Cancer letters最新文献

{"title":"Extrachromosomal DNA (ecDNA) drives hepatocellular carcinoma malignancy through high-copy amplification of chromosome 1q21-derived PIP5K1A oncogene","authors":"Ni Zhang ,&nbsp;Xiangyu Zhang ,&nbsp;Tinghao Yan ,&nbsp;Fen Liu ,&nbsp;Xinchen Tian ,&nbsp;Changlin Ma ,&nbsp;Huapeng Lin ,&nbsp;Yiming Zhang ,&nbsp;Lingli Hao ,&nbsp;Jiaqi Zhang ,&nbsp;Qingxia Xu ,&nbsp;Qingbin Liu ,&nbsp;Shulong Jiang","doi":"10.1016/j.canlet.2025.218004","DOIUrl":"10.1016/j.canlet.2025.218004","url":null,"abstract":"<div><div>Extrachromosomal circular DNA (eccDNA) drives oncogene amplification in multiple malignancies, yet its landscape and clinical relevance in hepatocellular carcinoma (HCC) remain poorly characterized. Here, we performed Circle-seq and RNA-seq on six pairs of HCC tumors and adjacent non-tumor tissues, identifying a 3 Mb extrachromosomal DNA (ecDNA) from chromosome 1q21 in 50 % tumor samples. This ecDNA contained multiple genes, but functional analysis prioritized <em>PIP5K1A</em> due to its central role in <em>PI3K/AKT</em> signaling and association with poor prognosis. The extrachromosomal localization of <em>PIP5K1A</em> was validated through outward PCR, inward PCR, Sanger sequencing, and fluorescence <em>in situ</em> hybridization (FISH) assays. Kaplan-Meier (KM) analysis demonstrated that elevated <em>PIP5K1A</em> expression was associated with an unfavorable prognosis in patients with HCC. <em>In vivo</em> and <em>in vitro</em> assays revealed that ecDNA-driven <em>PIP5K1A</em> amplification enhanced HCC proliferation, migration, and apoptosis resistance. Our study provides a genome-wide eccDNA profiling of HCC, implicating 1q21 ecDNA and <em>PIP5K1A</em> as prognostic markers and therapeutic targets, offering insights into HCC treatment strategies.</div></div>","PeriodicalId":9506,"journal":{"name":"Cancer letters","volume":"633 ","pages":"Article 218004"},"PeriodicalIF":10.1,"publicationDate":"2025-08-25","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144906975","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":"Protective role of epithelial deoxyhypusine synthase in colorectal carcinogenesis caused by deletion of the adenomatous polyposis coli gene","authors":"Alain P. Gobert ,&nbsp;Caroline V. Hawkins ,&nbsp;Lydia A. Snyder ,&nbsp;Kamery J. Williams ,&nbsp;Daniel P. Barry ,&nbsp;Margaret M. Allaman ,&nbsp;Mohammad Asim ,&nbsp;Kara M. McNamara ,&nbsp;Shane M. Carey ,&nbsp;Alberto G. Delgado ,&nbsp;Regina N. Tyree ,&nbsp;Kristie L. Rose ,&nbsp;Yu Wang ,&nbsp;Shilin Zhao ,&nbsp;Olivier Boutaud ,&nbsp;Irène Zagol-Ikapitte ,&nbsp;M. Blanca Piazuelo ,&nbsp;M. Kay Washington ,&nbsp;Lori A. Coburn ,&nbsp;Keith T. Wilson","doi":"10.1016/j.canlet.2025.218002","DOIUrl":"10.1016/j.canlet.2025.218002","url":null,"abstract":"<div><div>Mutations in the adenomatous polyposis coli (<em>APC</em>) gene lead to the formation of adenomatous polyps in the colon that can evolve into carcinoma. We have reported that deoxyhypusine synthase (DHPS), the rate-limiting enzyme for the synthesis of the amino acid hypusine on the eukaryotic translation initiation factor 5A, plays a major role in intestinal homoeostasis. Here, we investigated the role of hypusination in sporadic colorectal cancer (CRC). GEO database analyses revealed increases in polyamine metabolism genes, including <em>DHPS</em>, in human CRC. Tumors exhibited increased immunostaining for DHPS compared non-tumor tissues. Then, we generated mice with tamoxifen-inducible disruption of both <em>Apc</em> and <em>Dhps</em> in intestinal epithelial cells. Compared to animals with deletion of <em>Apc</em> only, survival and body weight loss were worsened in mice with specific deletion of both <em>Apc</em> and <em>Dhps</em>. Moreover, these