Oncology reports最新文献

{"title":"A novel regulatory role of microRNA‑5590‑3p in hepatocellular carcinoma via the HOXB2/MYC axis.","authors":"Bin Li, Lin Zhou","doi":"10.3892/or.2026.9130","DOIUrl":"https://doi.org/10.3892/or.2026.9130","url":null,"abstract":"<p><p>The present study aimed to investigate the effects of microRNA (miR)‑5590‑3p on the biological functions of hepatocellular carcinoma (HCC) cells through the homeobox B2 (HOXB2)/MYC axis. The expression levels of miR‑5590‑3p, HOXB2 and MYC were measured in HCC tissues and cell lines, and the relationships between miR‑5590‑3p, HOXB2, and the clinicopathological characteristics and prognosis of patients with HCC were analyzed. The Cell Counting Kit‑8 assay assessed cell proliferation, flow cytometry measured apoptosis rate, and the Transwell and wound healing assays evaluated the invasive and migratory abilities of cells. The targeting interactions between miR‑5590‑3p and HOXB2, and between HOXB2 and MYC were assessed. In addition, a subcutaneous HCC xenograft model was established to assess the effects of miR‑5590‑3p on tumor growth. The results revealed that miR‑5590‑3p expression was downregulated in HCC tissues and cells, whereas HOXB2 and MYC expression were upregulated. Notably, low miR‑5590‑3p expression and high HOXB2 expression were both associated with a poor prognosis in patients with HCC. miR‑5590‑3p directly targeted and suppressed HOXB2, whereas HOXB2 promoted MYC transcription. Furthermore, downregulation of miR‑5590‑3p enhanced the invasion, migration and proliferation of Huh7 cells, and reduced their apoptotic rate. By contrast, miR‑5590‑3p overexpression or HOXB2 silencing decreased invasion, migration and proliferation, while increasing apoptosis. Moreover, HOXB2 overexpression reversed the inhibitory effect of miR‑5590‑3p upregulation on HCC cell proliferation. HOXB2 appeared to promote Huh7 cell proliferation and motility through MYC transcriptional activation, whereas miR‑5590‑3p overexpression suppressed tumor growth <i>in vivo</i>. In conclusion, miR‑5590‑3p may inhibit HCC cell proliferation and motility, and induce apoptosis by targeting HOXB2 and suppressing MYC transcription.</p>","PeriodicalId":19527,"journal":{"name":"Oncology reports","volume":"56 1","pages":""},"PeriodicalIF":3.9,"publicationDate":"2026-07-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"147840306","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"[Retracted] SHIP1 is targeted by miR‑155 in acute myeloid leukemia.","authors":"Hua Xue, Luo-Ming Hua, Ming Guo, Jian-Min Luo","doi":"10.3892/or.2026.9129","DOIUrl":"https://doi.org/10.3892/or.2026.9129","url":null,"abstract":"<p><p>Subsequently to the publication of the above article, a concerned reader drew the Editor's attention to the fact that the left‑hand, outer edges of the β‑actin protein blot of lane 1 and the SHIP‑1 protein blot for lane 9 in Fig. 1B were hanging over the area representing the grey background of the gels, extending beyond the perceived boundary of these background regions and therefore raising possible concerns about post‑acquisition compositing or localized image processing during figure assembly. In addition, in the same figure, the control β‑actin western blots shown in Fig. 1B for the lanes 1‑8 and 9‑16 were apparently the same, albeit the bands in the lower set of blots (for lanes 9-16) were horizontally more compressed. In view of the potential anomalies described above for the data in Fig. 1B, the Editor of <i>Oncology Reports</i> has decided that this paper should be retracted from the Journal on account of a lack of confidence in the presented data. After having been in contact with the authors, they did not accept the decision to retract the paper. The Editor apologizes for any inconvenience caused. [Oncology Reports 32: 2253‑2259, 2014; DOI: 10.3892/or.2014.3435].