Oncogene最新文献

{"title":"Circular RNA MCM3 recruits USP49 to stabilize PTBP1 and promote cisplatin resistance in cervical squamous cell carcinoma","authors":"Chenchen Zhu, Ying Wei, Yuebo Li, Zhengzheng Chen, Ying Zhou, Hanyuan Liu","doi":"10.1038/s41388-026-03988-2","DOIUrl":"10.1038/s41388-026-03988-2","url":null,"abstract":"Circular RNA MCM3 is upregulated in platinum-resistant cervical squamous cell carcinoma (CSCC) and is associated with poor patient prognosis. However, its role in chemoresistance and the underlying mechanism remain undefined. Here, we demonstrate that circMCM3 drives cisplatin resistance both in vitro and in vivo by enhancing cell proliferation, inhibiting apoptosis and reducing DNA damage. Mechanistically, circMCM3 recruits the deubiquitinase USP49 to stabilize PTBP1, which binds to and stabilizes CCND1 mRNA, thereby facilitating cell cycle transition and reducing DNA damage. Notably, knockdown of PTBP1 or CCND1 abrogates circMCM3-mediated cisplatin resistance, supporting the existence of a functional circMCM3-USP49-PTBP1-CCND1 axis. Collectively, our findings identify circMCM3 as a critical regulator of platinum resistance and suggest that targeting this axis may represent a promising therapeutic strategy for patients with platinum-resistant CSCC.","PeriodicalId":19524,"journal":{"name":"Oncogene","volume":"45 43","pages":"4630-4646"},"PeriodicalIF":9.1,"publicationDate":"2026-09-12","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148945439","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":"Propionyl-CoA catabolism is a metabolic gatekeeper for fatty acid oxidation in pancreatic cancer","authors":"Weidong Yu, Bo Wang, Fanhao Meng, Xiaojun Ren, Danyi Zhou, Huanxin Wei, Zhengquan Yang, Hongwei Sun, Minghua Jiang, Tao Xia, Wei Cui, Hezhi Fang","doi":"10.1038/s41388-026-03979-3","DOIUrl":"10.1038/s41388-026-03979-3","url":null,"abstract":"Pancreatic ductal adenocarcinoma (PDAC) cells rely on fatty acid oxidation (FAO) for proliferation; however, the regulatory mechanisms governing this dependency and their clinical implications remain unclear. Here, we report that PDAC patients exhibit decreased plasma levels of propionyl-CoA intermediates, alongside accelerated propionyl-CoA catabolic activity within both human PDAC tumors and Pdx1-Cre/KrasG12D/+/Trp53R172H/+ (KPC) mouse tumors. Specifically, PDAC cells upregulate propionyl-CoA carboxylase (PCC) to accelerate propionyl-CoA catabolism, thereby establishing a metabolic signature distinct from that of healthy tissues. Mechanistically, PCC is essential for PDAC growth, not by fueling the TCA cycle, but by preventing toxic propionyl-CoA accumulation. We further demonstrate that elevated propionyl-CoA leads to the propionylation-induced inactivation of the mitochondrial fatty acid oxidation (FAO) enzyme ACAA2 at Lysine 137, thereby blocking the FAO flux required for tumor proliferation. Moreover, high PCCA expression in patient PDAC tumors is significantly associated with decreased lipid accumulation, and PDAC cells with high PCC levels are more sensitive to etomoxir-induced cell proliferation arrest. These findings establish the PCC-ACAA2 axis as a critical metabolic vulnerability and a promising target for diagnostic and therapeutic interventions in PDAC.","PeriodicalId":19524,"journal":{"name":"Oncogene","volume":"45 43","pages":"4597-4612"},"PeriodicalIF":9.1,"publicationDate":"2026-09-11","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148945380","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":"Tumor-derived CTHRC1 mediates ITGB3-dependent osteoclast differentiation to promote prostate cancer bone metastasis","authors":"Tao Xie, Tianming Peng, Qu Li, Mingzhao Li, Maoping Cai, Qianyi Li, Yu-Zhong Yu, Jiehui Zhong, Chong Wang, Ming-Kun Chen, Zhe-Sheng Chen, Xian-Lu Song, Di Gu, Shan-Chao Zhao","doi":"10.1038/s41388-026-03976-6","DOIUrl":"10.1038/s41388-026-03976-6","url":null,"abstract":"Bone metastasis is a leading cause of mortality in advanced prostate cancer (PCa), with limited therapeutic options. This study