Molecular Cancer最新文献

{"title":"Lymphatic system is the mainstream for breast cancer dissemination and metastasis revealed by single-cell lineage tracing","authors":"Kai Miao, Aiping Zhang, Xiaodan Yang, Yipeng Zhang, Anqi Lin, Lijian Wang, Xin Zhang, Heng Sun, Jun Xu, Jingyao Zhang, Yuzhao Feng, Fangyuan Shao, Sen Guo, Zhihui Weng, Peng Luo, Dong Wang, Shuai Gao, Xiao-Yang Zhao, Xiaoling Xu, Chu-Xia Deng","doi":"10.1186/s12943-025-02279-w","DOIUrl":"https://doi.org/10.1186/s12943-025-02279-w","url":null,"abstract":"Cancer metastasis is the primary cause of cancer-related death, yet the forces that drive cancer cells through various steps and different routes to distinct target organs/tissues remain elusive. In this study, we applied a barcoding system based single-cell lineage tracing approach to study the metastasis rate and route of breast cancer cells and their interactions with the tumor microenvironment (TME) during metastasis. The results indicate that only a small fraction of cells, accounting for fewer than 3% of total barcodes, can intravasate from the primary site into the blood circulation, whereas more cells disseminate through the lymphatic system to different organs. Tumor cells derived from the same progenitor cell exhibit different gene expression patterns in different soils, and the cancer cell-TME communication paradigm varies significantly between primary and metastatic tumors. Furthermore, metastable cells require a prewired particular cytokine expression ability which may be specific for lymph metastasis route although the underlying mechanism requires further investigation. In summary, leveraging a single-cell lineage tracing system, we demonstrate that the crosstalk between tumor cells and the TME is the driving force controlling the preferential metastatic fate of cancer cells through the lymphatic system. ","PeriodicalId":19000,"journal":{"name":"Molecular Cancer","volume":"68 1","pages":""},"PeriodicalIF":37.3,"publicationDate":"2025-03-12","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143599813","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":"Reprogramming of Thyroid Cancer Metabolism: from Mechanism to Therapeutic Strategy","authors":"Yuxuan Wan, Guoqing Li, Gaoyuan Cui, Saili Duan, Shi Chang","doi":"10.1186/s12943-025-02263-4","DOIUrl":"https://doi.org/10.1186/s12943-025-02263-4","url":null,"abstract":"Thyroid cancer as one of the most prevalent malignancies of endocrine system, has raised public concern and more research on its mechanism and treatment. And metabolism-based therapies have advanced rapidly, for the exclusive metabolic profiling of thyroid cancer. In thyroid cancer cells, plenty of metabolic pathways are reprogrammed to accommodate tumor microenvironment. In this review, we initiatively summarize recent progress in the full-scale thyroid cancer metabolic rewiring and the interconnection of various metabolites. We also discuss the efficacy and prospect of metabolic targeted detection as well as therapy. Comprehending metabolic mechanism and characteristics of thyroid cancer roundly will be highly beneficial to managing individual patients.","PeriodicalId":19000,"journal":{"name":"Molecular Cancer","volume":"19 1","pages":""},"PeriodicalIF":37.3,"publicationDate":"2025-03-11","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143589668","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":"Modulating lipid metabolism by nanoparticles (NPs)-mediated ACSL3 silencing to inhibit hepatocellular carcinoma growth and metastasis","authors":"Linzhuo Huang, Rui Xu, Siyu Chen, Chunhao Lin, Wende Li, Senlin Li, Phei Er Saw, Lei Zhang, Xiaoding Xu","doi":"10.1186/s12943-025-02274-1","DOIUrl":"https://doi.org/10.1186/s12943-025-02274-1","url":null,"abstract":"Abnormal lipid metabolism plays an important role in the development and progression of almost all cancer types, especially hepatocellular carcinoma (HCC) as the liver is the central organ for lipid storage and metabolism. However, the underlying mechanisms are complex and have not been completely elucidated. By analyzing the proteomic sequencing and single cell RNA-sequencing (scRNA-seq) results of HCC patients, we herein reveal that acyl-CoA synthase long chain family member 3 (ACSL3) is predominately expressed in HCC cells and high ACSL3 expression is positively correlated with abnormal lipid metabolism and predicts