Cancer Biology & Medicine最新文献

{"title":"Chinese expert consensus on additional surgery following endoscopic resection for early colorectal cancer (2025 edition).","authors":"Zhipeng Qi, Fuqiang Zhao, Xuhua Hu, Yunshi Zhong, Qian Liu, Zhongtao Zhang, Guiying Wang","doi":"10.20892/j.issn.2095-3941.2025.0784","DOIUrl":"10.20892/j.issn.2095-3941.2025.0784","url":null,"abstract":"<p><p>Early colorectal cancer is often treated through endoscopic procedures to remove tumors. However, when initial removal is incomplete or shows high-risk features, further major surgery is required to ensure no cancer remains. This consensus provides a standard for surgeons to decide when and how to perform this additional surgery. A multidisciplinary group of Chinese medical experts reviewed global research and clinical evidence published between 2010 and 2024. The medical experts formulated key clinical recommendations, which were then discussed and finalized through expert voting to ensure high agreement. The consensus identifies specific high-risk factors necessitating additional surgery. The consensus recommends that these follow-up surgeries should ideally take place approximately 4 weeks after the first procedure. Furthermore, the consensus provides detailed protocols for marking the tumor location and selecting the best surgical approach. These consensuses offer a practical framework to improve the safety and effectiveness of treating early colorectal cancer. By standardizing surgical decisions, the consensus aims to help patients achieve better long-term recovery and quality of life.</p>","PeriodicalId":9611,"journal":{"name":"Cancer Biology & Medicine","volume":" ","pages":""},"PeriodicalIF":12.4,"publicationDate":"2026-03-18","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC13326600/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"147472774","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":"Sequential nimotuzumab plus gemcitabine and nab-paclitaxel chemotherapy followed by irreversible electroporation in advanced pancreatic ductal adenocarcinoma: a retrospective real-world analysis.","authors":"Yang Liu, Dandan Wu, Xing Li, Xihao Zhang, Rentao Li, Yanmei Ou, Hao Wang, Tongguo Si, Rui Xia, Yong Xu, Huikai Li, Chuntao Gao, Jihui Hao","doi":"10.20892/j.issn.2095-3941.2025.0848","DOIUrl":"10.20892/j.issn.2095-3941.2025.0848","url":null,"abstract":"","PeriodicalId":9611,"journal":{"name":"Cancer Biology & Medicine","volume":" ","pages":""},"PeriodicalIF":12.4,"publicationDate":"2026-03-16","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC13326601/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"147466976","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":"Mitochondrial uncoupling inhibits serine catabolism <i>via</i> FTO activation in metastatic breast cancer.","authors":"Xin Jin, Albert M Li, Man Zhao, Haowen Jiang, Yiren Xiao, Michaela Yip, Stavros Melemenidis, Scott Jackson, Yanan Yang, Cathyrin Simmermaker, Meng-Ning Zhou, Subarna Sinha, Daniel J Cuthbertson, Erinn B Rankin, Jiangbin Ye","doi":"10.20892/j.issn.2095-3941.2025.0444","DOIUrl":"10.20892/j.issn.2095-3941.2025.0444","url":null,"abstract":"<p><strong>Objective: </strong>The mitochondrial serine catabolic pathway (MSCP) supports tumor proliferation and metastasis, yet no therapies target the MSCP. Because cancer cells rely on the MSCP when respiration is suppressed, we hypothesized that reactivating respiration would inhibit the MSCP.</p><p><strong>Methods: </strong>Mitochondrial respiration was activated in triple negative breast cancer (TNBC) cells using uncouplers [niclosamide ethanolamine (NEN) and BAM15]. Metabolic activity through the MSCP was assessed using U-¹³C-serine tracing and expression of key MSCP enzymes (SHMT2, MTHFD2, and MTHFD1L) were evaluated at the mRNA and protein levels. The NAD⁺:NADH ratio and 2-hydroxyglutarate (2-HG) levels were determined using liquid chromatography-mass spectrometry. The role of m⁶A RNA demethylase fat mass and obesity-associated protein (FTO) in regulating MSCP enzymes was examined using pharmacologic and genetic approaches. The therapeutic potential of mitochondrial uncoupling was tested <i>in vivo</i> using a lung metastasis model.