Cancer Science最新文献

{"title":"Regulation of R-Loop Dynamics by Proteins and Long Noncoding RNAs: An Emerging Paradigm for Cancer Treatment","authors":"Miho M. Suzuki,&nbsp;Keiko Shinjo,&nbsp;Tatsunori Nishimura,&nbsp;Yutaka Kondo","doi":"10.1111/cas.70272","DOIUrl":"10.1111/cas.70272","url":null,"abstract":"<p>R-loops are three-stranded nucleic acid structures comprising an RNA/DNA hybrid and a displaced single-stranded DNA. While transient R-loop formation is essential for various physiological processes, their persistent accumulation leads to genomic instability. Cancer cells exhibit elevated R-loop levels due to hypertranscription, replication stress, and impaired DNA repair pathways. In this review, we provide a comprehensive overview of the molecular machinery that resolves R-loops, including chromatin remodelers, transcriptional regulators, nucleases, and helicases. We also highlight the emerging roles of long noncoding RNAs (lncRNAs) in modulating R-loop dynamics and explore how these RNA-based mechanisms cooperate with canonical resolution pathways. Finally, we explore the potential of targeting R-loop regulatory networks as a novel therapeutic strategy in cancer treatment.</p>","PeriodicalId":9580,"journal":{"name":"Cancer Science","volume":"117 2","pages":"297-307"},"PeriodicalIF":4.3,"publicationDate":"2025-11-24","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12861113/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145589562","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":"Correction to “Trametinib Overcomes KRAS-G12V–Induced Osimertinib Resistance in a Leptomeningeal Carcinomatosis Model of EGFR-Mutant Lung Cancer”","authors":"","doi":"10.1111/cas.70278","DOIUrl":"10.1111/cas.70278","url":null,"abstract":"<p>K. Fukuda, S. Otani, S. Takeuchi, et al., “Trametinib Overcomes <i>KRAS</i>-G12V–Induced Osimertinib Resistance in a Leptomeningeal Carcinomatosis Model of <i>EGFR</i>-Mutant Lung Cancer,” Cancer Science 112 (2021): 3784–3795. https://doi.org/10.1111/cas.15035.</p><p>In the above article, Figure 6B is incorrect. In Figure 6B, the image for “Control, Day 7” was inadvertently duplicated from “Osimertinib, Day 7” during figure assembly. The corrected panel is shown below. The color scale and radiance range are identical to the published figure (1 × 10⁶ – 2 × 10⁸ p/sec/cm²/sr). This error is limited to the representative image and does not affect the quantitative data in Figure 6A, the text, or the conclusions of the article. We apologize for the oversight.</p><p>We apologize for this error.</p>","PeriodicalId":9580,"journal":{"name":"Cancer Science","volume":"117 2","pages":"577-578"},"PeriodicalIF":4.3,"publicationDate":"2025-11-24","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12861087/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145597924","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":"Impacts of Mitochondrial Status After Neoadjuvant Chemotherapy in Esophageal Squamous Cell Carcinoma Patients","authors":"Kotaro Sugawara,&nbsp;Shingo Sakashita,&nbsp;Takashi Fukuda,&nbsp;Chiaki Murakami,&nbsp;Daiji Oka,&nbsp;Gulanbar Amori,&nbsp;Yoshifumi Baba,&nbsp;Hiroaki Kanda,&nbsp;Noriko Motoi","doi":"10.1111/cas.70276","DOIUrl":"10.1111/cas.70276","url":null,"abstract":"<p>The prognostic significance of mitochondrial status after neoadjuvant chemotherapy (NAC) and its association with the tumor microenvironment (TME) in esophageal squamous cell carcinoma (ESCC) remains unclear. We analyzed 202 ESCC patients who underwent NAC followed by surgical resection. Mitochondrial status was quantified using an objective, immunohistochemistry-based scoring system (Mito-score). The optimal cut-off value was determined by receiver operating characteristic curve analysis. Clinicopathological features, TME parameters (T-cell density and programmed death ligand-1 [PD-L1] expression), and survival outcomes were compared between high and low Mito-score groups. Multivariate Cox regression identified independent prognostic factors for overall survival (OS) and cancer-specific survival (CSS). The high and low Mito-score groups comprised 140 (69.3%) and 62 (30.7%) patients, respectively. NAC response rates and ypStages III–IV frequencies were similar in the two groups. PD-L1 expression was significantly higher in high Mito-score tumors (<i>p</i> = 0.04), while T-cell densities did not differ. High Mito-score was associated with significantly worse OS (3-year OS: 51.9% vs. 72.6%, <i>p</i> = 0.001) across both ypStages I–II (<i>p</i> = 0.047) and ypStages III–IV (<i>p</i> = 0.01) subgroups. In ypStages III–IV, high Mito-score was also linked to poorer CSS (<i>p</i> = 0.01). Multivariate analysis confirmed high Mito-score to be an independent predictor of unfavorable OS and CSS. Overall, high Mito-score after NAC identifies ESCC patients with significantly poorer survival, particularly among those with advanced pathological stages, thereby possibly serving as an independent prognostic biomarker.</p>","PeriodicalId":9580,"journal":{"name":"Cancer Science","volume":"117 2","pages":"491-500"},"PeriodicalIF":4.3,"publicationDate":"2025-11-24","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12861109/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145597938","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":"Functional Difference of MYC and MYCN in Combined Hepatocellular–Cholangiocarcinoma: Regulation of Differentiation by HNF1B","authors":"Masanori Goto,&nbsp;Masahiro Yamamoto,&nbsp;Hiroki Tanaka,&nbsp;Yumiko Fujii,&nbsp;Kumi Takasawa,&nbsp;Yuki Kamikokura,&nbsp;Masayo Kamikokura,&nbsp;Nobuyuki Kobayashi,&nbsp;Taro Murakami,&nbsp;Yuji Nishikawa,&nbsp;Akira Takasawa","doi":"10.1111/cas.70233","DOIUrl":"10.1111/cas.70233","url":null,"abstract":"<p>MYC and MYCN oncogenes are frequently upregulated in human liver cancers, yet their functional differences remain unclear. We used a mouse model of intrahepatic cholangiocarcinoma (CCA), constructed by transposon-mediated somatic gene integration of <i>AKT</i> and <i>YAP</i> into hepatocytes, to investigate the effects of additional integration of <i>Myc</i> or <i>Mycn</i>. Both <i>Myc</i> and <i>Mycn</i> induced a poorly differentiated hepatocellular carcinoma (HCC) component, resulting in the formation of combined hepatocellular-cholangiocarcinoma (cHCC-CCA). Interestingly, the ratio of HCC to CCA components differed significantly; <i>AKT/YAP/Mycn</i> (AYN) tumors exhibited a lower proportion of CCA components than <i>AKT/YAP/Myc</i> (AYM) tumors. To explore the underlying mechanisms, we analyzed the expression levels of genes involved in liver differentiation. We found that AYN tumors, at both the mRNA and protein levels, exhibited lower expression of HNF1B, a transcription factor that is highly expressed in human CCA but not in HCC. When <i>Hnf1b</i> was co-introduced with AYN, the percentage of the CCA area increased significantly. Furthermore, these tumors exhibited increased expression of TEAD proteins, which interact with YAP to initiate transcription. Notably, treatment with a YAP-TEAD inhibitor suppressed <i>AKT/YAP/Mycn/Hnf1b</i> tumor growth. These findings indicate that <i>Myc</i> and <i>Mycn</i> play distinct roles in the phenotypic determination of primary liver tumors and suggest that their differential effects on <i>Hnf1b</i> expression and subsequent TEAD activation may be a key regulatory mechanism.