the poor prognosis of HCC patients. Mechanically, ACSL3 could promote the synthesis of 1-palmitoyl-2-oleoyl-sn-glycero-3-phosphocholine (POPC), which could activate peroxisome proliferator-activated receptor α (PPARα) pathway and enhance the transcription of downstream lipid metabolism-associated genes, thereby promoting HCC growth and metastasis via accelerating lipid catabolism and anabolism. Considering the lack of specific inhibitor for ACSL3, we further develop an endosomal pH-responsive nanoparticle (NP) platform for systemic delivery of ACSL3 siRNA (siACSL3) and demonstrate its ability to inhibit HCC tumor growth and metastasis. Our findings indicate that ACSL3 could be used to predict the prognosis of HCC patients and NPs-mediated ACSL3 silencing could be a promising strategy for effective HCC therapy.","PeriodicalId":19000,"journal":{"name":"Molecular Cancer","volume":"38 1","pages":""},"PeriodicalIF":37.3,"publicationDate":"2025-03-10","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143582752","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":"Bridging epigenomics and tumor immunometabolism: molecular mechanisms and therapeutic implications","authors":"Xiaowen Xie, Weici Liu, Zhiyuan Yuan, Hanqing Chen, Wenjun Mao","doi":"10.1186/s12943-025-02269-y","DOIUrl":"https://doi.org/10.1186/s12943-025-02269-y","url":null,"abstract":"Epigenomic modifications—such as DNA methylation, histone acetylation, and histone methylation—and their implications in tumorigenesis, progression, and treatment have emerged as a pivotal field in cancer research. Tumors undergo metabolic reprogramming to sustain proliferation and metastasis in nutrient-deficient conditions, while suppressing anti-tumor immunity in the tumor microenvironment (TME). Concurrently, immune cells within the immunosuppressive TME undergo metabolic adaptations, leading to alterations in their immune function. The complicated interplay between metabolites and epigenomic modulation has spotlighted the significance of epigenomic regulation in tumor immunometabolism. In this review, characteristics of the epigenomic modification associated with tumors are systematically summarized alongside with their regulatory roles in tumor metabolic reprogramming and immunometabolism. Classical and emerging approaches are delineated to broaden the boundaries of research on the crosstalk research on the crosstalk between tumor immunometabolism and epigenomics. Furthermore, we discuss potential therapeutic strategies that target tumor immunometabolism to modulate epigenomic modifications, highlighting the burgeoning synergy between metabolic therapies and immunotherapy as a promising avenue for cancer treatment.\u0000","PeriodicalId":19000,"journal":{"name":"Molecular Cancer","volume":"53 1","pages":""},"PeriodicalIF":37.3,"publicationDate":"2025-03-08","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143575267","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":"Small extracellular vesicles and particles (sEVPs) derived from tumor-free pre-metastatic organs promote breast cancer metastasis and support organotropism","authors":"Tasneem Cheytan, Martin Schneider, Roberto Würth, Paul Schwerd-Kleine, Ewgenija Gutjahr, Verena Thewes, Laura L. Michel, Rebecca Weber, Tim Vorberg, Sabrina Lohr, Katja Nitschke, Michelle Neßling, Peter Lichter, Andreas Schneeweiss, Karsten Richter, Dominic Helm, Martin Sprick, Andreas Trumpp","doi":"10.1186/s12943-025-02235-8","DOIUrl":"https://doi.org/10.1186/s12943-025-02235-8","url":null,"abstract":"Metastatic breast cancer remains largely incurable, partly due to our incomplete understanding of its intricate underlying mechanisms. Notably, intercellular communication mediated by small extracellular vesicles and particles (sEVPs) has emerged as a key feature of metastasis. While tumor-derived sEVPs have been extensively studied and are known to be pro-metastatic, the role of sEVPs from metastasis-prone normal tissue sites remains primarily undefined. Here, we characterized and studied the function of sEVPs secreted from tumor-free pre-metastatic organs (TuFMO-sEVPs) such as the brain and lungs in both immunocompetent and patient-derived xenograft models. TuFMO-sEVPs from the brain of mammary tumor-bearing mice were found to have a distinct protein content as compared to brain-sEVPs from tumor-free mice, suggesting that the primary