Carcinogenesis最新文献

{"title":"cAMP Signaling Pathway in TAMs: Molecular Mechanisms and Tumor Immunotherapy.","authors":"Yi Liu, Shuai Li, Wei Li, Mengting Zhou, Jie Liang, Xiaoli Liu, Xiao Wang, Yuanzhen Guo, Zhen Li, Bei Zhang, Luoyang Wang","doi":"10.1093/carcin/bgag026","DOIUrl":"https://doi.org/10.1093/carcin/bgag026","url":null,"abstract":"<p><p>Tumor-associated macrophages (TAMs) are the core innate immune cells in the tumor microenvironment (TME), and their phenotypic polarization and functional reprogramming determine the orientation of the tumor immune microenvironment and the efficacy of immunotherapy. As a key intracellular second messenger, cyclic adenosine monophosphate (cAMP) acts as a central hub regulating TAM function by activating two major downstream effector pathways: protein kinase A (PKA) and exchange protein directly activated by cAMP (Epac). This article systematically reviews the molecular mechanisms by which the cAMP-PKA/Epac signaling pathway regulates TAMs, the upstream regulatory factors in the TME, and targeted tumor immunotherapy strategies for this pathway. Studies have shown that cAMP mainly induces TAMs to polarize toward a pro-tumor \"M2-like phenotype\" through two classical pathways: cAMP-PKA-CREB and cAMP-PKA-STAT3/6. Meanwhile, it enhances the immunosuppressive, pro-angiogenic, and pro-fibrotic functions of TAMs via the cAMP-Epac pathway, inhibition of NF-κB signaling, and attenuation of M1 polarization. Furthermore, lactate and hypoxia-inducible factor-1α (HIF-1α) in the TME can further activate the intracellular cAMP signaling pathway in TAMs by activating G protein-coupled receptors and regulating the expression of adenylate cyclase, forming a cascade regulatory network with cAMP that exacerbates tumor immunosuppression. In addition, targeting the cAMP metabolic process, the downstream PKA pathway, and key molecules such as CREB/STAT/NF-κB can effectively reverse the \"M2-like phenotype\" of TAMs and restore their anti-tumor functions. Combination with immune checkpoint inhibitors can also significantly enhance the efficacy of tumor immunotherapy. By summarizing the core mechanisms of the cAMP-TAM regulatory axis and targeted intervention strategies, this article provides theoretical references and potential target directions for the development of novel tumor immunotherapy regimens based on TAM reprogramming.</p>","PeriodicalId":9446,"journal":{"name":"Carcinogenesis","volume":" ","pages":""},"PeriodicalIF":2.9,"publicationDate":"2026-05-06","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"147833530","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":"Characteristic genetic alterations associated with the partial deletion of chromosome 11 in mouse thymic lymphomas induced by high linear energy transfer irradiation with carbon ions.","authors":"Masaaki Sunaoshi, Erika Takahashi, Yoshiko Amasaki, Takamitsu Morioka, Kazuhiro Daino, Mayumi Nishimura, Yoshiya Shimada, Daisuke Iizuka, Shizuko Kakinuma","doi":"10.1093/carcin/bgag025","DOIUrl":"https://doi.org/10.1093/carcin/bgag025","url":null,"abstract":"<p><p>High linear energy transfer (LET) radiation is thought to induce highly complex DNA damage compared with photon radiation such as X-rays, suggesting a characteristic mechanism for the development of cancers associated with high-LET radiation exposure. However, few studies have investigated the carcinogenic mechanisms that are dependent on radiation quality or LET. This study analyzed mutations and gene expression in thymic lymphomas induced by high-LET carbon-ion irradiation to identify characteristic genetic alterations. The results revealed that thymic lymphomas arising after four-fractionated high-LET carbon-ion irradiation frequently exhibited loss of heterozygosity in the region containing the thymic lymphoma-associated gene Ikzf1 on chromosome 11 owing to extensive genomic deletions in the paternal allele. Nevertheless, for carbon ion-induced thymic lymphomas, those with only loss of heterozygosity without Ikzf1 alterations were observed at a relatively high frequency (16/39, 41.0%). Comprehensive RNA sequencing and reverse-transcription PCR analysis of neighboring genes of Ikzf1 revealed highly upregulated expression of Grb10 (17/39, 43.6%), an imprinted gene that is barely expressed in the normal thymus. In thymic lymphomas expressing Grb10, enhanced interferon signaling and Pten mutations, along with activation of the PI3K-AKT-mTOR signaling pathway, were suggested to promote cell proliferation and survival. These results suggest that extensive genomic deletions caused by high-LET carbon-ion irradiation may contribute to carcinogenesis by altering the expression of multiple genes located in the deleted region.