Cancer Cell International最新文献

{"title":"Advancements and challenges in CAR-T cell therapy for solid tumors: A comprehensive review of antigen targets, strategies, and future directions.","authors":"Jiajun Zhu, Jianming Zhou, Yiting Tang, Ruotong Huang, Chengjia Lu, Ke Qian, Qingyu Zhou, Jingjun Zhang, Xiaoyi Yang, Wenhan Zhou, Jiaqiang Wu, Qiudan Chen, Yong Lin, Shuying Chen","doi":"10.1186/s12935-025-03938-0","DOIUrl":"10.1186/s12935-025-03938-0","url":null,"abstract":"","PeriodicalId":9385,"journal":{"name":"Cancer Cell International","volume":"25 1","pages":"313"},"PeriodicalIF":6.0,"publicationDate":"2025-08-23","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12374352/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144944140","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Transcriptomics assisted by metabolomics analysis provides insights into regulation mechanisms during carcinogenic process in a hydrodynamically transfected liver cancer model.","authors":"Qi Zhang, Yongfeng Li, Xiaojing Cheng, Zhouxiang Liao, Sha Wen, Xuejing Huang, Zhenyu Song, Min He, Lichao Yang","doi":"10.1186/s12935-025-03937-1","DOIUrl":"10.1186/s12935-025-03937-1","url":null,"abstract":"<p><strong>Background: </strong>Hepatocellular carcinoma (HCC) ranks among the most prevalent malignancies with a substantial mortality rate, and its pathogenesis is relatively complex. Animal models provide valuable tools for exploring the causes and mechanisms of malignancy. This study uses a novel hydrodynamic transfection mouse model to investigate the changes in key genes and metabolites during the development of HCC. By combining metabolomics-assisted transcriptomics assay, this research seeks to provide new insights into HCC development.</p><p><strong>Methods: </strong>A mouse model of HCC was established using hydrodynamic transfection coupled with the SB11 transposon system and the CRISPR-Cas9 system. C57BL/6J mice were used as experimental animals, with mice arbitrarily split into the control and experimental groups. The experimental group of mice underwent hydrodynamic transfection using mixed recombination carcinogenic plasmids that knocked out the tumor suppressor genes Pten and P53, while overexpressing the oncogenes β-catenin and c-Met. In contrast, the control group of mice was transfected with corresponding empty vectors. All mice were monitored for weight, activity, and blood routine examinations during the modeling phase. All mice were sacrificed upon completion of the modeling phase, and their liver specimens were harvested for pathological evaluations and metabolomics-assisted transcriptomics investigation.</p><p><strong>Results: </strong>In contrast to the control group, the experimental group mice exhibited notably smaller weight gain (P < 0.01) and markedly elevated serum ALT and AST levels (P < 0.001). At the end of the modeling period, visible white nodules appeared in the liver; hematoxylin and eosin (H&E) staining, immunohistochemistry, and electron microscopy revealed pathological features of HCC in the experimental group. Transcriptome analysis ascertained 2757 differentially expressed genes (DEGs) between HCC tissues and control liver tissues, with 2273 elevated and 484 diminished genes. KEGG pathway evaluation indicated substantial clustering of DEGs in cell cycle signaling pathways. Metabolome analysis showed the enrichment of differential metabolites in pathways related to ascorbate and alternate metabolism, choline metabolism in cancer, and glycerophospholipid metabolism. Notably, we observed significant differences in HCC progression between male and female mice after modeling, with female mice showing a higher incidence of HCC, greater liver-to-body weight ratios, and larger tumors than males. Transcriptome analysis and subsequent qRT-PCR demonstrated a significant downregulation of several glutathione transferase family genes (Gata1, Gata2, Gstp1, Mgst1) in the liver tissues of female mice versus males in the experimental group. Liver metabolome analysis revealed that female mice in the experimental group had 57 metabolites that differed from those of male mice, with 24 metabolites being upregulated and 33 do","PeriodicalId":9385,"journal":{"name":"Cancer