tumor can systemically influence the cargo of TuFMO-sEVPs. Importantly, mice orthotopically injected with breast cancer cells which had been educated with either brain or lung TuFMO-sEVPs prior to transplantation showed significantly increased metastasis to the respective organ. We further demonstrated that TuFMO-sEVPs induced the expression of the enzyme dihydrofolate reductase (DHFR) upon uptake by breast cancer cells, leading to their enhanced metastatic capacity. Organ-specific signatures generated from TuFMO-sEVP educated tumor cells were found to be increased in metastatic samples from breast cancer patients as compared to the primary tumor or normal tissue samples and these signatures also significantly correlated with poorer patient outcome. Collectively, our data reveals a novel facet of the metastatic cascade, implicating a role for TuFMO-sEVPs in directing metastasis and providing a potential therapeutic strategy for targeting this process.","PeriodicalId":19000,"journal":{"name":"Molecular Cancer","volume":"14 1","pages":""},"PeriodicalIF":37.3,"publicationDate":"2025-03-08","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143575273","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":"Contract to kill: GNAS mutation","authors":"Pratima Raut, Poompozhil Mathivanan, Surinder K. Batra, Moorthy P. Ponnusamy","doi":"10.1186/s12943-025-02247-4","DOIUrl":"https://doi.org/10.1186/s12943-025-02247-4","url":null,"abstract":"The mutation in Gsα-coding GNAS exons, popular as gsp oncogene, is the most frequent mutation across all heterotrimeric G proteins involved in oncogenesis. GNAS R201, the most frequently mutated, followed by Q227, are found predominantly across various neoplasms and cancers such as IPMN, pituitary, thyroid, appendiceal, colorectal, etc. This review emphasizes the pivotal significance of the gsp oncogene and its ramifications underpinning the sustained addiction to GNAS mutation. Recent studies delineating the mechanistic intricacies that provide solid evidence of the profound impact of oncogenic GNAS on tumor formation, progression, and maintenance are highlighted. We have leveraged the discoveries of Gsα as an ideal neoantigen candidate for vaccine therapy, allele-specific inhibitors, and cyclic peptide-based small molecular inhibitors for G proteins and explored the therapeutic potential to target oncogenic GNAS directly. Alternative therapeutic modalities and patient-centric studies to mitigate the impact of GNAS mutations are also discussed. The exposition of novel studies and strategies designed to address the potential challenges inherent in these approaches of targeting the activating mutations of GNAS, along with probable avenues for further investigation, are highlighted. This review aims to reverberate the current understanding of the oncogenic potential of GNAS, the genomic and biological landscape of GNAS-driven neoplasms and cancers, and potential therapeutic strategies against them.\u0000","PeriodicalId":19000,"journal":{"name":"Molecular Cancer","volume":"212 1","pages":""},"PeriodicalIF":37.3,"publicationDate":"2025-03-07","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143569445","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":"Engineered multifunctional nanoparticles for enhanced radiation therapy: three-in-one approach for cancer treatment","authors":"Tejaswini Appidi, Debarghya China, George-Răzvan Ștefan, Michele Moreau, Serena Mao, Esteban Velarde, Ngeh Toyang, Henry Lowe, Aravind Kumar Rengan, Kai Ding, Wilfred Ngwa","doi":"10.1186/s12943-025-02266-1","DOIUrl":"https://doi.org/10.1186/s12943-025-02266-1","url":null,"abstract":"Clinical cancer treatment modalities include radiation as one of the first-line therapies used for treating almost two-thirds of cancer patients. Combinational therapy for cancer is becoming extremely popular, with multiple therapies and their pharmacological effects expected to provide a synergistic outcome. The nanotechnology-based combinational therapeutic approach is emerging as a more effective strategy, for its advantages include simultaneous loading of multiple drugs, on-demand drug delivery controlled by external or internal stimulus, targeting a particular site, and the potential to combine physical treatment modalities (like radiation, thermal therapies, etc.) with chemical interventions (like chemotherapy, immunotherapy, etc.). We