animals had increased tumor number, tumor burden, and adenomas with low-grade or high-grade dysplasia. Differential label-free quantitative proteomic analysis on colonic epithelial cells demonstrated that DHPS activity in the tumors supported the translation of enzymes implicated in detoxification of deleterious electrophiles. Thus, tumors from mice with <em>Apc</em> and <em>Dhps</em> deletion exhibited increased malondialdehyde-dilysyl crosslinks. Further, the exacerbated tumorigenesis in mice with deletion of <em>Apc</em> and <em>Dhps</em> was significantly reduced by treatment with a scavenger of electrophiles, 2-hydroxybenzylamine. Thus, epithelial hypusination is essential to dampen the initiation of adenoma formation, notably by reducing the deleterious effects of reactive aldehydes. Strategies to enhance hypusination, such as by spermidine supplementation, may have potential for chemoprevention of CRC.</div></div>","PeriodicalId":9506,"journal":{"name":"Cancer letters","volume":"633 ","pages":"Article 218002"},"PeriodicalIF":10.1,"publicationDate":"2025-08-24","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144912453","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":"Proteomics and single cell profiling identify keratin driven preexisting immunity influences lung squamous carcinoma neoadjuvant therapy","authors":"Jiangnan Zhao ,&nbsp;Mo Shen ,&nbsp;Xia Xu ,&nbsp;Shunxian Ji ,&nbsp;Shumin Xu ,&nbsp;Lei Xu ,&nbsp;Ying Yang ,&nbsp;Minhua Ye ,&nbsp;Yunkun Lu ,&nbsp;Pingli Wang ,&nbsp;Kai Wang","doi":"10.1016/j.canlet.2025.218000","DOIUrl":"10.1016/j.canlet.2025.218000","url":null,"abstract":"<div><div>Lung squamous cell carcinoma (LUSC) demonstrates heterogeneous responses to neoadjuvant immune checkpoint blockade, necessitating biomarkers for outcome prediction. Here, we identify tumor keratinization as a key determinant of therapeutic resistance. In 470 LUSC patients, elevated serum CYFRA 21-1 correlated with non-complete pathological response (non-CPR), while CK5/6 immunohistochemistry revealed strong association between keratinization and residual tumor burden. Proteomic profiling of 167 treatment-naïve biopsies stratified patients into distinct subtypes based on keratinization levels. KRT_L (low keratinization) exhibited enhanced immune infiltration, a markedly lower residual viable tumor percentage (P &lt; 0.001), and superior survival outcomes (, P = 0.034) compared to the KRT_H (high keratinization). Conversely, KRT_H displayed upregulation of keratin proteins, activation of metabolic pathways, and enhanced cancer stemness features, alongside notable immunosuppression. Single-cell RNA analysis confirmed higher keratinization, metabolism and stemness in non-CPR tumors, with trajectory analysis linking undifferentiated states to keratin overexpression. Through integrated proteomic and single-cell analyses, our findings establish keratinization as a hallmark of immune-cold LUSC microenvironments, mechanistically linking elevated keratin expression with both stemness features and impaired immunotherapy efficacy, proposing keratin-based stratification for personalized therapy.</div></div>","PeriodicalId":9506,"journal":{"name":"Cancer letters","volume":"633 ","pages":"Article 218000"},"PeriodicalIF":10.1,"publicationDate":"2025-08-22","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144902634","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":"Synergistic targeting of FASN and HMGCS1 by cerulenin enhances tumor cell ferroptosis sensitivity through rewiring lipid metabolism and blocking GPX4 biosynthesis","authors":"Chaoyi Xia ,&nbsp;Xue Sun ,&nbsp;Yang Wang ,&nbsp;Jingshu Min ,&nbsp;Wenxia Zhang ,&nbsp;Chong Wei ,&nbsp;Lianchao Gao ,&nbsp;Feiyang Zhao ,&nbsp;Abdur