Cell International","volume":"25 1","pages":"312"},"PeriodicalIF":6.0,"publicationDate":"2025-08-22","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12372400/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144944249","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Elucidating the dynamic tumor microenvironment through deep transcriptomic analysis and therapeutic implication of MRE11 expression patterns in hepatocellular carcinoma.","authors":"Ruiqiu Chen, Chaohui Xiao, Zizheng Wang, Guineng Zeng, Shaoming Song, Gong Zhang, Lin Zhu, Penghui Yang, Rong Liu","doi":"10.1186/s12935-025-03931-7","DOIUrl":"10.1186/s12935-025-03931-7","url":null,"abstract":"<p><strong>Aim: </strong>This study aims to explore the dynamic tumor microenvironment of hepatocellular carcinoma (HCC) through deep transcriptomic analysis and to identify key regulatory genes, among which MRE11 was further validated for its immunomodulatory and prognostic significance.</p><p><strong>Methods: </strong>We performed Summary-data-based Mendelian Randomization (SMR) analysis to identify genes causally associated with HCC and intersected these with DNA damage repair (DDR) genes, leading to the identification of MRE11. A comprehensive evaluation of MRE11 expression in HCC was conducted using transcriptomic data analysis. We collected data from 92 HCC patient samples and validated MRE11 expression differences in HCC tissues through qPCR, immunohistochemistry, and Western blotting. Publicly available single-cell RNA sequencing (scRNA-seq) data and spatial transcriptomics were utilized to explore MRE11's dynamic mechanisms in the tumor microenvironment (TME) of both primary and post-immunotherapy cases. We also screened for differentially expressed genes and constructed a robust HCC prognosis model using 101 machine-learning algorithms.</p><p><strong>Results: </strong>Our results demonstrated that high MRE11 expression is strongly associated with poor prognosis in HCC. In the primary TME, MRE11 regulates immune responses, facilitating immune evasion. Single-cell analysis revealed significant tumor heterogeneity in MRE11 high-expression groups, particularly in macrophages and malignant cells, where MRE11 regulates immune evasion and tumor progression via the cGAS-STING pathway and HGF-MET axis. Under immunotherapy, high MRE11 expression facilitated epithelial-mesenchymal transition (EMT) and extensive remodeling of the TME. Furthermore, MRE11 dynamically enhanced macrophage regulation, exhibiting immunosuppressive and tumor-invasive features. Finally, our prognostic model exhibited strong predictive accuracy across multiple datasets.</p><p><strong>Conclusion: </strong>High MRE11 expression is crucial in regulating the immune microenvironment in HCC, fostering immune evasion and driving tumor progression. MRE11 emerges as a promising biomarker for HCC diagnosis and a potential target for personalized immunotherapy.</p>","PeriodicalId":9385,"journal":{"name":"Cancer Cell International","volume":"25 1","pages":"311"},"PeriodicalIF":6.0,"publicationDate":"2025-08-21","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12369108/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144944098","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"The endoplasmic reticulum stress-ferroptosis reciprocal signaling orchestrates anti-tumor effect of anlotinib in anaplastic thyroid cancer.","authors":"Yehao Guo, Juyong Liang, Lingling Ding, Jiajun Wu, Weidong Teng, Jiafeng Wang, Liehao Jiang, Zhuo Tan","doi":"10.1186/s12935-025-03947-z","DOIUrl":"10.1186/s12935-025-03947-z","url":null,"abstract":"<p><strong>Background: </strong>Ferroptosis-induced therapy is a promising approach for treating anaplastic thyroid carcinoma (ATC), a highly lethal form of cancer. However, the specific effects of two anti-angiogenic agents, lenvatinib and anlotinib, on ferroptosis in ATC are not well understood.