</p>","PeriodicalId":9446,"journal":{"name":"Carcinogenesis","volume":" ","pages":""},"PeriodicalIF":2.9,"publicationDate":"2026-05-06","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"147833723","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":"The Effects of Black Raspberry Lozenges on 4-Hydroxy-1-(3-pyridyl)-1-butanone-Releasing DNA Adducts in Buccal Cells and Urinary Levels of N'-Nitrosonornicotine and its Glucuronide in Active Smokers.","authors":"Kun-Ming Chen, Nicolle M Krebs, Yuan-Wan Sun, Dongxiao Sun, Jiangang Liao, Lisa Reinhart, Susan R Mallery, Karam El-Bayoumy","doi":"10.1093/carcin/bgag019","DOIUrl":"https://doi.org/10.1093/carcin/bgag019","url":null,"abstract":"<p><p>The tobacco constituent, N'-nitrosonornicotine (NNN) is a potential etiological agent in the development of oral cancer. NNN is metabolically activated to form DNA adducts that release 4-hydroxy-1-(3-pyridyl)-1-butanone (HPB) which was detected at higher levels in the oral cavity of smokers than non-smokers. Black raspberry (BRB) has been proposed as a preventive agent of oral cancer. In a phase 0 clinical trial, 40 active smokers (16 males, 24 females) consumed 5g of BRB lozenges daily for eight weeks. Each participant served as his/her own control. Buccal cells and urine were collected at baseline, during BRB administration, and washout period. In all smokers, BRB reduced, but not significantly, the levels of HPB-releasing DNA adducts (Baseline: 0.97 ± 0.51 and End-BRB: 0.61 ± 0.23 HPB/106 Guanine). A sex-specific response to BRB was observed: BRB had no effects in men, but in 16 of 24 women BRB significantly reduced the levels of HPB. We further tested the hypothesis that detoxification of NNN via N-glucuronidation by BRB may, in part, account for the inhibition of HPB levels. The ratio of NNN-N-Gluc to free NNN significantly increased (p = 0.028) from 1.29 ± 0.40 (baseline) to 2.77 ± 0.76 (End-BRB) in all 40 women as well as in female responders from 1.24 ± 0.60 (baseline) to 2.87 ± 1.00, but not in non-responders. The metabolic changes of NNN observed in our clinical trial indicate that BRB is a promising candidate for cancer interception and prevention of oral cancer in some, but not in all active smokers.</p>","PeriodicalId":9446,"journal":{"name":"Carcinogenesis","volume":" ","pages":""},"PeriodicalIF":2.9,"publicationDate":"2026-04-30","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"147811242","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":"Chronic Stress Promotes Oral Squamous Cell Carcinoma Progression via GLUD1-Mediated Metabolic Reprogramming.","authors":"Huiqing Long, Yu Zhang, Yuqi Qin, Fangzhi Lou, Yiyun Liu, Juncai Pu, Xiaogang Zhong, Li Yan, Shihong Luo, Ping Ji, Bing Yang, Xin Jin","doi":"10.1093/carcin/bgag022","DOIUrl":"https://doi.org/10.1093/carcin/bgag022","url":null,"abstract":"<p><p>Stress is a risk factor for the development of various types of cancer. However, its impact and related underlying mechanisms in oral squamous cell carcinoma (OSCC) progression remain unclear. Therefore, the present study aimed to investigate how chronic stress affects OSCC progression. We assessed mitochondrial metabolism by investigating tumor growth and performing behavioral analysis and molecular assessment, including non-targeted metabolomics and U-13C5-glutamine isotope metabolic flow analysis. We knocked down glutamate dehydrogenase 1 (GLUD1) using lentiviral vectors and investigated it both in vitro (HSC3 and HN6 cells) and in vivo (xenograft models). Our results indicated that chronic stress enhanced glutamate oxidative deamination and tricarboxylic acid cycle metabolism in OSCC cells. It also increased α-ketoglutarate (α-KG) levels, adenosine triphosphate synthesis, and oxygen consumption. Notably, GLUD1-knockdown suppressed these metabolic pathways and significantly inhibited tumor growth both in vitro and in vivo. Furthermore, under chronic stress, GLUD1 regulated OSCC progression through histone H3 trimethylation at lysine 4. However, α-KG supplementation partially reversed GLUD1-knockdown-induced OSCC progression inhibition. Collectively, our results indicate the glutamate-dependent metabolic phenotype regulated by the GLUD1-α-KG metabolic axis is involved in the progression of OSCC under chronic stress.