Cancer Science最新文献

{"title":"Advances in Radiotherapy for Neoadjuvant Therapy of Stage III Non-Small Cell Lung Cancer.","authors":"Qinrong Mao, Yuanchun Yu, Yan Fang, Shaofeng Zhu, Chengjin Tang, Jing Cai","doi":"10.1111/cas.70535","DOIUrl":"10.1111/cas.70535","url":null,"abstract":"<p><p>This review aims to systematically summarize the mechanisms of action, clinical evolution, and application prospects of radiotherapy in neoadjuvant therapy for stage III non-small cell lung cancer. Focusing on three core techniques: spatially fractionated radiotherapy, stereotactic body radiotherapy, and low-dose radiotherapy, key study data were screened across different treatment eras. Data extraction covers the unique mechanisms of the three radiotherapy modalities, as well as the efficacy and safety of treatment regimens before and after the immunotherapy era, including pathological response rate, survival benefit, adverse reactions, and other core endpoints. Comprehensive data analysis indicates that the three radiotherapy techniques have distinct characteristics; radioimmunotherapy synergy and triple regimens in the immunotherapy era significantly improve pathological response rates and long-term disease control. Spatially fractionated radiotherapy demonstrates unique advantages due to its low toxicity and dual mechanisms of action. In conclusion, radiotherapy shows prominent value in neoadjuvant therapy for stage III non-small cell lung cancer, and spatially fractionated radiotherapy is expected to become an important therapeutic option. However, its optimal dose-fractionation regimen, standardized procedures, and other issues still require further validation by multicenter randomized controlled trials to promote the development of more precise, safe, and effective treatments.</p>","PeriodicalId":48943,"journal":{"name":"Cancer Science","volume":" ","pages":""},"PeriodicalIF":4.3,"publicationDate":"2026-09-18","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC13587753/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148992004","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Limitations of PIV Biomarker Analysis Related to Chemoradiotherapy and Unadjusted Confounders.","authors":"Hongbo Gao, Wencai Weng","doi":"10.1111/cas.70543","DOIUrl":"10.1111/cas.70543","url":null,"abstract":"<p><p>The pan-immune-inflammation value (PIV) derived from four blood cell counts warrants cautious interpretation in rectal-cancer immunotherapy, as CRT cannot be disentangled from anti-PD-1 effects within the small n = 16 subgroup.</p>","PeriodicalId":48943,"journal":{"name":"Cancer Science","volume":" ","pages":""},"PeriodicalIF":4.3,"publicationDate":"2026-09-17","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC13586479/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148991991","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Clinical Significance of a Cell-Of-Origin-Based Classification in Pancreatic Ductal Adenocarcinoma.","authors":"Tatsuya Kikuchi, Soichiro Ako, Hironari Kato, Hideaki Kinugasa, Masaki Uchida, Takashi Oda, Ryosuke Hirai, Akihiro Matsumi, Kazuya Miyamoto, Hiroyuki Terasawa, Yuki Fujii, Daisuke Uchida, Kazuyuki Matsumoto, Koichiro Tsutsumi, Shigeru Horiguchi, Kazuya Yasui, Tomokazu Fuji, Kosei Takagi, Hirokazu Kato, Tomoyuki Honda, Fumio Otsuka, Motoyuki Otsuka","doi":"10.1111/cas.70533","DOIUrl":"10.1111/cas.70533","url":null,"abstract":"<p><p>Pancreatic ductal adenocarcinoma (PDAC) remains one of the most lethal malignancies, with limited therapeutic options and poor clinical outcomes. Although PDAC has traditionally been thought to arise from ductal epithelial cells, recent studies using genetically engineered mouse models have demonstrated that acinar cells can also serve as a cell of origin, giving rise to tumors with distinct biological properties. Here, we investigated whether such lineage-specific differences are preserved in human PDAC. RNA sequencing was performed on resected specimens from 40 treatment-naïve patients with PDAC, and tumors were classified into Acinar- and Ductal-subtypes using lineage-specific gene expression signatures derived from mouse models. This classification strategy was further applied to human PDAC cell lines, followed by in vitro drug sensitivity assays. Patients with Acinar-subtype tumors had