</p><p><strong>Methods: </strong>Methods: To investigate the anticancer activity of lenvatinib and anlotinib in vivo, a subcutaneous tumor model was established in mice. The pharmacological effects of these agents on ATC cells were assessed using various assays, including CCK-8, colony formation, transwell, and sphere-forming assays. Angiogenesis was evaluated using a tubule formation assay. Reactive oxygen species (ROS) levels were measured by flow cytometry, and levels of ferroptosis and endoplasmic reticulum (ER) stress were determined through western blot assays. Immunohistochemistry analyses were used to profile the expression of GPX4, HO-1, PERK, and CHOP in tumor tissues.</p><p><strong>Results: </strong>Both lenvatinib and anlotinib demonstrated dose- and time-dependent inhibition of Luciferase-8505 C-induced subcutaneous tumors in mice, with anlotinib showing greater efficacy than lenvatinib. In vitro experiments revealed that while both drugs were effective at inhibiting angiogenesis, anlotinib displayed superior antitumor effects in terms of cell viability, proliferation, tumor sphere formation, migration, and invasion. Mechanistic studies indicated that anlotinib induced ROS-mediated ferroptosis through the ER stress pathway, a response not observed with lenvatinib treatment.</p><p><strong>Conclusion: </strong>Anlotinib showed superior efficacy in treating ATC compared to lenvatinib, independent of their anti-angiogenic properties. The ability of anlotinib to induce ER stress-mediated ferroptosis suggests that targeting ferroptosis may hold promise as a therapeutic strategy for ATC.</p>","PeriodicalId":9385,"journal":{"name":"Cancer Cell International","volume":"25 1","pages":"310"},"PeriodicalIF":6.0,"publicationDate":"2025-08-21","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12369195/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144944093","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"The components and regulation of the Hippo pathway and its relationships with the progression and treatment of Non-small cell lung cancer (NSCLC).","authors":"Yuheng Feng, Xueting Gan, Xuezhu Rong, Qiang Han","doi":"10.1186/s12935-025-03946-0","DOIUrl":"10.1186/s12935-025-03946-0","url":null,"abstract":"","PeriodicalId":9385,"journal":{"name":"Cancer Cell International","volume":"25 1","pages":"309"},"PeriodicalIF":6.0,"publicationDate":"2025-08-20","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12366177/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144882244","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"CAFs exosomal miR-21-5p suppresses ferroptosis and promotes proliferation and migration in osteosarcoma.","authors":"Xiaoying Niu, Wen Tian, Yuanmeng Ke, Yifan Li, Xinxin Zhang","doi":"10.1186/s12935-025-03930-8","DOIUrl":"10.1186/s12935-025-03930-8","url":null,"abstract":"<p><strong>Background: </strong>Osteosarcoma is one of the malignant tumors in children and adolescents patients. Uncontrolled and unlimited proliferation and metastasis lead to poor overall survival. CAFs play a pivotal role in the osteosarcoma tumor microenvironment, exerting significant influence on prognosis and treatment outcomes. However, there remains a need for further exploration into the intricate molecular mechanisms underlying CAFs.</p><p><strong>Methods: </strong>Single-cell RNA sequencing was employed to characterize the microenvironment of osteosarcoma. Tissue exosomal miRNA sequencing was conducted on tumor tissues and adjacent normal tissues to screen for abnormal expression of exosomal miRNAs. WGCNA analysis was used to identify target exosomal miRNAs. The relative expression of miR-21-5p was analyzed using qRT-PCR. The proliferation rate and migration ability of tumor cells were assessed using the CCK8 and Transwell method, respectively. Exosomes derived from cells were extracted and characterized via transmission electron microscopy and NTA analysis. siRNA interference was utilized to disrupt the expression of miR-21-5p in CAFs. Experiments in vivo validated the role of exosomal miR-21-5p in promoting malignant characteristics in osteosarcoma.</p><p><strong>Results: </strong>Single-cell RNA sequencing analysis of GSE162454 revealed the crucial role of CAFs in the pathogenesis of osteosarcoma. Tissue exosomal miRNA sequencing unveiled significant differential expression of miR-21-5p. Subsequently, aberrant upregulation of exosomal miR-21-5p exhibited a strong correlation with advanced clinical stage and poor prognosis in osteosarcoma. Further experiments in vitro indicated that elevated levels of miR-21-5p significantly enhanced proliferation and migration of osteosarcoma cells by suppressing ferroptosis. Moreover, experiments in vivo validated the capacity of CAFs-derived exosomal miR-21-5p to promote tumor growth and weight, thereby demonstrating their ability to deliver miR-21-5p to osteosarcoma cells and induce proliferation and migration through inhibition of ferroptosis.