</p>","PeriodicalId":9580,"journal":{"name":"Cancer Science","volume":"117 2","pages":"536-547"},"PeriodicalIF":4.3,"publicationDate":"2025-11-24","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12861104/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145589533","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":"Stromal Defense Against Cancer: An Unprecedented Mechanism Limiting Cancer Invasion Into the Bone","authors":"Masayuki Tsukasaki,&nbsp;Hiroshi Takayanagi","doi":"10.1111/cas.70273","DOIUrl":"10.1111/cas.70273","url":null,"abstract":"<p>Decades of research into the immune regulation of cancer have revolutionized oncology, leading to the clinical success of immune checkpoint inhibitors. In contrast, the roles of nonimmune systems in tumor regulation remain largely undefined. Our recent study of cancer bone invasion has uncovered a previously unrecognized host defense mechanism: stromal cells in the periosteum, the membranous tissue enveloping the bone, actively respond to tumor proximity and facilitate periosteum thickening that physically impedes tumor invasion into the bone. We propose a new concept, “stromal defense against cancer (SDAC),” a unique mechanism of tumor regulation orchestrated by stromal cells. In this review, we summarize the molecular and cellular mechanisms underlying SDAC and discuss its clinical implications.</p>","PeriodicalId":9580,"journal":{"name":"Cancer Science","volume":"117 2","pages":"308-315"},"PeriodicalIF":4.3,"publicationDate":"2025-11-23","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12861099/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145589540","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":"Spatial Location of SPP1+TAMs and Mutually Exclusive Subsets Based on Single-Cell and Transcriptome Data","authors":"Xuan Luo,&nbsp;JianGuo Xu,&nbsp;ZhiYuan Wang,&nbsp;XiaoFang Wang,&nbsp;YangHao Wang,&nbsp;Yu Zhang,&nbsp;FangFang Li,&nbsp;Hui Fang,&nbsp;XiaoYun Huang,&nbsp;MuYe Li,&nbsp;XiaoJuan Liu,&nbsp;JiHong Tang,&nbsp;PeiYang Fan,&nbsp;GuoJing Zhao,&nbsp;YongWen He,&nbsp;Li Bian","doi":"10.1111/cas.70247","DOIUrl":"10.1111/cas.70247","url":null,"abstract":"<p>To clarify locations and mutually exclusive subsets of SPP1⁺tumor associated macrophages (SPP1⁺TAMs) in lung adenocarcinoma (LUAD). Analyze the polarization type, mutually exclusive cell subset, and spatial location of SPP1⁺TAMs based on the transcriptome data of the Cancer Genome Atlas (TCGA) and Genotype-Tissue Expression (GTEx) database, single-cell and spatial transcriptome data of the Gene Expression Omnibus database (GEO), immunohistochemical data of the Human Protein Atlas (HPA) database and local LUAD to provide a scientific basis for precision treatment of LUAD. Secreted phosphoprotein-1 (SPP1) was identified as the central regulatory gene of LUAD. The single-cell transcriptome data showed that SPP1 is up-regulated in invasive lung carcinoma (ILC), while macrophage receptor with collagenous structure (MARCO) is up-regulated in adenocarcinoma in situ (AIS). MARCO⁺M2 macrophages and SPP1⁺M2 macrophages clustered in different positions in the uniform manifold approximation and projection (UMAP) to form mutually exclusive cell subsets. SPP1⁺M2 plays a major role in ILC and MARCO⁺M2 plays a major role in AIS. The spatial transcriptome data showed that some SPP1⁺M2 were clustered at the edge of the tumor, and this particular spatial location may increase tumor invasiveness. Further spatial distance analysis showed that the distance was greater from the SPP1⁺M2 to alveolar type 2 epithelial cell (AT2) than from the MARCO⁺M2. Immunohistochemical analysis showed that SPP1 expression was up-regulated in the tumor or ILC group and notably higher in inflammatory cells. In summary, SPP1⁺M2 and MARCO⁺M2 form mutually exclusive cell subsets, and MARCO⁺M2 and SPP1⁺M2 synergistically promote different stages of tumor progression.