Raheem Aleem ,&nbsp;Wanting Peng ,&nbsp;Yiren Hu ,&nbsp;Qiang Zhang ,&nbsp;Caiyun Fu","doi":"10.1016/j.canlet.2025.217992","DOIUrl":"10.1016/j.canlet.2025.217992","url":null,"abstract":"<div><div>Ferroptosis, an iron-dependent form of regulated cell death driven by lipid peroxidation, has emerged as a promising therapeutic target for cancer. However, accumulating evidence indicates that tumor cells exhibit insensitivity to classic ferroptosis inducers. In the present study, through high-throughput screening of a metabolite library, we identified cerulenin as a potent ferroptosis sensitizer. Mechanistically, cerulenin dually targets fatty acid synthase (FASN) and hydroxymethylglutaryl-CoA synthase 1 (HMGCS1), thereby inhibiting their enzymatic activity. FASN inhibition unexpectedly promoted ferroptosis via suppressing carnitine O-palmitoyltransferase 1 (CPT1)-mediated lipid β-oxidation, thereby triggering polyunsaturated fatty acid (PUFA) accumulation to drive ferroptosis. Simultaneously, HMGCS1 inhibition disrupted the mevalonate pathway, leading to impaired selenocysteine tRNA maturation and subsequent suppressing the synthesis of the glutathione peroxidase 4 (GPX4) protein, which enhances the sensitivity of tumor cells to ferroptosis inducers. Clinical bioinformatics analysis of TCGA datasets revealed significant co-overexpression of solute carrier family 7 member 11 (<em>SLC7A11</em>), <em>FASN</em>, and <em>HMGCS1</em> in multiple malignancies, which correlated with poor patient survival rates. <em>In vivo</em>, cerulenin synergized with classic ferroptosis inducer erastin to suppress xenograft tumor growth without observable toxicity. Collectively, this study revealed that cerulenin dual-targets FASN/HMGCS1 and obtained with remarkable pro-ferroptosis properties, providing a mechanistically distinct therapeutic paradigm for precision cancer therapy.</div></div>","PeriodicalId":9506,"journal":{"name":"Cancer letters","volume":"633 ","pages":"Article 217992"},"PeriodicalIF":10.1,"publicationDate":"2025-08-21","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144888778","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":"Response to the letter to the editor titled: “Polyploid giant cancer cells: unveiling a latent axis of resistance and tumor evolution in HER2-targeted therapy”","authors":"Mark Barok ,&nbsp;Narjes Yazdi ,&nbsp;Heikki Joensuu","doi":"10.1016/j.canlet.2025.217997","DOIUrl":"10.1016/j.canlet.2025.217997","url":null,"abstract":"","PeriodicalId":9506,"journal":{"name":"Cancer letters","volume":"631 ","pages":"Article 217997"},"PeriodicalIF":10.1,"publicationDate":"2025-08-21","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144944142","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":"SUSD2 hypersialylation promotes early lung adenocarcinoma progression by driving ECM remodeling and pro-tumorigenic fibroblast activation","authors":"Dong Zhou ,&nbsp;Jiao Zhang ,&nbsp;Xufeng Deng ,&nbsp;Xiao Lu,&nbsp;Xiaobing Liu,&nbsp;Juncheng Yu,&nbsp;Hong Zheng,&nbsp;Jigang Dai","doi":"10.1016/j.canlet.2025.217995","DOIUrl":"10.1016/j.canlet.2025.217995","url":null,"abstract":"<div><div>Cancer-associated fibroblasts (CAFs) play a crucial role in promoting the invasion and metastasis of lung adenocarcinoma (LUAD). The mechanism by which CAFs promote this process remains unclear. We employed glycoproteomics to investigate the dynamic changes in glycosylation between normal and early-stage LUAD tissues, and explore the roles of related glycoproteins and site-specific polysaccharides through <em>in vitro</em> and <em>in vivo</em> experiments. Using mass spectrometry-based glycoproteomics, we identified 242 N-glycosylated proteins with significantly increased expression and 17 with decreased