</p><p><strong>Results: </strong>Activation of mitochondrial respiration with NEN or BAM15 inhibited MSCP activity, as indicated by reduced labeling of glycine and purines from U-¹³C-serine. Mitochondrial uncoupling markedly decreased the levels of SHMT2, MTHFD2, and MTHFD1L protein, despite unchanged or elevated mRNA levels. This post-transcriptional suppression was mediated by an increased NAD⁺:NADH ratio, leading to reduced 2-HG production and subsequent activation of FTO. Inhibition of FTO, either pharmacologically or genetically, restored MSCP enzyme protein levels. Dietary mitochondrial uncoupling significantly suppressed lung metastasis <i>in vivo</i>.</p><p><strong>Conclusions: </strong>The findings herein demonstrated that mitochondrial uncouplers inhibit MSCP through FTO-dependent m⁶A demethylation. This work identified mitochondrial uncoupling as a novel and promising therapeutic approach for promoting m⁶A demethylation and targeting MSCP in metastatic breast cancer.</p>","PeriodicalId":9611,"journal":{"name":"Cancer Biology & Medicine","volume":" ","pages":""},"PeriodicalIF":12.4,"publicationDate":"2026-03-12","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC13617950/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"147442853","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":"Click chemistry-driven tumor theranostics: recent advances, challenges, and future perspectives.","authors":"Dayong Hou, Xiangpeng Li, Niyuan Zhang, Xingyan Fu, Hao Wang","doi":"10.20892/j.issn.2095-3941.2025.0667","DOIUrl":"10.20892/j.issn.2095-3941.2025.0667","url":null,"abstract":"<p><p>Tumor theranostics, which integrates accurate diagnosis and precise therapy, has emerged as a pivotal approach in modern oncology for improving treatment efficacy and reducing off-target toxicity. Click chemistry, which is characterized by high efficiency, selectivity, biocompatibility, and modularity, has become an indispensable tool for constructing versatile theranostic systems. This review systematically summarizes the recent progress in click chemistry-based tumor theranostic systems, starting with an overview of core click reactions and the unique features in biomedical applications. We then focus on the application of click chemistry within a diagnosis-therapy-theranostics framework to three key aspects of tumor theranostics: (i) tumor diagnosis (molecular imaging probes and circulating tumor cell detection); (ii) tumor therapy (chemotherapy, phototherapy, immunotherapy, and gene therapy); and (iii) integrated theranostics (multimodal imaging-guided combinatorial therapy). Furthermore, the current challenges, such as the biocompatibility of catalysts and <i>in vivo</i> reaction efficiency, are critically discussed. Finally, we highlight promising directions, including stimuli-responsive click reactions, AI-assisted probe design, and personalized theranostic systems. This review not only serves as a comprehensive reference for researchers but also highlights how click chemistry uniquely bridges molecular design with clinical functionality, distinguishing click chemistry from conventional conjugation or labeling methods by enabling spatiotemporal control, modular integration, and bioorthogonal precision in complex biological settings.</p>","PeriodicalId":9611,"journal":{"name":"Cancer Biology & Medicine","volume":" ","pages":""},"PeriodicalIF":12.4,"publicationDate":"2026-03-12","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC13115431/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"147442772","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":"Targeting tumor-infiltrating regulatory T cells based on immunometabolism.","authors":"Na Li, Dexue Tian","doi":"10.20892/j.issn.2095-3941.2025.0645","DOIUrl":"10.20892/j.issn.2095-3941.2025.0645","url":null,"abstract":"<p><p>The immune checkpoint blockade (ICB) approach in cancer therapy involves the disruption of immune checkpoint inhibitory signals on tumor-specific CD8+ T cells, thereby reinstating the immune activity of CD8+ T cells and yielding therapeutic efficacy. However, due to the co-expression of immune checkpoint molecules, such as CTLA-4 