</p><p><strong>Conclusions: </strong>Our findings indicate that exosomal miR-21-5p could potentially serve as a therapeutic target in osteosarcoma, providing initial evidence for further clinical investigation.</p>","PeriodicalId":9385,"journal":{"name":"Cancer Cell International","volume":"25 1","pages":"308"},"PeriodicalIF":6.0,"publicationDate":"2025-08-19","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12362868/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144871606","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"FPR3 orchestrates macrophage polarization in breast cancer: multi-omics dissection of prognostic relevance and therapeutic targeting.","authors":"Ying Chen, Xin Tang, Liran Zhu, Yi Wang, Gaopeng Li, Wulin Yang","doi":"10.1186/s12935-025-03942-4","DOIUrl":"10.1186/s12935-025-03942-4","url":null,"abstract":"<p><strong>Background: </strong>The N-formyl peptide receptor family (FPRs) is implicated in the progression of diverse cancer types, yet studies specifically exploring their roles in breast cancer remain scarce.</p><p><strong>Methods: </strong>A comprehensive analysis integrating bulk RNA-seq transcriptomics, methylomics, single-cell transcriptomics, and spatial single-cell transcriptomics data was conducted to elucidate the distinctive characteristics of FPRs in breast cancer. This study particularly focused on delineating the e xpression profiles of FPR3 across distinct breast cancer subtypes, while systematically investigating its prognostic implications and association with macrophage polarization patterns in breast cancer patients. Furthermore, molecular docking analysis was performed to screen potential therapeutic compounds targeting FPR3, providing insights into its druggability.</p><p><strong>Results: </strong>Notably, FPR3 was found to be highly expressed in macrophages within breast cancer tissues, with a notably elevated level in HER2-positive and triple-negative breast cancer (TNBC) subtypes, both of which are associated with poor prognosis. FPR3 expression inversely correlates with promoter methylation levels. Further analysis of pan-cancer immune infiltration patterns uncovered a striking association between FPR3 and macrophage infiltration, as well as their polarization status. Knockdown of FPR3 expression in macrophages markedly enhanced the expression of IL6, TNF-α, and TGF-β, while significantly reducing IL10 levels, indicative of a shift towards an M1-like macrophage phenotype. Through computational molecular docking analyses, Otamixaban and Rivaroxaban emerged as promising candidate inhibitors of FPR3.</p><p><strong>Conclusions: </strong>These findings underscore the profound infiltration of FPR3 + macrophages in breast cancer patients with adverse prognoses, highlighting FPR3 as a potential therapeutic target for intervening breast cancer aggressiveness.</p>","PeriodicalId":9385,"journal":{"name":"Cancer Cell International","volume":"25 1","pages":"306"},"PeriodicalIF":6.0,"publicationDate":"2025-08-18","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12359989/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144871607","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Oxypalmatine promotes apoptosis and protective autophagy in lung cancer cells via the PI3K/AKT pathway.","authors":"Ge Qiao, Zhanghao Huang, Youlang Zhou, Jiahai Shi","doi":"10.1186/s12935-025-03939-z","DOIUrl":"10.1186/s12935-025-03939-z","url":null,"abstract":"","PeriodicalId":9385,"journal":{"name":"Cancer Cell International","volume":"25 1","pages":"307"},"PeriodicalIF":6.0,"publicationDate":"2025-08-18","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12360002/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144871608","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Precise stratification of prognosis in pancreatic