investigates the molecular mechanisms underlying PCa bone metastasis and identifies potential therapeutic targets. Using in vitro co-culture systems and in vivo mouse models, we demonstrated that tumor-derived Collagen Triple Helix Repeat Containing 1 (CTHRC1) promotes osteoclast differentiation, thereby contributing to the development of osteolytic lesions in PCa bone metastasis. Mechanistically, CTHRC1 cooperates with receptor activator of nuclear factor-κB ligand (RANKL) signaling to promote osteoblast-derived RANKL-mediated osteoclastogenesis by disrupting the RANKL/osteoprotegerin (OPG) system. Furthermore, CTHRC1 directly binds to integrin beta 3 (ITGB3) on osteoclasts to activate the FAK/MEK/ERK1/2 pathway and dissociate SRC signaling, jointly mediating osteoclast differentiation. Blocking the CTHRC1-ITGB3 axis significantly weakened CTHRC1-induced osteoclast differentiation and bone resorption. Collectively, our findings identify CTHRC1 as a novel mediator in the bone microenvironment, providing a potential therapeutic target for inhibiting the occurrence and progression of PCa bone metastasis.","PeriodicalId":19524,"journal":{"name":"Oncogene","volume":"45 43","pages":"4613-4629"},"PeriodicalIF":9.1,"publicationDate":"2026-09-11","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148945404","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":"CircRHBDD1(4,5) drives malignant progression of oral squamous cell carcinoma by enhancing DKK1 mRNA stability through facilitating m6A-dependent IGF2BP2 binding","authors":"Daixi Ren, Jiarong Zhang, Mao Huang, Jie Wu, Mei Yang, Yixuan Liu, Pingjuan Xiang, Hongke Qu, Dan Wang, Junshang Ge, Qijia Yan, Lei Shi, Bo Xiang, Wei Xiong, Guiyuan Li, Chunmei Fan, Zhaoyang Zeng","doi":"10.1038/s41388-026-03986-4","DOIUrl":"10.1038/s41388-026-03986-4","url":null,"abstract":"Oral squamous cell carcinoma (OSCC) is a malignant tumor arising from the oral mucosa and is highly prevalent in Southeast Asia and the Pacific region. Recurrence and metastasis significantly contribute to poor clinical outcomes, highlighting the importance of understanding the underlying molecular mechanisms. Circular RNAs (circRNAs), a class of covalently closed non-coding RNAs, have emerged as key regulators of tumor development and progression. However, their roles in OSCC remain largely unexplored. In this study, we identified for the first time that circRHBDD1(4,5) (hsa_circ_0058493, a 656-nt circRNA generated by back-splicing of exons 4 and 5 of the RHBDD1 gene) is markedly upregulated in OSCC and promotes tumor cell proliferation, invasion, and metastasis. Mechanistically, circRHBDD1(4,5) functions as a molecular scaffold that brings IGF2BP2 and DKK1 mRNA into close proximity, thereby facilitating the m6A-dependent recognition of DKK1 mRNA by IGF2BP2, which is mediated by WTAP. This interaction enhances DKK1 mRNA stability, leading to increased DKK1 expression and subsequent activation of the PI3K-AKT signaling pathway, thereby driving the malignant progression in OSCC. Collectively, our findings highlight the critical role of the circRHBDD1(4,5)/IGF2BP2/DKK1 axis in OSCC pathogenesis and provide a potential foundation for developing novel targeted therapeutic strategies.","PeriodicalId":19524,"journal":{"name":"Oncogene","volume":"45 42","pages":"4581-4596"},"PeriodicalIF":9.1,"publicationDate":"2026-09-11","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148930860","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":"A step-wise, deterministic and fatal mouse model of myeloid neoplasm with spontaneous acquisition of patient-relevant RTK–RAS mutations","authors":"Marija A. Zarocsinceva, Moosa Qureshi, Nicola K. Wilson, George Giotopoulos, Blaise Musabe, Katherine H. M. Sturgess, M. S. Vijayabaskar, Sarah J. Kinston, Ryan Asby, David J. Adams, Brian J. P. Huntly, Fernando J. Calero-Nieto, Berthold Göttgens","doi":"10.1038/s41388-026-03964-w","DOIUrl":"10.1038/s41388-026-03964-w","url":null,"abstract":"Leukaemia arises through the stepwise transformation of healthy haematopoietic