and PD-1 on tumor-infiltrating Tregs (TI-Tregs) and conventional T cells (Tconvs), immune checkpoint inhibitors (ICIs) inadvertently amplify the immunosuppressive activity of Tregs while targeting CD8+ T cells, which contributes to the failure of immune therapy. Conventional strategies targeting Tregs, including ICI/conventional kinase and chemokine/chemokine receptor blockade, generally induce systemic Treg depletion, which triggers autoimmune diseases. Thus, achieving high selectivity and specificity in targeting TI-Tregs is of paramount importance in mitigating adverse immunologic reactions. Targeting metabolism-based TI-Tregs has been shown to enhance target precision, providing potential for the development of adjunctive immunotherapeutic strategies. This article explores the reciprocal interaction between TI-Tregs and the tumor microenvironment (TME), elucidating metabolic reprogramming, while envisioning plausible high-selectivity targets for TI-Tregs without compromising systemic immune homeostasis and immune reactivity of effector T cells.</p>","PeriodicalId":9611,"journal":{"name":"Cancer Biology & Medicine","volume":"23 2","pages":""},"PeriodicalIF":12.4,"publicationDate":"2026-03-10","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12980038/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"147431125","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":"BEX2 influences the MCL1-Hedgehog signaling axis to regulate the potential of stemness characterization in colorectal cancer.","authors":"Yucheng Qian, Jingsun Wei, Yuan Bian, Yinuo Tan, Yimin Fang, Liubo Chen, Kai Jiang, Dongliang Fu, Xiaoxu Ge, Tianyi Ling, Qian Xiao, Kefeng Ding, Yeting Hu","doi":"10.20892/j.issn.2095-3941.2025.0120","DOIUrl":"10.20892/j.issn.2095-3941.2025.0120","url":null,"abstract":"<p><strong>Objective: </strong>Colorectal cancer (CRC) progression is driven by cancer stem cells (CSCs) that evade treatment through dynamic phenotype modulation. Our previous research identified BEX2 as a significant regulator of CRC malignancy involving the Hedgehog (Hh) pathway. This study aimed to elucidate the influence of BEX2 on CRC stemness and the interaction with the Hh signaling pathway, potentially uncovering innovative therapeutic strategies for combating CRC.</p><p><strong>Methods: </strong>TCGA and GEO data were analyzed to correlate BEX2 expression with clinical outcomes and stemness markers in CRC. Functional assays, including spheroid formation, flow cytometry, extreme limiting dilution assay (ELDA), Transwell, wound healing, and cell viability assay, were performed in DLD1 and HCT116 cell lines. Immunoblotting and qRT-PCR assessed BEX2 expression with <i>in vivo</i> validation in NOD/SCID mice.</p><p><strong>Results: </strong>The findings revealed a negative correlation between BEX2 expression and the levels of stemness-associated genes with a significant association with CRC patient' prognosis. Overexpression of <i>BEX2</i> diminished CRC stemness potential, whereas BEX2 knockdown led to a pronounced enhancement of these stem-like characteristics. Further investigation revealed that BEX2 inhibited the Hh pathway. BEX2 interacted with MCL1, promoting ubiquitination and degradation, thereby decreasing MCL1 stability. Low <i>BEX2</i> expression stabilized MCL1, which enhanced stemness potential. These results suggested BEX2 modulates CRC stemness <i>via</i> MCL1 downregulation.</p><p><strong>Conclusions: </strong>Taken together, the current study findings highlight BEX2 and MCL1 as potential therapeutic targets in CRC with BEX2 emerging as a key regulator of stemness, chemoresistance, and invasiveness. These findings advance our understanding of CRC and pave the way for more effective therapies.