</p>","PeriodicalId":9446,"journal":{"name":"Carcinogenesis","volume":" ","pages":""},"PeriodicalIF":2.9,"publicationDate":"2026-04-13","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"147670539","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":"Current progress of CDC20 in cancer development and targeting CDC20 for cancer therapy.","authors":"Yingtong Chen, Shuang Gao, Ping Yang, Shuozi Liu, Weilong Zhang, Jing Wang, Hongmei Jing","doi":"10.1093/carcin/bgag021","DOIUrl":"10.1093/carcin/bgag021","url":null,"abstract":"<p><p>Cell division cycle 20 homolog (CDC20), a critical substrate-recruiting subunit of the anaphase-promoting complex/cyclosome (APC/C), binds to APC/C to form the active APC/C-CDC20 complex, which regulates the degradation of key cell cycle substrates to ensure accurate and timely mitotic progression. Accumulating evidence demonstrates that CDC20 functions as an oncogenic factor, with its overexpression observed in various malignancies. Its dysregulation is closely associated with tumor initiation, progression, drug resistance, and poor clinical outcomes, underscoring its potential as a therapeutic target in anti-cancer strategies. In this review, we describe the biological functions of CDC20 in cancers, discuss its role and underlying mechanisms in solid tumors and hematological malignancies, and elucidate currently reported CDC20-targeted inhibitors along with their clinical benefits and challenges. By emphasizing the oncogenic significance of CDC20, we propose that the development of specific, safe, and potent CDC20 inhibitors could provide a promising therapeutic approach for cancer patients exhibiting CDC20 overexpression.</p>","PeriodicalId":9446,"journal":{"name":"Carcinogenesis","volume":" ","pages":""},"PeriodicalIF":2.9,"publicationDate":"2026-04-09","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"147509851","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":"Ultraviolet A plays a protective role in ultraviolet B-induced squamous cell carcinoma through c-Fos/XRCC4 axis.","authors":"Yifei Xie, Ke Yao, Yongfeng Wu, Caoyuan Ding, Sally E Dickinson, Jian Li, Yanan Jiang, Simin Zhao, Eunmiri Roh, Kangdong Liu, Zigang Dong","doi":"10.1093/carcin/bgag014","DOIUrl":"10.1093/carcin/bgag014","url":null,"abstract":"<p><p>For decades, there has been a strong epidemiological association between solar ultraviolet (UV) radiation and skin cancer. UVB and UVA are the major UV bands that can penetrate the atmosphere, playing vital roles in skin carcinogenesis. Our research group previously discovered that a specific dose of UVA can inhibit the increase of activator protein 1 (AP-1) activity caused by UVB. It is unclear whether UVA plays a particular role in UVB-induced skin cancer. Here, we report that UVA was protective in UVB-induced cutaneous squamous cell carcinoma (cSCC) by attenuating UVB-induced DNA damage. DNA repair chip array results showed that the mRNA level of X-ray cross-complementing protein 4 (XRCC4) significantly increased in the UVA/B group compared with the UVB group, and knockdown of XRCC4 partly blocked the protective effect of UVA in UVB-induced DNA damage. AP-1, the predicted transcriptional regulatory factor of XRCC4, exhibited no sensitivity to UVB radiation upon pretreatment with UVA. More importantly, the luciferase reporter assay showed that c-Fos, which is the critical component of AP-1, inhibited the transcription of XRCC4, and mutation of c-Fos (cys154 > serine) partly enhanced this effect and promoted keratinocyte transformation. UVA was protective in UVB-induced cSCC by interacting with the c-Fos/XRCC4 axis.