report a combination of radiotherapy and chemotherapy mediated by a multifunctional lipo-polymeric hybrid nanosystem coated with gold, demonstrating the three different functionalities using a single nanosystem: a) radio sensitization, b) radiation-triggered delivery of drugs, and c) application as an X-ray/CT contrast agent. The lipo-polymeric hybrid nanoparticles, synthesized using a modified hydrogel isolation method, were loaded with a natural plant-derived anti-cancer agent “Caflanone.” These nanoparticles were further subjected to in-situ reduction for a surface coating of gold, which provided enhanced radiosensitivity, radiation triggered drug delivery and X-ray/CT imaging. This approach using a multifunctional nanosystem leverages the biocompatibility of the lipo-polymeric hybrid system for the loading of drugs, precise spatiotemporal controllability of radiation for drug release, and the cytotoxicity of the plant-derived anti-cancer agent “Caflanone.” A significant therapeutic efficacy in vitro against breast cancer (p = 0.0002), pancreatic cancer (p < 0.0001), and glioblastoma (p < 0.0001) was demonstrated with the combinational approach. The application of the nanosystem as an X-ray/CT contrast agent has been shown in vivo in tumor-bearing mice and the safety profile and histopathology evaluated in healthy mice showed no adverse effects. A significant increase (p = 0.01) in the survival of breast tumor-bearing mice treated with a combinational approach was also demonstrated. The engineered multifunctional nanoparticles enhanced the radiation therapy and triggered the drug release at the tumor site, triggering the action of encapsulated chemotherapeutic agents while providing image guidance.","PeriodicalId":19000,"journal":{"name":"Molecular Cancer","volume":"36 1","pages":""},"PeriodicalIF":37.3,"publicationDate":"2025-03-06","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143560615","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":"Harnessing myeloid cells in cancer","authors":"Su-Yeon Park, Ekaterina Pylaeva, Vikas Bhuria, Adriana Rosa Gambardella, Giovanna Schiavoni, Dimitrios Mougiakakos, Sung-Hoon Kim, Jadwiga Jablonska","doi":"10.1186/s12943-025-02249-2","DOIUrl":"https://doi.org/10.1186/s12943-025-02249-2","url":null,"abstract":"Cancer-associated myeloid cells due to their plasticity play dual roles in both promoting and inhibiting tumor progression. Myeloid cells with immunosuppressive properties play a critical role in anti-cancer immune regulation. Cells of different origin, such as tumor associated macrophages (TAMs), tumor associated neutrophils (TANs), myeloid derived suppressor cells (also called MDSCs) and eosinophils are often expanded in cancer patients and significantly influence their survival, but also the outcome of anti-cancer therapies. For this reason, the variety of preclinical and clinical studies to modulate the activity of these cells have been conducted, however without successful outcome to date. In this review, pro-tumor activity of myeloid cells, myeloid cell-specific therapeutic targets, in vivo studies on myeloid cell re-polarization and the impact of myeloid cells on immunotherapies/genetic engineering are addressed. This paper also summarizes ongoing clinical trials and the concept of chimeric antigen receptor macrophage (CAR-M) therapies, and suggests future research perspectives, offering new opportunities in the development of novel clinical treatment strategies.","PeriodicalId":19000,"journal":{"name":"Molecular Cancer","volume":"34 1","pages":""},"PeriodicalIF":37.3,"publicationDate":"2025-03-06","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143560927","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":"Circular RNA circCLASP2 promotes nasopharyngeal carcinoma progression through binding to DHX9 to enhance PCMT1 translation","authors":"Miao Peng, Shanshan Zhang, Pan Wu, Xiangchan Hou, Dan Wang, Junshang Ge, Hongke Qu, Chunmei Fan, Yujuan Zhou, Bo Xiang, Qianjin Liao, Ming Zhou, Ming Tan, Guiyuan Li, Wei Xiong, Pan Chen, Zhaoyang Zeng, Zhaojian Gong","doi":"10.1186/s12943-025-02272-3","DOIUrl":"https://doi.org/10.1186/s12943-025-02272-3","url":null,"abstract":"Circular RNAs (circRNAs), characterized by their covalently closed-loop structures, constitute a distinct class of non-coding RNAs. They play pivotal regulatory roles within cells and