significantly longer overall survival than those with Ductal-subtype tumors (median, 54.0 vs. 26.5 months; p < 0.01), and multivariate analysis identified the ductal cell-derived tumor signature as an independent predictor of poor prognosis (HR, 3.74 [95% CI, 1.41-9.97]; p = 0.01). Among patients who developed postoperative recurrence, Acinar-subtype tumors were associated with more durable disease control (≥ 10 months) following gemcitabine-based chemotherapy than Ductal-subtype tumors (63.6% vs. 16.7%; p = 0.02). Consistently, pancreatic cancer cell lines classified as Acinar-subtype showed greater sensitivity to gemcitabine (p < 0.01) and paclitaxel (p < 0.05). These findings extend the clinical relevance of cell-of-origin signatures beyond prognostic stratification, highlighting the potential of cell-of-origin-based classification for treatment stratification and precision medicine in PDAC.</p>","PeriodicalId":48943,"journal":{"name":"Cancer Science","volume":" ","pages":""},"PeriodicalIF":4.3,"publicationDate":"2026-09-13","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC13571873/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148963803","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"EPHX2 Loss Promotes CRC Migration via EET-Dependent Chemokine Elevation and Mitochondrial Defect.","authors":"Jianjun Zhu, Jingjia Chang, Zhiyong Li, Jin Wu, Pengfei Yu, Jingjing Zheng, Li Li, Jia Tao, Hao Wu, Yintao Li, Ming Liu","doi":"10.1111/cas.70537","DOIUrl":"10.1111/cas.70537","url":null,"abstract":"<p><p>Epoxide hydrolase 2 (EPHX2) is a key enzyme in fatty acid metabolism that metabolizes epoxyeicosatrienoic acids (EETs), lipid mediators involved in inflammation, angiogenesis, and carcinogenesis. However, the role and mechanism of EPHX2 in colorectal cancer (CRC) migration remain unclear. In this study, we employed an integrated approach of bioinformatics and functional experiments to examine EPHX2 expression, its clinical implications, and its mechanistic role in CRC migration. Our results showed that EPHX2 was significantly downregulated in CRC tissues, and its low expression correlated with poor prognosis. Overexpression of EPHX2 led to accumulation of HDHA, HEPE, and HETE in CRC cells, whereas loss of EPHX2 increased CXCL levels and suppressed mitochondrial biogenesis via EET accumulation. Furthermore, loss of EPHX2 promoted cell migration through ROS and CXCL signaling. Collectively, loss of EPHX2 accelerates cell migration via EET accumulation-dependent chemokine elevation and mitochondrial biogenesis impairment in CRC. These findings reveal a novel metabolic-mitochondrial axis in CRC progression and highlight EPHX2 as a potential therapeutic target.</p>","PeriodicalId":48943,"journal":{"name":"Cancer Science","volume":" ","pages":""},"PeriodicalIF":4.3,"publicationDate":"2026-09-13","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC13571872/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148963765","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Advances in Spatial Heterogeneity and Cellular Localization Specificity of Intratumoral Bacteria.","authors":"Minlan Ren, Jing Jia, Tingting Li, Yiwei Li, Nanxiang Shen, Yun Shi, Zhe Wang, Hao Fan, Guangli Sun, Guanying Xiong, Gang Li, Rui Peng","doi":"10.1111/cas.70536","DOIUrl":"10.1111/cas.70536","url":null,"abstract":"<p><p>Bacteria in tumors are increasingly recognized to be a part of the tumor microenvironment and their biological function depends on the location and relative abundance of a given microorganism or microbial community. Genetic sequencing data directly from tissue samples to detection of active metabolic signals from microorganisms, cell-microbiome interactions, ultrastructural localization of microorganisms; these are all different kinds of inferences about the functional role of the microbiome, and the evidence for \"microbial presence and function\" grows in a stepwise fashion. Furthermore, most current microbial detection methods do not, alone, predict the viability, biological activity, or functional properties of microorganisms. In this review, we compare different existing microbial detection techniques and distinguish three spatial paradigms: organized communities in tissue, intracellular bacteria, and extracellular bacteria. We summarize how each