expression in LUAD tissues. Sialylated modifications constitute the largest proportion of N-glycosylation and promote extracellular matrix (ECM) release by CAFs, enhancing their pro-cancer potential. Stage I LUAD patients with high levels of sialylation modifications have poor overall survival (OS) rates. Further findings revealed that ST3GAL4-mediated sialylation in CAFs is a key driver of ECM secretion, and that early-stage LUAD patients with high infiltration of ST3GAL4-positive CAFs have poor OS. Quantitative analysis of intact glycopeptides showed that core sialylation of SUSD2-Asn(N)162 was significantly upregulated and correlated with the ability of CAFs to secrete ECM. Sialylated SUSD2 binds to AKT and Smad2, enhancing their phosphorylation and ECM secretion, thereby increasing the pro-tumorigenic effects of CAFs. These findings offer new directions for developing glycosylation-centric therapies and biomarkers to treat early-stage LUAD, to improve patient outcomes by targeting CAF-driven drug resistance mechanisms.</div></div>","PeriodicalId":9506,"journal":{"name":"Cancer letters","volume":"633 ","pages":"Article 217995"},"PeriodicalIF":10.1,"publicationDate":"2025-08-20","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144944127","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":"C18-trans-fatty acids in cancer immunosurveillance","authors":"Tewodros Shegute ,&nbsp;Chen-Shiou Wu ,&nbsp;Wei-Chao Chang ,&nbsp;Chung-Yu Chen ,&nbsp;Yi-Chuan Li ,&nbsp;Muhammad Zeshan ,&nbsp;Hirohito Yamaguchi ,&nbsp;Yu-Fu Chen ,&nbsp;Zong-Shin Lin ,&nbsp;Shin-Lei Peng ,&nbsp;Hsiao-Fan Chen ,&nbsp;Mien-Chie Hung","doi":"10.1016/j.canlet.2025.217994","DOIUrl":"10.1016/j.canlet.2025.217994","url":null,"abstract":"","PeriodicalId":9506,"journal":{"name":"Cancer letters","volume":"633 ","pages":"Article 217994"},"PeriodicalIF":10.1,"publicationDate":"2025-08-20","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144902635","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 multicenter, real-world study analysis: pembrolizumab changes treatment strategy for the patient with recurrent/metastatic head and neck squamous cell carcinoma","authors":"Man Hu ,&nbsp;Xia Li ,&nbsp;Hong Feng ,&nbsp;Qiao Qiao ,&nbsp;Guangyuan Hu ,&nbsp;Kunyu Yang ,&nbsp;Xicheng Song ,&nbsp;Yuandong Cao ,&nbsp;Min Kang ,&nbsp;Ruozheng Wang ,&nbsp;Rui Liu ,&nbsp;Yani Zhang ,&nbsp;Luo Huang ,&nbsp;Xiujuan Cao ,&nbsp;Wenjun Liao ,&nbsp;Wenyu Ma ,&nbsp;Xueming Sun ,&nbsp;Bin Sun ,&nbsp;Xueying Liu ,&nbsp;Sangang Wu ,&nbsp;Jinming Yu","doi":"10.1016/j.canlet.2025.217996","DOIUrl":"10.1016/j.canlet.2025.217996","url":null,"abstract":"<div><div>Anti-PD-1/PD-L1 has made breakthrough progress in the treatment of recurrent and metastatic head and neck squamous cell carcinoma (R/M HNSCC). However, the Asian population in KEYNOTE-048 only accounts for 13.2 % of the total population, and there is a lack of data on the mainland Chinese population. This multi-center trial (ChiCTR2400090060) evaluated the efficacy and safety of pembrolizumab in patients with R/M HNSCC. Between July 2020 and January 2024, 291 patients who received pembrolizumab-based therapy were enrolled from 20 hospitals across China. All patients were divided into two cohort: cohort 1 included patients unable surgery or radiotherapy (RT), who received first-line treatment of pembolizumab-based, and cohort 2 included patients eligible for surgery or RT, who received pembrolizumab-based treatment with or without local therapy. The primary endpoint was overall survival (OS), while secondary endpoints included time of pembrolizumab treatment (TOPT), immune-related adverse events (irAEs), and best overall response (BOR). With a median follow-up of 18.5 months, the mOS was not reached, with a 18mo-OS rate was 63.2 %. The mOS for cohort 1 was 21.2 months. Interestingly, mOS for cohort 2 was not reached. Patients who received local therapy had a significantly improvement on 18mo-OS rate compared to those who did not (86.1 % vs. 65.8 %, p = 0.021). A total of 24.7 % of patients experienced irAEs. The study was the first report that the patient who was eligible for local treatment had a benefit from pembrolizumab, especially the OS was significantly improved for pembrolizumab followed by surgery or RT.