</p>","PeriodicalId":9580,"journal":{"name":"Cancer Science","volume":"117 2","pages":"548-565"},"PeriodicalIF":4.3,"publicationDate":"2025-11-21","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12861114/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145574806","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":"Drug Repurposing Screen Identifies Pimozide as a ROS-Inducing Therapy With Anti-Tumor Efficacy in HNSCC PDX Models","authors":"Shogo Okazaki,&nbsp;Shintaro Nakamura,&nbsp;Tomoya Soma,&nbsp;Momoko Yoshikawa,&nbsp;Seiji Asoda,&nbsp;Yurika Nakajima,&nbsp;Kenji Tsuchihashi,&nbsp;Mitsuyo Ohmura,&nbsp;Ryo Goitsuka,&nbsp;Kenichi Imai,&nbsp;Hideyuki Saya,&nbsp;Osamu Nagano,&nbsp;Hiroyuki Ozawa","doi":"10.1111/cas.70253","DOIUrl":"10.1111/cas.70253","url":null,"abstract":"<p>Redox regulation is a key mechanism supporting tumor survival and an attractive therapeutic target. In this study, we screened 1161 FDA-approved compounds to identify agents that induce reactive oxygen species (ROS) accumulation in head and neck squamous cell carcinoma (HNSCC) cells. Pimozide, a dopamine D2 receptor antagonist, emerged as the most potent ROS inducer. It selectively suppresses the growth of HNSCC cells with high oxidative stress resistance while exhibiting only modest effects on less resistant cells and normal keratinocytes. Notably, pimozide exhibited anti-tumor effects as a monotherapy and in combination with paclitaxel at clinically relevant doses. Mechanistic analysis revealed that pimozide rapidly induced ROS accumulation via a mechanism distinct from its known action on dopamine D2 receptors and STAT3/5. To identify markers of ROS-induced responses, we examined ROS-responsive genes and found that early growth response 1 (EGR1) was selectively induced in sensitive cells and correlated with pimozide responsiveness. Functional analysis revealed that EGR1 knockdown suppressed pimozide-induced cytotoxicity, suggesting its role as a functional pharmacodynamic marker of pimozide sensitivity. In a patient-derived xenograft model of HNSCC, pimozide significantly reduced the tumor burden alone and in combination with paclitaxel. While tumor volume reduction in the combination group was not statistically greater than that in the monotherapy group, fluorescence immunohistochemistry revealed a marked decrease in undifferentiated tumor cells, indicating enhanced therapeutic effects of combination treatment. Taken together, these findings indicate that pimozide is a promising candidate for repurposing as a novel therapeutic agent against HNSCC.</p>","PeriodicalId":9580,"journal":{"name":"Cancer Science","volume":"117 2","pages":"511-521"},"PeriodicalIF":4.3,"publicationDate":"2025-11-20","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12861098/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145565910","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":"Prognostic Impact of DPP4 Inhibitors on Systemic Drug Therapy for Advanced Kidney Cancer Patients","authors":"Shuhei Kamada,&nbsp;Sachi Kitayama,&nbsp;Ryosuke Yamase,&nbsp;Kazuhiro Ikeda,&nbsp;Wataru Sato,&nbsp;Tomokazu Sazuka,&nbsp;Hideki Takeshita,&nbsp;Shinichi Sakamoto,&nbsp;Akihiro Yano,&nbsp;Kuniko Horie,&nbsp;Tomohiko Ichikawa,&nbsp;Satoru Kawakami,&nbsp;Satoshi Inoue","doi":"10.1111/cas.70250","DOIUrl":"10.1111/cas.70250","url":null,"abstract":"<p>Unmet challenges in systemic therapy persist for advanced renal cell carcinoma (RCC) despite the widespread use of anti-angiogenetic tyrosine kinase inhibitors (TKIs) and immune checkpoint inhibitors (ICIs). We previously showed that dipeptidyl peptidase 4 inhibitor (DPP4i) improved TKI sensitivity using patient-derived RCC cells and experimental TKI-resistant models. To address whether DPP4i is clinically useful for the enhancement of RCC systemic therapy, including ICIs, we analyzed 320 cases with RCC who underwent systemic therapy. Patients with DPP4i treatment exhibited longer overall survival (hazard ratio: 0.50, 95% confidence interval: 0.30–0.82, <i>p</i> = 0.0060). In the Cox proportional hazards model, the use of DPP4is, along with BMI ≥ 25, no metastasis, low serum