</p>","PeriodicalId":19527,"journal":{"name":"Oncology reports","volume":"56 1","pages":""},"PeriodicalIF":3.9,"publicationDate":"2026-07-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"147840297","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"[Retracted] PTEN enhances G2/M arrest in etoposide‑treated MCF‑7 cells through activation of the ATM pathway.","authors":"Ruopeng Zhang, Li Zhu, Lirong Zhang, Anli Xu, Zhengwei Li, Yijuan Xu, Pei He, Maoqing Wu, Fengxiang Wei, Chenhong Wang","doi":"10.3892/or.2026.9127","DOIUrl":"10.3892/or.2026.9127","url":null,"abstract":"<p><p>Subsequently to the publication of the above article, a concerned reader drew to the Editor's attention that the β‑actin bands featured in Fig. 1A were also apparently included in the 'Ctrl' experiments for the phospho‑P53 protein bands in Fig. 1B. In addition, a specific pair of P53 bands in Fig. 1B had also apparently been re‑used as phospho‑CDC25C bands in Fig. 6A, suggesting that these figures may have potentially undergone inappropriate editing. After having evaluated these data independently in the Editorial Office, the concerns of the reader were shown to have been well‑founded. Therefore, in view of the uncertainties regarding the assembly of some of the western blot data in Figs. 1 and 6, the Editor of <i>Oncology Reports</i> has decided that this paper should be retracted from the Journal on account of uncertainties with the presentation of the abovementioned data. The authors were asked for an explanation to account for these concerns, but the Editorial Office did not receive a reply.The Editor apologizes to the readership for any inconvenience caused. [Oncology Reports 35: 2707‑2714, 2016; DOI: 10.3892/or.2016.4674].</p>","PeriodicalId":19527,"journal":{"name":"Oncology reports","volume":"56 1","pages":""},"PeriodicalIF":3.9,"publicationDate":"2026-07-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC13153861/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"147777740","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Chronic stress and cancer progression through neuro‑endocrine‑immune networks (Review).","authors":"Zhangxiang Zhu, Xiaohu Zhang, Jing Yan, Mingquan Wang, Yang Lv, Wuqiong Zhang, Hui Guo, Aimei Zheng","doi":"10.3892/or.2026.9128","DOIUrl":"https://doi.org/10.3892/or.2026.9128","url":null,"abstract":"<p><p>Chronic stress may influence cancer trajectories; however, the majority of current frameworks do not clearly define how organism‑level regulation interacts with tumor behavior. The present review summarizes mechanistic and translational evidence to propose a testable model in which cancer progression can, in selected contexts, be understood as over‑adaptation to sustained stress within a hierarchical neuro‑endocrine‑immune network. Within this framework, stress‑related signals converge in brainstem‑hypothalamic control circuits, and engage sympathetic, hypothalamic‑pituitary‑adrenal and vagal effector pathways, which may influence cellular programs, microenvironmental remodeling and systemic dissemination. The evidence is organized into three sections: Cellular adaptation, microenvironmental remodeling and systemic progression. This multiscale perspective provides a host‑context framework for understanding how chronic stress‑related physiology may interact with tumor‑intrinsic processes. Therapeutic implications are also discussed, including psychosocial support, exercise, mindfulness‑based interventions, vagal modulation and perioperative β‑blocker/COX‑2 strategies. At present, the strongest clinical evidence for these approaches supports improvements in symptoms, patient‑reported outcomes and selected biomarkers, whereas durable effects on tumor control or survival remain uncertain. Overall, this framework is presented as a conceptual and testable model intended to guide future research on host‑tumor interactions in cancer.</p>","PeriodicalId":19527,"journal":{"name":"Oncology reports","volume":"56 1","pages":""},"PeriodicalIF":3.9,"publicationDate":"2026-07-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"147840320","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Perturbation of BRD4 and p300 activity suppresses super enhancer‑driven <i>KLF6</i> expression in renal carcinoma.","authors":"Nurul Nadia Mohamad Zamberi, Asmaa Y Abuhamad, Siti Nur Hasanah Mohd Yusuf, Nur Qurratu Athirah A Rahman, Mohamad Aimanuddin Mohtar, Saiful Effendi Syafruddin","doi":"10.3892/or.2026.9118","DOIUrl":"10.3892/or.2026.9118","url":null,"abstract":"<p><p>Super enhancers (SEs) are involved in regulating cell identity and lineage‑specific gene expression, and drive cancer‑associated gene expression. The transcription factor Kruppel‑like factor 6 (KLF6) promotes the growth and progression of clear cell renal cell carcinoma (ccRCC), with its high expression driven by one of the strongest SEs in ccRCC. However, the mechanisms that establish and maintain <i>KLF6</i> SE activity, particularly the roles of epigenetic regulators bromodomain-containing 