating the nuclear translocation of p65 and activating the NF-κB signaling pathway. These findings suggest that VPS35 may serve as a prognostic biomarker and a promising therapeutic target in GC.","PeriodicalId":9577,"journal":{"name":"Cancer gene therapy","volume":"33 10","pages":"1113-1125"},"PeriodicalIF":6.4,"publicationDate":"2026-08-20","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148788453","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Advanced gene editing technologies for oncology mechanisms, applications, and clinical implementation","authors":"Soham Bindu,&nbsp;Archishman Ash,&nbsp;Koustav Sarkar","doi":"10.1038/s41417-026-01070-3","DOIUrl":"10.1038/s41417-026-01070-3","url":null,"abstract":"Advanced gene editing tools have transformed oncology by facilitating precise molecular therapies aimed at the hereditary basis of cancer. This thorough study examines the mechanisms, applications, and clinical implementation of advanced genome editing technologies in cancer treatment. This review commences with the molecular principles of genome editing and DNA repair mechanisms, systematically analyzing established technologies such as Zinc Finger Nucleases, Transcription Activator-Like Effector Nucleases, and various CRISPR/Cas systems (Cas9, Cas12, Cas13), in addition to novel advancements including base editors, prime editors, and the PASTE system. Additionally, hybrid platforms such as ARCUS, MegaTALs, and modified recombinases are examined, highlighting their amalgamation with artificial intelligence, biosensors, and synthetic biology concepts. The study outlines significant applications including functional genomics, disease modeling, synthetic lethality screening, and direct therapeutic interventions, with a specific focus on CAR-T cell engineering and immune checkpoint regulation. Applications unique to various cancer types are thoroughly examined throughout lung, breast, colorectal, hematologic, liver, pancreatic, head &amp; neck, esophageal, prostate, gastric, and brain cancers. Significant obstacles such as delivery optimization via viral and non-viral vectors, tumor-specific targeting, off-target effects, immunogenicity, and ethical issues related to germline vs somatic editing are comprehensively examined. The translational landscape is analyzed via current clinical trials, regulatory structures, and the incorporation of organoid models and patient-derived xenografts for the advancement of personalized therapies. This review highlights the transformative impact of gene editing on cancer medicine, advancing toward more accurate, effective, and personalized therapeutic approaches.","PeriodicalId":9577,"journal":{"name":"Cancer gene therapy","volume":"33 10","pages":"1150-1176"},"PeriodicalIF":6.4,"publicationDate":"2026-08-20","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148788492","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}