ductal adenocarcinoma patients based on pre- and postoperative genomic information.","authors":"Kokichi Miyamoto, Ryuichi Yoshida, Kazuya Yasui, Kunitoshi Shigeyasu, Kazuhiro Yoshida, Tomokazu Fuji, Kosei Takagi, Yuzo Umeda, Kazuyuki Matsumoto, Yuki Fujii, Toshiaki Takahashi, Kazuya Moriwake, Masashi Kayano, Takeyoshi Nishiyama, Yasuo Nagai, Hideki Yamamoto, Hironari Kato, Hiroshi Tazawa, Mizuki Morita, Motoyuki Otsuka, Toshiyoshi Fujiwara","doi":"10.1186/s12935-025-03894-9","DOIUrl":"10.1186/s12935-025-03894-9","url":null,"abstract":"<p><strong>Background: </strong>Pancreatic ductal adenocarcinoma (PDAC) has the highest mortality rate among all cancers; hence, multidisciplinary treatment is essential for patients with PDAC. Although the resectability status, tumour marker, KRAS circulating tumour DNA (mutKRAS-ctDNA) mutations, and GATA binding 6 (GATA6) expression status are promising prognostic biomarkers, their effective integration before and after surgery remains unclear.</p><p><strong>Methods: </strong>In this retrospective cohort study, patients with PDAC who had undergone radical resection were enrolled, and pre- and postoperative independent factors associated with poor prognosis were identified using Cox hazard modelling. Risk stratification systems were developed using the identified prognostic factors and investigated for the ability to predict prognosis.</p><p><strong>Results: </strong>A total of 91 patients with PDAC were included (median follow-up duration, 28 months). Borderline resectable or locally advanced cancer at diagnosis, elevated carbohydrate antigen 19-9 (CA19-9) level, and mutKRAS-ctDNA-positive status were identified as independent preoperative factors associated with poor prognosis. The postoperative factors significantly associated with shorter overall survival were low GATA6 expression, elevated CA19-9 level, and mutKRAS-ctDNA-positive status. Finally, the preoperative and postoperative risk scoring systems developed using Cox modelling hazard ratio values could significantly stratify prognosis after curative resection for PDAC.</p><p><strong>Conclusion: </strong>A risk stratification system based on liquid biopsy, specialised for each phase (pre- and post-surgery), has been proven to be a useful, simple, and practical prognostic prediction clinical tool to determine the optimal multidisciplinary treatment protocol for PDAC.</p>","PeriodicalId":9385,"journal":{"name":"Cancer Cell International","volume":"25 1","pages":"305"},"PeriodicalIF":6.0,"publicationDate":"2025-08-18","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12359879/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144871609","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Research progress on the mechanisms of CSF3R mutations in leukemogenesis and treatment strategies.","authors":"Ningxuan Wang, Xiangan Li, Chenyang She, Jun Zhang","doi":"10.1186/s12935-025-03941-5","DOIUrl":"10.1186/s12935-025-03941-5","url":null,"abstract":"<p><p>Leukemia is a malignant clonal disease originating from hematopoietic stem cells. Its pathogenesis is associated with multiple factors, including biological, physical, chemical, genetic, and other hematological diseases. Previous studies have shown that a high mutation rate (>80%) of colony-stimulating factor receptor 3 (CSF3R) is observed in chronic neutrophilic leukemia (CNL) patients, and these mutations activate downstream signaling pathways, leading to the proliferation of neutrophils. In-depth research on the CSF3R genes and their related mechanisms will help further reveal the mechanisms of leukemia development and provide potential targets for treatment. Therefore, this paper mainly focuses on the roles of colony-stimulating factor 3 (CSF3R) in hematopoiesis and the occurrence of leukemia, with particular attention to the roles of CSF3R in the JAK-STAT, PI3K-AKT, and MAPK-ERK signaling pathways.</p>","PeriodicalId":9385,"journal":{"name":"Cancer Cell International","volume":"25 1","pages":"304"},"PeriodicalIF":6.0,"publicationDate":"2025-08-14","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12351999/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144854653","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}