</p>","PeriodicalId":9611,"journal":{"name":"Cancer Biology & Medicine","volume":"23 2","pages":""},"PeriodicalIF":12.4,"publicationDate":"2026-03-10","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12980035/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"147431091","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":"From concept to clinic: emerging paradigms and novel insights into liquid biopsy.","authors":"Wenjie Guo, Yang Liu, Haiying Dong, Xiang Li, Xu Guo, Haitao Guo, Kaixiang Zhou, Jinliang Xing","doi":"10.20892/j.issn.2095-3941.2025.0830","DOIUrl":"10.20892/j.issn.2095-3941.2025.0830","url":null,"abstract":"","PeriodicalId":9611,"journal":{"name":"Cancer Biology & Medicine","volume":"23 2","pages":""},"PeriodicalIF":12.4,"publicationDate":"2026-03-10","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12980030/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"147431070","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":"Cancer-immunity cycle-based molecular subtypes in breast cancer predict the response to immune checkpoint inhibitors.","authors":"Di Shao, Tianjian Yu, Yi Xiao, Zhiming Shao","doi":"10.20892/j.issn.2095-3941.2025.0611","DOIUrl":"10.20892/j.issn.2095-3941.2025.0611","url":null,"abstract":"<p><strong>Objective: </strong>The cancer-immunity cycle (CIC) outlines key steps of anti-tumor immunity from antigen release to T cell effector function. A comprehensive evaluation of the CIC in patients with breast cancer is lacking, which limits the accurate assessment of immune status and selection of patients suitable for immune checkpoint inhibitor (ICI) therapy.</p><p><strong>Methods: </strong>A signature that describes the six steps of the CIC in the primary tumor was constructed. This signature was used to calculate a CIC score in our previously published breast cancer cohort (<i>n</i> = 752) and classify patients into 3 distinct CIC clusters. The predictive value of the ICI response was validated in pan-cancer ICI-treated cohorts. Clusters with distinct characteristics were further identified through multi-omic analyses, including genomics, metabolomics, and single-cell RNA sequencing.</p><p><strong>Results: </strong>Breast cancer patients were classified into three CIC clusters: cluster 1 [C1] (immune-cold); cluster 2 [C2] (antigen presentation-deficient); and cluster 3 [C3] (immune-hot). C3 showed abundant immune infiltration that correlated with a better ICI response. In addition to reduced immune infiltration, C1 patients exhibited macrophage phenotypic conversion. The tumor microenvironment of C2 was marked by elevated regulatory T cells and dysfunctional dendritic cells. Genomic analysis of C2 showed a high tumor mutational burden with frequent HLA loss of heterozygosity. C1 was enriched in lipid metabolism pathways and C3 in glycolysis features. <i>PSAT1</i>, a serine-related gene, was identified as a key metabolic regulator in C2, suggesting a role in influencing immunoregulatory molecules.</p><p><strong>Conclusions: </strong>This study provided a novel framework for classifying tumors based on the CIC characteristics, revealing distinct biological and clinical profiles and suggesting broad clinical significance.</p>","PeriodicalId":9611,"journal":{"name":"Cancer Biology & Medicine","volume":" ","pages":""},"PeriodicalIF":12.4,"publicationDate":"2026-03-05","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC13326604/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"147364032","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":"Expansion of IL-2-independent tumor-infiltrating lymphocytes through a feeder-free process: a preclinical study for solid tumors.","authors":"Ying Zhang, Sicheng Du, Rongrui Liu, Chuanhua Zhao, Juan Li, Sisi Ye, Man Zhang, Xingming Ma, Zhou He, Wenjia Zhuang, Huajun Jin, Jianming Xu","doi":"10.20892/j.issn.2095-3941.2025.0441","DOIUrl":"10.20892/j.issn.2095-3941.2025.0441","url":null,"abstract":"<p><strong>Objective: </strong>Conventional tumor-infiltrating lymphocyte (TIL) therapy for solid tumors relies on high-dose interleukin-2 (IL-2) during expansion and post-infusion, and promotes T-cell exhaustion and toxicity. Herein, we developed a feeder-free, low-dose IL-2 TIL expansion protocol and evaluated whether hydroxychloroquine (HCQ) or programmed cell death protein 1 (PD-1) blockade might enhance therapeutic efficacy and decrease IL-2 dependence.