cells, yet the asymptomatic premalignant phase and its progression to overt disease remain poorly understood. To model this process, we engineered a patient-derived CEBPA mutation into Hoxb8-FL multipotent murine progenitors and transplanted them into syngeneic mice, capturing a clinically silent premalignant stage. All recipients developed overt disease after ~12 months with 100% penetrance and all acquired secondary RTK–RAS mutations, often with identical amino acid changes to those in patients. Single-cell transcriptomics and phenotypic profiling showed that premalignant mutant cells adopt a plasmacytoid dendritic progenitor–like state in vitro which generates both myeloid and B-lymphoid lineages during premalignancy in vivo, with individual tumours restricted to one lineage. The specificity for RTK-RAS mutations coupled with ongoing differentiation, reflects clinically relevant biological contexts thus providing a tractable model of myeloid neoplasm for mechanistic studies and drug discovery.","PeriodicalId":19524,"journal":{"name":"Oncogene","volume":"45 42","pages":"4551-4563"},"PeriodicalIF":9.1,"publicationDate":"2026-09-04","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.nature.comhttps://www.nature.com/articles/s41388-026-03964-w.pdf","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148892210","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":"ITGA5 promotes homologous recombination mediated radioresistance in esophageal squamous cell carcinoma by upregulating RAD51AP1 expression","authors":"Xinyi Huang, Jiayi Liu, Jiao Ren, Jupeng Yuan, Wen Huo, Zengfu Zhang, Minxin Chen, Baoqing Tian, Dawei Chen","doi":"10.1038/s41388-026-03966-8","DOIUrl":"10.1038/s41388-026-03966-8","url":null,"abstract":"Radiotherapy resistance represents a critical barrier to successful treatment of esophageal squamous cell carcinoma (ESCC), driving tumor recurrence and poor patient survival. We identify constitutive overexpression of integrin α5 (ITGA5) as a key molecular determinant of ESCC radioresistance. Clinically, elevated ITGA5 expression correlates with radiation therapy failure and reduced overall survival. Mechanistically, ITGA5 sustains persistent FAK/AKT/GSK-3β/β-Catenin signaling activation, which drives MYC-dependent transactivation of RAD51AP1. This signaling axis enhances homologous recombination repair efficiency by facilitating RAD51 chromatin loading, enabling effective DNA damage resolution and radioresistance maintenance. Genetic validation confirms the indispensable roles of RAD51AP1 and MYC in this process. Critically, pharmacological inhibition of ITGA5 with ATN-161 restores radiation sensitivity in preclinical models, suppressing tumor growth and enhancing DNA damage accumulation. Our work defines the ITGA5/FAK/β-catenin/MYC/RAD51AP1 pathway as a key mechanistic driver of radioresistance and validates ITGA5 as a potential clinical target for ESCC therapy.","PeriodicalId":19524,"journal":{"name":"Oncogene","volume":"45 42","pages":"4564-4580"},"PeriodicalIF":9.1,"publicationDate":"2026-09-04","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.nature.comhttps://www.nature.com/articles/s41388-026-03966-8.pdf","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148892145","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":"The RNA-binding protein La/SSB is associated with HNSCC progression and TFAP2C/FSCN1-linked transcriptional regulation","authors":"Shixian Liu, Deshang Chen, Wentao Zhang, Hui Li, Jie Peng, Xiaomin Wang, Mingjie Zhang, Weiwei Liu, Junjie Zhang, Mengjun Wang, Guoying Han, Changqi Cai, Shencheng Liu, Xiaoli You, Qun Xu, Yuefeng Han, Xiaojun Zha, Shiyin Ma","doi":"10.1038/s41388-026-03959-7","DOIUrl":"10.1038/s41388-026-03959-7","url":null,"abstract":"Head and neck squamous cell carcinoma (HNSCC) is characterized by aggressive progression, frequent therapeutic resistance, and poor clinical outcomes. Although the RNA-binding protein La/SSB is aberrantly expressed in multiple malignancies, its functional and mechanistic role in HNSCC remains incompletely