are intricately associated with the progression of malignant tumors. However, their roles and the underlying mechanisms in nasopharyngeal carcinoma (NPC) progression have yet to be fully uncovered and comprehensively understood. Employing RNA sequencing technology, high-abundance circular RNAs in NPC were identified. Expression analysis of circCLASP2 in NPC tissues was conducted using quantitative real-time polymerase chain reaction (qRT-PCR) and in situ hybridization experiments. Through in vitro and in vivo functional assays, the influence of circCLASP2 on the proliferation and metastasis of NPC was investigated. LC–MS/MS technology analyzed the binding partners of circCLASP2, its differentially regulated targets, and the associated proteins of PCMT1. Interactions among circCLASP2, DHX9 protein, and PCMT1 mRNA were elucidated through RNA immunoprecipitation and RNA pull-down techniques. The effects of circCLASP2 and DHX9 on RNA G-quadruplex (rG4) structures and PCMT1 mRNA translation were explored through immunofluorescence (IF), ribosomal gradient separation, and dual-luciferase reporter assays. Immunoprecipitation (IP) revealed the downstream effector of the circCLASP2-DHX9-PCMT1 regulatory axis and Phalloidin staining confirmed its ultimate effect on the cytoskeleton. PDS treatment was applied for interventions in NPC, demonstrating potential therapeutic avenues. Our research revealed that circCLASP2, a novel circRNA that has not been reported in tumors, is upregulated in NPC and fosters cell proliferation and metastasis both in vitro and in vivo. Mechanistically, circCLASP2 acts as a molecular scaffold, facilitating the approximation of DHX9 to PCMT1 mRNA. DHX9 unwinds the inhibitory rG4 structure near the translation initiation site on PCMT1 mRNA, increasing PCMT1 expression. PCMT1 binds to and upregulates cytoskeleton-associated proteins, modulating cytoskeleton strength and dynamics and ultimately driving NPC cell proliferation and metastasis. In both in vitro and in vivo experiments, PDS significantly inhibits NPC growth and metastasis, showcasing promising therapeutic potential. Our investigation pinpointed a circular RNA, circCLASP2, which is upregulated in NPC and augments cytoskeletal functions via the DHX9-PCMT1 axis, contributing to the malignancy progression of NPC. This pathway holds promise as a potential therapeutic target for NPC. Furthermore, these molecules could also serve as biomarkers for adjunct diagnosis and prognosis assessment in NPC.","PeriodicalId":19000,"journal":{"name":"Molecular Cancer","volume":"11 1","pages":""},"PeriodicalIF":37.3,"publicationDate":"2025-03-06","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143560617","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":"The epigenetic hallmarks of immune cells in cancer","authors":"Yu Ji, Chu Xiao, Tao Fan, Ziqin Deng, Di Wang, Wenpeng Cai, Jia Li, Tianle Liao, Chunxiang Li, Jie He","doi":"10.1186/s12943-025-02255-4","DOIUrl":"https://doi.org/10.1186/s12943-025-02255-4","url":null,"abstract":"Targeting the dysregulation of epigenetic mechanisms in cancer has emerged as a promising therapeutic strategy. Although the significant rationale progress of epigenetic therapies in blocking cancer cells, how epigenetic regulation shapes tumor microenvironment (TME) and establishes antitumor immunity remains less understood. Recent study focus has been put on the epigenetic-mediated changes in the fate of immune cells, including the differentiation, expansion, recruitment, functionalization, and exhaustion of T cells, natural killer (NK) cells, tumor-associated macrophages (TAMs), dendritic cells (DCs), myeloid-derived suppressor cells (MDSCs), and B cells within the TME. Here, we review the latest molecular and clinical insights into how DNA modifications, histone modification, and epitranscriptome-related regulations shape immune cells of various cancers. We also discuss opportunities for leveraging epigenetic therapies to improve cancer immunotherapies. This review provides the epigenetic foundations of cancer immunity and proposes the future direction of combination therapies.","PeriodicalId":19000,"journal":{"name":"Molecular Cancer","volume":"12 1","pages":""},"PeriodicalIF":37.3,"publicationDate":"2025-03-05","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143546147","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}