</p>","PeriodicalId":9446,"journal":{"name":"Carcinogenesis","volume":" ","pages":""},"PeriodicalIF":2.9,"publicationDate":"2026-04-09","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"147442446","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":"Stromal NNMT Overexpression as an Independent Prognostic Biomarker in Lung Adenocarcinoma and Breast Carcinoma.","authors":"Yanzhong Wang, Yiping Wu, Shuyang Zheng, Xiaotian Yan, Xingtong Yu, Yuzhen Gao, Shuduo Xie, Zhinong Jiang, Rui An, Guoli Li, Jun Yang, Qingchao Tong, Xinyou Xie, Jun Zhang","doi":"10.1093/carcin/bgag020","DOIUrl":"https://doi.org/10.1093/carcin/bgag020","url":null,"abstract":"<p><p>This study investigated the expression profile and prognostic significance of nicotinamide N-methyltransferase (NNMT) in pan-cancer stroma, with focused validation in lung adenocarcinoma (LUAD) and breast carcinoma (BC). Integrated analysis of Genotype-Tissue Expression and The Cancer Genome Atlas databases revealed tumor-specific NNMT mRNA upregulation in these malignancies. Subsequently, the relationship between NNMT mRNA expression levels and clinical parameters across multiple cancer types was examined, with particular emphasis on LUAD, BC, and CRC. Single-cell RNA sequencing data further revealed elevated NNMT expression specifically within stromal compartments, with fibroblasts exhibiting the highest NNMT expression levels among stromal cell populations. Protein-level validation using the Human Protein Atlas database, the National Cancer Institute's Proteomics Data Commons, and the quantitative immunohistochemistry of our independent clinical cohorts demonstrated elevated stromal NNMT protein expression, particularly in cancer-associated fibroblasts. Cox regression analysis and survival curve analysis established stromal NNMT expression as an independent prognostic factor for overall survival in LUAD and BC patients (p < 0.05). In conclusion, high stromal NNMT levels correlated with poor prognosis, establishing it as a promising biomarker for risk stratification in LUAD and BC.</p>","PeriodicalId":9446,"journal":{"name":"Carcinogenesis","volume":" ","pages":""},"PeriodicalIF":2.9,"publicationDate":"2026-03-30","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"147580245","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":"Role of P450 enzymes of the Cyp2abfgs gene subfamilies in tobacco smoke-induced lung tumorigenesis in mice.","authors":"Lisa M Tran, Patricia C Edwards, Weizhu Yang, Qing-Yu Zhang, Weiguo Han, Nataliia Kovalchuk, Liang Ding, Xiangmeng Wu, Xiaoyu Fan, Angel Arredondo, Robin Jordan Agustin Merluza, David G Besselsen, J Rachel Reader, Laura S Van Winkle, Xinxin Ding","doi":"10.1093/carcin/bgag017","DOIUrl":"https://doi.org/10.1093/carcin/bgag017","url":null,"abstract":"<p><p>Many chemical carcinogens in tobacco smoke require bioactivation by cytochrome P450 enzymes. While the roles of P450 enzymes in carcinogenesis have been demonstrated in vivo using several individual carcinogens at relatively high doses, no data has been reported on their contributions to carcinogenesis induced by tobacco smoke, a complex mixture of >4000 compounds. The present study aims to address this important knowledge gap, using mice deficient in the expression of enzymes of the Cyp2abfgs gene subfamilies, which are known to bioactivate multiple chemical carcinogens in tobacco smoke. Male and female wild-type (WT) and Cyp2abfgs-null mice on the A/J genetic background were exposed to environmental tobacco smoke (ETS), a mixture of mainstream and sidestream smoke, for 6 hours/day, 5 days/week, for 5 months, at a target dose of 0 or 120 mg/m3 suspended total particulate matter. All mice were returned to filtered air (FA) for 4 months after cessation of ETS exposure. At approximately 11 months of age, mice were euthanized, and lungs were collected for tumor enumeration. ETS exposure increased tumor multiplicity (number of tumors per lung) in WT mice by 2.5-fold (p<0.0001), but only by 1.7-fold in Cyp2abfgs-null mice (p<0.001), compared to FA-exposed mice (n=∼180 per group, male and female). Multiplicity of ETS-induced tumors was significantly reduced (by 50%; p<0.01) in Cyp2abfgs-null relative to WT mice. These results demonstrate for the first time, in vivo, that bioactivation of ETS constituents by P450 enzymes, of the Cyp2abfgs gene subfamilies, play an important role in tobacco-smoke induced lung tumorigenesis in mice.