understood. Here, by integrating transcriptomic and chromatin accessibility profiling with comprehensive in vitro and in vivo analyses, we identify La/SSB as a putative regulator associated with HNSCC progression and cisplatin (CDDP) resistance. La/SSB was markedly upregulated in HNSCC tissues and cell lines, and elevated expression was associated with unfavorable survival. Genetic depletion of La/SSB suppressed proliferation, migration, and invasion, promoted apoptosis, and reduced tumor growth and metastatic colonization, whereas ectopic expression exerted the opposite effects. Multi-omics analyses implicated FSCN1 as a functionally relevant downstream candidate associated with La/SSB-dependent phenotypes. Mechanistically, La/SSB depletion was associated with reduced H3K27ac enrichment and diminished TFAP2C occupancy at the FSCN1 promoter, supporting a TFAP2C/FSCN1-linked regulatory framework. Importantly, loss of La/SSB significantly enhanced CDDP responsiveness in the PDO model established in this study and in vivo conditional knockout models. Clinically, elevated La/SSB showed independent prognostic value, whereas TFAP2C and FSCN1 supported a biologically associated regulatory framework linked to aggressive disease features. Collectively, our findings identify La/SSB as a clinically relevant factor associated with HNSCC progression and CDDP responsiveness, and support a TFAP2C/FSCN1-linked regulatory framework that may contribute to malignant phenotypes.","PeriodicalId":19524,"journal":{"name":"Oncogene","volume":"45 42","pages":"4533-4550"},"PeriodicalIF":9.1,"publicationDate":"2026-09-03","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.nature.comhttps://www.nature.com/articles/s41388-026-03959-7.pdf","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148888234","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":"The GSEC-encoded polypeptide GESP drives colorectal cancer tumorigenesis via NPM1-c-Myc-mediated repression of NDRG1","authors":"Yoshihiro Kawasaki, Tomoatsu Hayashi, Akane Kitta-Kunihiro, Lumi Negishi, Sakiko Suda, Chiemi Furuya-Ikude, Nao Taniguchi, Tetsu Akiyama, Eisaku Kondo","doi":"10.1038/s41388-026-03958-8","DOIUrl":"10.1038/s41388-026-03958-8","url":null,"abstract":"Expression of long non-coding RNAs (lncRNAs) is frequently dysregulated in human cancers. We previously reported that the lncRNA GSEC accelerates colorectal cancer (CRC) cell motility by inhibiting the RNA helicase DHX36. Here, we demonstrated that a nuclear polypeptide (designated ‘GESP’) is translated from a short ORF encoded by GSEC, which is highly expressed in CRC cells. In vivo experiments using CRC cell-xenografted mice revealed that GESP is required for development of immature tumors through suppression of a critical differentiation factor, NDRG1. Suppression of GESP by shRNA-mediated knockdown of GSEC caused growth retardation associated with tumor differentiation. At the molecular level, GESP recruits c-Myc to the promoter region of NDRG1 by forming a GESP-NPM1-c-Myc complex, which consequently represses transcription of NDRG1. Collectively, these data indicate a novel lncRNA product, GESP, plays a pivotal role in CRC tumor development/progression by suppression of tumor cell differentiation through the GESP-NDRG1 axis.","PeriodicalId":19524,"journal":{"name":"Oncogene","volume":"45 42","pages":"4522-4532"},"PeriodicalIF":9.1,"publicationDate":"2026-09-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.nature.comhttps://www.nature.com/articles/s41388-026-03958-8.pdf","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148874950","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":"Neuromedin U ‘innervation’ reprograms myeloid immunosuppression in neuroendocrine prostate cancer","authors":"Michela Perego, Jozef Madzo, Andrew V. Kossenkov, F. Cansu Atilgan, Marcella Tazzari, Maria Maddalena Tumedei, Francesco Limarzi, Cristian Lolli, Giorgia Gurioli, Alessandro Fatatis, Mary V. Iacocca, Nicholas J. Petrelli, Justine J. Jacobi, David W. Goodrich, Lucia R. Languino, Dario