</div></div>","PeriodicalId":9506,"journal":{"name":"Cancer letters","volume":"634 ","pages":"Article 217996"},"PeriodicalIF":10.1,"publicationDate":"2025-08-20","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144944105","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":"Corrigendum to “Pharmacological inhibition of DUSP6 suppresses gastric cancer growth and metastasis and overcomes cisplatin resistance” [Cancer Lett. (2018) 412 243–255]","authors":"Qi-Nian Wu ,&nbsp;Yi-Fu Liao ,&nbsp;Yun-Xin Lu ,&nbsp;Yun Wang ,&nbsp;Jia-Huan Lu ,&nbsp;Zhao-Lei Zeng ,&nbsp;Qi-Tao Huang ,&nbsp;Hui Sheng ,&nbsp;Jing-Ping Yun ,&nbsp;Dan Xie ,&nbsp;Huai-Qiang Ju ,&nbsp;Rui-Hua Xu","doi":"10.1016/j.canlet.2025.217983","DOIUrl":"10.1016/j.canlet.2025.217983","url":null,"abstract":"","PeriodicalId":9506,"journal":{"name":"Cancer letters","volume":"630 ","pages":"Article 217983"},"PeriodicalIF":10.1,"publicationDate":"2025-08-19","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144944135","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":"WZ4003 sensitizes hepatocellular carcinoma to OSI-027 by inhibiting ARK5-mediated autophagy","authors":"Bryan Wei Chen ,&nbsp;Jie-Ni Xiong ,&nbsp;Xiao Zhi ,&nbsp;Qi Chen ,&nbsp;Hui-liang Li ,&nbsp;Tao Ma ,&nbsp;Ting-bo Liang","doi":"10.1016/j.canlet.2025.217989","DOIUrl":"10.1016/j.canlet.2025.217989","url":null,"abstract":"<div><div>Mammalian target of rapamycin kinase inhibitors (mTOR-KIs) represent a novel promising treatment option for cancer therapy. OSI-027, a typical mTOR-KI, has been confirmed to suppress the proliferation of hepatocellular carcinoma (HCC) in preclinical models. However, mTOR-KIs confer limited therapeutic response against HCC, and the underlying mechanism remains enigmatic. The present study aimed to reveal the interaction between NUAK inhibitor WZ4003 and OSI-027 in HCC. Treatment with OSI-027 was found to result in up-regulation of ARK5 (also known as NUAK1), whereas both <em>ARK5</em> knockdown and WZ4003 sensitized HCC cells to OSI-027. Intriguingly, knockdown of <em>ARK5</em> abrogated the synergistic anti-HCC effect observed with the combination of WZ4003 and OSI-027. Additionally, OSI-027 triggered autophagy, an effect that could be reversed by WZ4003. Furthermore, WZ4003 was found to regulate autophagy in an ARK5-dependent manner, and phosphorylation of unc-51 like autophagy activating kinase 1 (ULK1) at Ser757 served as a downstream effector of ARK5. Notably, both chloroquine treatment and ULK1-S757E transfection abolished the OSI-027/WZ4003 synergy. We also confirmed a synergism pattern between OSI-027 and WZ4003 in an HCC xenograft model. Moreover, elevated ARK5 expression was observed in HCC specimens and was independently associated with an unfavorable recurrence-free survival (RFS). Our findings propose a novel strategy for augmenting sensitivity to OSI-027 in HCC, further underscoring the significance of ARK5 and autophagy as cancer therapeutic targets.</div></div>","PeriodicalId":9506,"journal":{"name":"Cancer letters","volume":"632 ","pages":"Article 217989"},"PeriodicalIF":10.1,"publicationDate":"2025-08-18","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144864204","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}