4 (BRD4) and p300, remain poorly understood. This study investigated the roles of BRD4 and p300 in modulating <i>KLF6</i> SE activity. The effects of JQ1‑mediated BRD4 and A‑485‑mediated p300 inhibition were assessed using cell viability and colony formation assays. Reverse transcription‑quantitative (q)PCR and ChIP‑qPCR were employed to evaluate the impact of BRD4 and p300 inhibition, as well as CRISPR‑mediated deacetylation of individual constituent enhancers, on <i>KLF6</i> expression and SE activity. Chemical inhibition of BRD4 and p300 significantly reduced ccRCC cell viability and colony formation, and decreased KLF6 expression and levels of acetylation at lysine 27 of histone H3 (H3K27ac) at <i>KLF6</i> enhancer regions SE_1, SE_2 and SE_3, suggesting decreased chromatin accessibility. On the other hand, deacetylation of SE_1 using dead Cas9 fused to histone deacetylase 3, led to <i>KLF6</i> downregulation, which was associated with decreased H3K27ac signals at this region. The present results demonstrated that BRD4 and p300 are key for maintaining <i>KLF6</i> SE activity and driving high <i>KLF6</i> expression in ccRCC. However, deacetylation of  individual enhancer regions using CRISPR was insufficient to fully suppress <i>KLF6</i> transcription, emphasizing the robustness of the KLF6 SE and its modular role in sustaining high <i>KLF6</i> expression. Overall, the present study deepens the understanding of growth‑promoting KLF6 transcriptional networks in ccRCC and offers insights to support the development of diagnostic or therapeutic strategies.</p>","PeriodicalId":19527,"journal":{"name":"Oncology reports","volume":"55 6","pages":""},"PeriodicalIF":3.9,"publicationDate":"2026-06-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC13107101/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"147699404","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Role of CHD4 in tumor progression, DNA damage response and treatment resistance (Review).","authors":"Shuo Li, Quan Ma, Keying Lian, Zhisheng Jiang, Yun Ma","doi":"10.3892/or.2026.9112","DOIUrl":"10.3892/or.2026.9112","url":null,"abstract":"<p><p>Chromodomain helicase DNA‑binding protein 4 (CHD4) is a core adenosine triphosphate (ATP)‑dependent chromatin‑remodeling factor of the nucleosome‑remodeling and deacetylase (NuRD) complex. It plays a crucial role in chromatin structure regulation, gene expression regulation, and DNA damage response. It has been demonstrated that CHD4 has context‑dependent functions in tumor development and progression. It can influence tumor progression via such mechanisms as regulating tumor‑related signaling pathways, maintaining the silencing of tumor suppressor genes, and promoting metabolic adaptation; it can also exert tumor‑suppressive effects in specific transcriptional regulatory environments. Additionally, during DNA damage response, CHD4 participates in chromatin remodeling at damage sites, in cell cycle recovery, and in repair pathway selection. It is also involved in the development of tumor treatment resistance through mechanisms that include regulation of DNA repair, cell cycle progression, drug efflux, the tumor immune microenvironment, and replication fork stability. It has also been shown that various non‑coding RNAs participate in the functional regulation of CHD4 by modulating its expression, localization, and protein stability. In summary, as a key node connecting chromatin regulation, genome stability, and tumor treatment response, CHD4 holds significant importance in tumor progression and treatment.</p>","PeriodicalId":19527,"journal":{"name":"Oncology reports","volume":"55 6","pages":""},"PeriodicalIF":3.9,"publicationDate":"2026-06-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC13088044/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"147609481","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"NF‑κB‑driven LUZP1 promotes metastasis and chemoresistance in head and neck squamous cell carcinoma.","authors":"Chen-Yuan Lin, Ching-Yun Hsieh, Hsin-Chi Lan, Ching-Chan Lin, Tzu-Ting Chen, Wei-Chi Tseng, Yung-An Tsou, Wei-Chao Chang","doi":"10.3892/or.2026.9115","DOIUrl":"10.3892/or.2026.9115","url":null,"abstract":"<p><p>Head and neck squamous cell carcinoma (HNSCC) remains a highly aggressive malignancy with poor prognosis driven by metastasis and therapeutic resistance. Through comparative proteomic profiling of tumor specimens from patients with long‑ and