paradigm influences signal transduction, metabolism, metastatic spread, treatment resistance, antitumor immunity, and immunotherapy responses. We focus on low-biomass contamination, batch effects, negative controls, absolute quantification, and orthogonal validation. Finally, we classify results according to localization, biological role, clinical evidence, application, and applications, while distinguishing observations of human patients from mechanistic and therapeutic preclinical studies. Spatial microbiology provides useful information about tumor-microbial interactions, but clinically actionable conclusions require standard analysis, reproducible localization, viability or activity, and functional disruption experiments to demonstrate microbial effects and independent clinical validation.</p>","PeriodicalId":48943,"journal":{"name":"Cancer Science","volume":" ","pages":""},"PeriodicalIF":4.3,"publicationDate":"2026-09-13","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC13572861/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148963778","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Integrated Analysis of HER2 Expression and ERBB2 Alterations in Bladder Cancer.","authors":"Kensuke Hirosuna, Kazuki Nishimura, Moritoshi Sakamoto, Satoshi Tokushige, Keita Nakamori, Tomohisa Matsunaga, Yuki Yoshikawa, Takeshi Tsutsumi, Ryoichi Maenosono, Takuya Tsujino, Masahiko Ajiro, Haruhito Azuma, Akihide Yoshimi, Kazumasa Komura","doi":"10.1111/cas.70534","DOIUrl":"10.1111/cas.70534","url":null,"abstract":"<p><p>Human epidermal growth factor receptor 2 (HER2) has emerged as a potential therapeutic target in bladder cancer (BC), particularly with the advent of next-generation antibody-drug conjugates (ADCs) like trastuzumab deruxtecan (T-DXd). However, the complex relationship between HER2 protein expression, genetic status, and clinical outcomes remains incompletely understood. We conducted an integrated multi-omics analysis of 445 BC cases (306 muscle-invasive [MIBC] and 139 non-muscle-invasive [NMIBC]) from the OMPU-NCC cohort, a uniform Japanese clinical database. The study utilized whole-exome sequencing, RNA sequencing, and refined HER2 immunohistochemistry (IHC) scoring. HER2 IHC positivity (1+/2+/3+) was identified in 30.1% of the cohort. An additional 8.5% exhibited faint membrane staining despite being IHC 0, indicating that detectable HER2 membrane staining was present in approximately 38.5% of cases. HER2 IHC scores showed no prognostic value, whereas ERBB2 amplification, detected in 7.8% of cases, was associated with poorer survival and remained an independent adverse prognostic factor in multivariable analysis (HR, 1.76; 95% CI: 1.08-2.87). ERBB2 amplification was accompanied by frequent co-amplification of genes within the 17q12 amplicon, including GRB7, MIEN1, and PGAP3. Molecular subtyping revealed that ERBB2 amplification was enriched in the Luminal Unstable (LumU) subtype. In contrast, detectable HER2 membrane staining significantly correlated with high NECTIN4 expression, indicating an overlap between tumors expressing these two ADC targets. HER2 protein expression and ERBB2 amplification represent distinct features of BC. Their integrated assessment may improve molecular stratification and guide future biomarker-driven studies.</p>","PeriodicalId":48943,"journal":{"name":"Cancer Science","volume":" ","pages":""},"PeriodicalIF":4.3,"publicationDate":"2026-09-13","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC13571850/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148963770","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Integrated Transcriptomics of Human and Canine Osteosarcoma Reveals Species Stemness and Trabectedin Sensitivity.","authors":"Kenta Kono, Yomogi Shiota, Ting-Ting Shu, Hayato Shibahara, Daiki Kato, Takayuki Nakagawa, Seiji Ohtori, Tadashi Kondo","doi":"10.1111/cas.70524","DOIUrl":"10.1111/cas.70524","url":null,"abstract":"<p><p>Canines share close environmental and physiological homologies with humans, making them essential large-animal models in preclinical drug discovery. However, species-specific discrepancies in therapeutic responsiveness often limit the direct extrapolation of canine data to human clinical scenarios. Although osteosarcoma (OS) spontaneously occurs in large-breed dogs