</p>","PeriodicalId":9446,"journal":{"name":"Carcinogenesis","volume":" ","pages":""},"PeriodicalIF":2.9,"publicationDate":"2026-03-19","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"147484757","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":"Microplastics in Early Onset Carcinogenesis.","authors":"Anne M Bailey, Lorne J Hofseth","doi":"10.1093/carcin/bgaf093","DOIUrl":"https://doi.org/10.1093/carcin/bgaf093","url":null,"abstract":"<p><p>Plastics have become integral to modern life, but their persistence has generated vast quantities of microplastics (MPs, <5 mm) and nanoplastics (NPs, <1 µm) that now contaminate food, water, air, and human tissues. Although not yet classified as carcinogens by the International Agency for Research on Cancer, accumulating experimental and epidemiologic evidence raises concern that MPs may contribute to cancer development. Global plastic production has risen from 2 megatons in 1950 to more than 450 megatons annually in 2022, leaving behind pervasive waste that fragments into MPs and NPs. These particles act as xenobiotics, carrying toxic additives and adsorbed pollutants, provoking oxidative stress, chronic inflammation, DNA damage, and microbiome disruption; all processes central to carcinogenesis. MPs have been detected in human cancers, and animal studies show tissue accumulation, fibrosis, and genomic instability following exposure. Importantly, the proliferation of plastics parallels a global rise in early-onset cancers (diagnosed before age 50), suggesting a possible, though unproven, temporal association. Individuals born after the 1950s plastic boom have experienced continuous MP exposure beginning in utero, potentially predisposing them to carcinogenic pathways later in life. In this review, we integrate human biomonitoring data, experimental findings, and clinical observations to evaluate the emerging hypothesis that chronic MP exposure contributes to cancer risk. While causality has not been established, the biological plausibility and mounting evidence underscore the urgent need for mechanistic and epidemiologic studies to clarify the role of MPs and NPs in cancer development. It also underscores an urgent need for research into causal pathways and preventive mechanisms.</p>","PeriodicalId":9446,"journal":{"name":"Carcinogenesis","volume":" ","pages":""},"PeriodicalIF":2.9,"publicationDate":"2026-01-12","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145951570","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":"Adverse events and recent advances in CAR-T-cell therapy.","authors":"Zhimin Bai, Xiaoyu Huang, Hui Jia, Zenghua Lin, Hong Liu","doi":"10.1093/carcin/bgaf083","DOIUrl":"10.1093/carcin/bgaf083","url":null,"abstract":"<p><p>Chimeric antigen receptor (CAR-T) cell therapy has been widely used in haematological malignancies and has achieved remarkable results. However, two major toxicities of CAR-T-cell therapy, cytokine release syndrome and immune effector cell-associated neurotoxicity syndrome, have been reported in many studies and often require hospitalization. There is evidence that CAR-T-cell therapy is being increasingly used clinically, so it is important to pay attention to its serious adverse events that may be life-threatening. In this review, we provide a detailed discussion of the clinical manifestations, classification, risk factors, and management and treatment of serious adverse events to provide theoretical support for clinicians to manage such cases. Although the clinical application of CAR-T cells continues to expand, adverse events associated with CAR-T-cell therapy are inevitable. With the identification of risk factors and the application of various new therapeutic approaches, the incidence and severity of these adverse events can be effectively controlled.</p>","PeriodicalId":9446,"journal":{"name":"Carcinogenesis","volume":" ","pages":""},"PeriodicalIF":2.9,"publicationDate":"2025-12-26","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145833139","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}