lactate dehydrogenase (LDH), and low serum C-reactive protein (CRP), was a favorable prognostic factor. Additionally, more pronounced tumor shrinkage was observed in a within-subgroup comparison of patients receiving TKI or ICI as first-line therapies. Consistently, we found that DPP4 high RCC tumors exhibit reduced immune infiltration and lower scores for effector T cell infiltration-related signatures based on the RNA sequencing data from the CheckMate-009, 010, and 025 studies. These findings can potentially change the interpretation of the prognostic impact of type 2 diabetes mellitus on RCC and bolster the rationale for initiating a prospective clinical trial to evaluate concurrent use of DPP4i with RCC therapeutic strategies.</p>","PeriodicalId":9580,"journal":{"name":"Cancer Science","volume":"117 2","pages":"468-475"},"PeriodicalIF":4.3,"publicationDate":"2025-11-19","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12861088/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145551498","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":"Correction to “MZT2A Promotes NSCLC Viability and Invasion by Increasing Akt Phosphorylation via the MOZART2 Domain”","authors":"","doi":"10.1111/cas.70271","DOIUrl":"10.1111/cas.70271","url":null,"abstract":"<p>Wang H, Jiang X, Cheng Y, et al. MZT2A promotes NSCLC viability and invasion by increasing Akt phosphorylation via the MOZART2 domain. <i>Cancer Sci</i>. 2021;112:2210–2222. https://doi.org/10.1111/cas.14900</p><p>In the above article, Figure 3E is incorrect. The correct image is shown below:</p><p>We apologize for this error.</p>","PeriodicalId":9580,"journal":{"name":"Cancer Science","volume":"117 2","pages":""},"PeriodicalIF":4.3,"publicationDate":"2025-11-18","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12861090/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145551526","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":"Mutant p53 Regulates Pyruvate Dehydrogenase Kinase 1 (PDK1) to Promote Proliferation and Migration in Breast Cancer","authors":"Yan Ye,&nbsp;Zuli Ou,&nbsp;Canling Li,&nbsp;Qingyu Liao,&nbsp;Qian Zeng,&nbsp;Xiaoqian Ju,&nbsp;Dian Zhang,&nbsp;Yu Wei,&nbsp;Xiang Zhang,&nbsp;Tao Zhang,&nbsp;Kejia Wu","doi":"10.1111/cas.70252","DOIUrl":"10.1111/cas.70252","url":null,"abstract":"<p>Tumor suppressor p53 is the most frequently mutated gene in cancers. Mutations in p53 not only result in the loss of its classical tumor-suppressive functions but also confer new oncogenic properties. The protein stabilization of mutant p53 (mutp53) is a prerequisite for gain-of-function manifestation. Here, we report the novel mechanism that pyruvate dehydrogenase kinase1 (PDK1) modulates both wild-type and mutant p53, and facilitates proliferation and migration of TP53 mutant breast cancer. On the one hand, we identified PDK1 as a direct transcriptional repression target of wild-type p53, whereas transcriptional activation of PDK1 in mutp53 cells is initiated by the EGR1 axis. On the other hand, PDK1 promoted mutp53 protein accumulation by binding to mutp53 and inhibiting its degradation. Taken together, mutp53 activated a positive feedback loop by upregulating PDK1 to enhance p53 protein stability and promote the malignancy of breast cancer. Moreover, PDK1 inhibition increased the therapeutic effect of APR-246 on TP53 mutant breast cancer in xenograft tumors. Our results suggested that intervention of PDK1 could potentially emerge as a new therapeutic strategy to impede the progression of TP53 mutant breast cancer.</p>","PeriodicalId":9580,"journal":{"name":"Cancer Science","volume":"117 2","pages":"335-352"},"PeriodicalIF":4.3,"publicationDate":"2025-11-17","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12861101/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145534812","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}