at an incidence 30-fold higher than in humans, the underlying interspecies molecular differences governing tumor behavior and drug sensitivity remain poorly understood. This study aimed to systematically evaluate the translational reliability and limitations of the canine OS model by comparing human and canine malignant architectures at baseline and during anti-cancer drug exposure. By integrating single-cell RNA sequencing (scRNA-seq) from treatment-naive patient specimens with multi-conditional temporal bulk RNA-seq of representative cell lines, we interrogated their dynamic transcriptomic responses to Trabectedin. Integrated single-cell analysis revealed that human OS possesses a highly primitive, high-stemness subpopulation hierarchy and a more primed tumor-infiltrating lymphocyte (TIL) profile than canine OS. Pharmacogenomic assays demonstrated that these distinct cellular architectures dictate therapeutic vulnerabilities: The rigid, high-stemness hierarchy of human OS facilitates transcriptomic robustness and adaptive drug resistance. In contrast, the fluid, less primitive network of canine OS renders its tumor cells prone to immediate, stochastically driven functional network collapse and superior Trabectedin sensitivity. Collectively, our study provides a comprehensive comparative molecular framework for human and canine OS. These findings emphasize the necessity of accounting for species-specific stemness and immune landscapes, ultimately accelerating the precision development of next-generation OS therapeutics.</p>","PeriodicalId":48943,"journal":{"name":"Cancer Science","volume":" ","pages":""},"PeriodicalIF":4.3,"publicationDate":"2026-09-11","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC13563635/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148945978","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Lung Cancer Brain Metastasis: Brain Microenvironmental Adaptation, Therapeutic Resistance and Translational Strategies.","authors":"Jun Yang, Junyi Xiong, Li Ying, Yanyang Zeng, Ziqiang Ouyang, Mei Liu, Meihua Li","doi":"10.1111/cas.70527","DOIUrl":"10.1111/cas.70527","url":null,"abstract":"<p><p>Lung cancer brain metastasis (LCBM) remains one of the most challenging clinical conditions limiting survival and neurological function. The development of LCBM is shaped by continuous exchange of molecular signals between tumor cells and the brain microenvironment, involving blood-brain barrier remodeling, glial and immune reprogramming, neuronal signaling, and metabolic adaptation. Together, these phenomena support brain colonization, immune escape, and therapeutic resistance. The management of LCBM has improved with the advent of stereotactic radiotherapy, targeted therapy, immunotherapy, chemoimmunotherapy, and antibody-drug conjugates. Yet durable intracranial control is still limited by intrinsic barrier heterogeneity, protected residual intracranial disease, and molecular resistance. This review summarizes recent advances in biology, preclinical modeling, therapeutic resistance, and translational treatment strategies of LCBM. By linking brain-specific metastatic biology with evolving therapeutic approaches, this review provides a framework for understanding LCBM progression and for developing more effective strategies to overcome intracranial resistance.</p>","PeriodicalId":48943,"journal":{"name":"Cancer Science","volume":" ","pages":""},"PeriodicalIF":4.3,"publicationDate":"2026-09-10","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC13562432/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148931545","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"The DNA/RNA Helicase SETX Maintains R-Loop Homeostasis to Promote Chemoresistance in Ovarian Cancer.","authors":"Zi-Wei Hu, Tu-Nan Xu, Zi-Ying Wang, Xin Zheng, Duan-Yong Feng, Xiao-Min Wang, Er-Suo Jin, Ming Ren, Xiao-Min Yang, Xian-Chao Zhang, Xuan Che, Wei-Wei Pan, Zha-Jun Zhan, Shu-Qun Cheng","doi":"10.1111/cas.70520","DOIUrl":"10.1111/cas.70520","url":null,"abstract":"<p><p>Ovarian cancer is a lethal malignancy that frequently develops resistance to platinum-based chemotherapies. Elucidating the genes that regulate DNA damage repair could lead to more effective treatments for ovarian cancer. Senataxin (SETX), an RNA-DNA helicase, maintains R-loop homeostasis