</p><p><strong>Methods: </strong>TILs from multiple solid tumors were expanded <i>ex vivo</i> with decreased-dose IL-2, IL-7, and IL-15 plus CD3/CD28 co-stimulation, without feeder cells. TIL products were assessed via quality control, T-cell phenotypes, and exhaustion markers. Cytotoxic activity was measured <i>in vitro</i> through interferon-gamma (IFN-<b>γ</b>) release and real-time cell analysis (RTCA). HCQ-induced changes in major histocompatibility complex class I (MHC-I) and programmed death-ligand 1 (PD-L1) expression were assessed in tumor cell lines, and RTCA-based cytotoxicity was evaluated using T-cell receptor-engineered T cells (TCR-T cells). The <i>in vivo</i> efficacy of HCQ and PD-1 blockade separately combined with TIL therapy was examined in a colorectal cancer patient-derived xenograft (PDX) model.</p><p><strong>Results: </strong>The protocol consistently produced viable TILs of favorable quality across tumor types, with variable CD8⁺ and memory T-cell profiles. Expanded TILs showed effector-to-target (E:T) ratio-dependent tumor cell killing in RTCA and secreted IFN-<b>γ</b> across multiple tumor types. HCQ significantly upregulated MHC-I expression <i>in vitro</i> (<i>P</i> < 0.05) without affecting PD-L1 expression or impairing TIL proliferation, and enhanced early TCR-T-mediated killing. In the PDX model, TIL plus HCQ, compared with TIL, showed less tumor growth and greater MHC-I expression, although these differences were not significant, given the small sample size. TIL plus low-dose PD-1 blockade significantly reduced tumor volume versus the control group (<i>P</i> = 0.002) and maintained higher body weights than the TIL-only and control groups.</p><p><strong>Conclusions: </strong>The feasibility of a feeder-free, low-dose IL-2 TIL expansion system was demonstrated. PD-1 blockade significantly enhanced antitumor activity and treatment tolerability, thus supporting its promise as an alternative to high-dose IL-2. HCQ demonstrated potential immunomodulatory effects, although its <i>in vivo</i> benefit was minimal. This strategy warrants further clinical evaluation in solid tumors.</p>","PeriodicalId":9611,"journal":{"name":"Cancer Biology & Medicine","volume":" ","pages":""},"PeriodicalIF":12.4,"publicationDate":"2026-03-05","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC13326599/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"147363993","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":"First-line immunotherapy for advanced HER2-negative gastric cancer: differences between Asian and non-Asian patients.","authors":"Chuanhua Zhao, Sisi Ye, Meng Chen, Jing Qian, Jianming Xu","doi":"10.20892/j.issn.2095-3941.2025.0398","DOIUrl":"10.20892/j.issn.2095-3941.2025.0398","url":null,"abstract":"<p><p>Emerging evidence suggests that the efficacy of immunotherapy in patients with advanced HER2-negative gastric cancer differs between Asian and non-Asian populations. This review examines potential factors contributing to these disparities, including differences in demographic and clinicopathologic characteristics, somatic mutations, molecular subtypes, tumor immunity, <i>Helicobacter pylori (H. pylori)</i> infection, dietary habits, and gut microbiome composition. These factors may serve as predictors of immunotherapy response in gastric cancer patients. For example, the prevalence of molecular subtypes and somatic mutations have been linked to variations in immunotherapy efficacy between Asian and non-Asian populations. In addition, differences in <i>H. pylori</i> infection rates, dietary habits, and gut microbiota composition may influence systemic immune responses, and consequently, immunotherapy outcomes. Understanding the factors contributing to these disparities in immunotherapy response is crucial for optimizing treatment strategies and improving outcomes for patients with gastric cancer. Further research into the mechanisms underlying racial and ethnic disparities in immunotherapy response is needed to identify potential biomarkers predictive of immunotherapy response in diverse patient populations.</p>","PeriodicalId":9611,"journal":{"name":"Cancer Biology & Medicine","volume":" ","pages":""},"PeriodicalIF":12.4,"publicationDate":"2026-02-27","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12980032/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"147324685","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}