C. Altieri","doi":"10.1038/s41388-026-03969-5","DOIUrl":"10.1038/s41388-026-03969-5","url":null,"abstract":"Neuroendocrine prostate cancer (NEPC) is an increasingly recognized, highly aggressive disease variant with no actionable therapeutic targets and a life expectancy of 7 months or less. Using a transgenic mouse model, we now show that early stages of NEPC are associated with increased intraprostatic recruitment of Ly6G+ polymorphonuclear neutrophils (PMN) and reduced infiltration of CD8+ T cells. This coincided with expansive transcriptional changes of increased cell viability and cell migration, as well as upregulation of multiple neuronal mediators with the neuropeptide, Neuromedin U (NMU) as the top hit (Z score = 4.34; FDR < 5%; p = 3.62 × 10−9). Analysis of a large cohort of human patient samples revealed that NMU was highly expressed in early and late stage prostate cancer, preferentially segregating with AR-/NE+ metastases. Exposure of PMN to recombinant NMU was sufficient to stimulate cell migration, inflammatory gene expression with increased levels of the cytokine-like alarmin, S100A9 and suppression of T cell proliferation. Genetic or pharmacological targeting of NMU/S100A9 signaling inhibited NEPC growth, reinvigorated an intratumoral immune microenvironment via recruitment of tumor antigen-specific CD8+ T cells with ‘stem-like’ (TCF1+/PD1+) and cytotoxic (GrzB+/KLRG1+) properties and enhanced the activity of therapeutic immune checkpoint inhibition, in vivo. Therefore, NMU ‘innervation’ drives myeloid immunosuppression in NEPC and provides a therapeutic target to restore sensitivity to immunotherapy in this highly refractory malignancy.","PeriodicalId":19524,"journal":{"name":"Oncogene","volume":"45 41","pages":"4442-4453"},"PeriodicalIF":9.1,"publicationDate":"2026-09-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148865692","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":"Frequently amplified SHANK2 promotes esophageal squamous cell carcinoma progression through the DVL/YAP axis","authors":"Cuicui Wang, Wei Zhao, Man Li, Min He, Cuicui Xu, Jianming Hu, Jun Hou, Lianghai Wang","doi":"10.1038/s41388-026-03974-8","DOIUrl":"10.1038/s41388-026-03974-8","url":null,"abstract":"SHANK2 is crucial for neuronal synapse development and has been implicated in certain tumors; however, its role in esophageal squamous cell carcinoma (ESCC) remains underexplored. In this study, the expression and prognostic significance of SHANK2 in ESCC were assessed through bioinformatics analyses and immunohistochemical staining. We examined the relationship between SHANK2 expression and genetic alterations across multiple ESCC datasets. The effects of SHANK2 on cell proliferation, migration, and invasion were evaluated using cell-based assays. Potential SHANK2-interacting proteins were identified via co-immunoprecipitation followed by mass spectrometry and further validated using immunoprecipitation and immunoblotting. Additionally, we investigated the in vivo role of SHANK2 in ESCC progression using tumor xenograft mouse models. Our findings demonstrated that SHANK2 expression was significantly elevated in ESCC tissues, with high levels correlating with poor patient prognosis. Genetic amplification of SHANK2 was frequently observed in ESCC samples. SHANK2 promoted the proliferation, motility, and epithelial-mesenchymal transition of ESCC cells. Mechanistically, SHANK2 may activate the YAP signaling through competitive binding with DVL2, thereby facilitating malignant progression. In vivo studies indicated that targeting YAP signaling can mitigate SHANK2-induced ESCC growth. Taken together, SHANK2 is upregulated in ESCC and activates YAP signaling by interacting with DVL2, contributing to tumor progression. The SHANK2/DVL/YAP axis presents a potential therapeutic target for ESCC.","PeriodicalId":19524,"journal":{"name":"Oncogene","volume":"45 42","pages":"4512-4521"},"PeriodicalIF":9.1,"publicationDate":"2026-08-31","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148865236","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}