to ensure replication fork progression, and its deficiency is linked to neurodegenerative diseases. However, its clinical relevance to solid tumors is not understood. We aimed to investigate the clinical significance and functional role of SETX in ovarian cancer progression and chemotherapy resistance. SETX expression was analyzed in ovarian cancer tissues, followed by CRISPR-Cas9-mediated knockout, mechanistic analyses, and RNASEH1 rescue experiments to investigate its role in ovarian cancer progression and chemoresistance. SETX was significantly overexpressed in ovarian tumors, and its high expression was correlated with cisplatin resistance and poor patient survival. SETX depletion significantly impaired tumor cell proliferation and invasion and sensitized cells to cisplatin-induced apoptosis. Mechanistically, SETX deficiency triggered pathological R-loop accumulation, which was accompanied by replication stress, DNA double-strand breaks, and activation of DNA damage response. RNA-seq analysis also revealed splicing alterations and U2AF1 interaction. Critically, R-loop degradation induced by RNASEH1 overexpression rescued the DNA damage phenotype and growth defects induced by SETX loss. These findings reveal a dual oncogenic role for SETX. Maintaining R-loop homeostasis supports malignant progression while conferring chemotherapy resistance. Therefore, SETX represents a promising therapeutic target, as its inhibition simultaneously suppresses tumor growth and overcomes chemotherapy resistance in ovarian cancer.</p>","PeriodicalId":48943,"journal":{"name":"Cancer Science","volume":" ","pages":""},"PeriodicalIF":4.3,"publicationDate":"2026-09-09","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC13555362/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148913797","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Spatiotemporal CD8⁺ T-Cell Dynamics: Clonal Replacement and Expansion as Determinants of Sustainable Antitumor Response.","authors":"Satoshi Ueha, Hiroyasu Aoki, Munetomo Takahashi, Shigeyuki Shichino, Kouji Matsushima","doi":"10.1111/cas.70531","DOIUrl":"10.1111/cas.70531","url":null,"abstract":"<p><p>The clinical success of immune checkpoint inhibitors (ICI) has shifted the paradigm of cancer treatment, yet the fundamental mechanisms governing the long-term sustainability of antitumor T-cell responses remain elusive. Emerging evidence suggests that the efficacy of ICI depends not only on the reinvigoration of pre-existing tumor-infiltrating lymphocytes but also on the continuous mobilization and replacement of T-cell clones from systemic reservoirs. In this review, we propose a \"spatiotemporal ecosystem model\" of the antitumor T-cell response. We first delineate the spatial dynamics of T-cell clones, where tumor-reactive progenitors primed in the tumor-draining lymph nodes (dLN) circulate through the peripheral blood to replenish the tumor microenvironment (TME). We highlight that TCR avidity emerges as a key determinant of clonal fate; while high-avidity clones provide potent early cytotoxicity, their susceptibility to accelerated terminal exhaustion eventually creates an available niche that allows for the subsequent expansion of intermediate-avidity successor clones. Furthermore, we discuss how single-cell multi-omics integration (transcriptome, TCR repertoire, and epigenome) reveals that clonal fate is functionally encoded in the molecular and metabolic poise of T cells prior to their expansion. Finally, we discuss the potential of monitoring these clonal dynamics through liquid biopsy as a non-invasive window into the resilience of the immune ecosystem, distinguishing responders with sustainable, polyclonal mobilization from non-responders with frustrated, oligoclonal responses. By integrating clonal evolution, metabolic fitness, and inter-organ crosstalk, this ecosystem perspective offers a comprehensive framework for predicting therapeutic outcomes and developing next-generation precision immunotherapies.</p>","PeriodicalId":48943,"journal":{"name":"Cancer Science","volume":" ","pages":""},"PeriodicalIF":4.3,"publicationDate":"2026-09-07","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC13550973/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148907712","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}