short‑term survival, the present study identified leucine zipper protein 1 (LUZP1) as one of the most upregulated proteins in tumors from short‑term survivors. Functional assays revealed that LUZP1 knockdown impaired migration, invasion, invadopodia formation and epithelial‑mesenchymal transition, while enhancing sensitivity to docetaxel and cisplatin. Analysis of paired primary and metastatic tumors further confirmed elevated LUZP1 expression in metastatic sites. Mechanistically, NF‑κB inhibition markedly reduced LUZP1 expression, whereas stimulation with IL‑1β or TNF‑α induced its upregulation and rescued the migration defect caused by LUZP1 depletion, implicating NF‑κB as a key upstream regulator. Immunohistochemical analysis of clinical samples demonstrated that high LUZP1 expression was associated with shorter overall and progression‑free survival. Collectively, these findings identify LUZP1 as a novel NF‑κB‑regulated effector that promotes metastasis and chemoresistance and highlight its potential as a prognostic biomarker and therapeutic target in HNSCC.</p>","PeriodicalId":19527,"journal":{"name":"Oncology reports","volume":"55 6","pages":""},"PeriodicalIF":3.9,"publicationDate":"2026-06-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC13107151/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"147639480","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"E3 ubiquitin ligase RNF40: Structure, function and its context‑dependent roles in tumorigenesis (Review).","authors":"Zikun Wu, Hang Yang, Guanglong Chen, Weijie Zhao, Banghe Bao, Chai Luv, Wenpu Zhu, Faqiang Liu, Huihan Ai, Zhi Li","doi":"10.3892/or.2026.9126","DOIUrl":"10.3892/or.2026.9126","url":null,"abstract":"<p><p>The ubiquitin‑proteasome system, a key protein degradation machinery in humans, mediates substrate recognition and proteolysis through ubiquitin‑tagged targeting of macromolecular proteins to the 26S proteasome. This evolutionarily conserved system orchestrates fundamental cell processes, including cell cycle progression, DNA damage repair, immune regulation, signal transduction and clearance of misfolded proteins. Its functional integrity is involved in the pathogenesis of various malignancies (breast and small cell lung cancer and colorectal adenocarcinoma) and degenerative diseases (Parkinson's disease). As a really interesting new gene‑type E3 ubiquitin ligase, ring finger protein (RNF)40 has emerged as a key regulator of both physiological homeostasis and disease progression. The present review systematically examines RNF40 structural architecture and its multifaceted roles in ubiquitination‑dependent proteostasis, epigenetic modulation and DNA repair mechanisms, as well as its tumor‑specific regulatory networks across cancer subtypes and therapeutic potential as a novel drug target.</p>","PeriodicalId":19527,"journal":{"name":"Oncology reports","volume":"55 6","pages":""},"PeriodicalIF":3.9,"publicationDate":"2026-06-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC13150416/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"147777485","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Inhibitory role of angiopoietin‑like 4 for cancer progression in oropharyngeal squamous cell carcinoma.","authors":"Takuya Mikoshiba, Mariko Sekimizu, Nana Nakahara, Shin Saito, Keisuke Yoshihama, Ryoto Nagai, Takeyuki Kono, Hiroyuki Ozawa","doi":"10.3892/or.2026.9122","DOIUrl":"https://doi.org/10.3892/or.2026.9122","url":null,"abstract":"<p><p>The mortality rate of head and neck squamous cell carcinoma (HNSCC), one of the most prevalent types of cancer, has remained unchanged despite advances in treatment strategies. Angiopoietin‑like 4 (ANGPTL4) exhibits both pro‑ and anti‑tumorigenic roles in various cancers depending on the tissue context. The present study investigated the role of ANGPTL4 expression in oropharyngeal squamous cell carcinoma (OPSCC). Data from 137 patients with OPSCC who underwent initial treatment were retrospectively analyzed. ANGPTL4 expression in tumor tissues was determined via immunohistochemistry. Survival outcomes [overall survival (OS) and disease‑free survival (DFS)] and clinicopathological correlations were evaluated. Tumor cell proliferation was assessed using an CellTiter‑Glo 2.0 luminescence‑based cell viability assay, immunofluorescence staining, and reverse transcription‑quantitative polymerase chain reaction following small interfering RNA‑mediated knockdown in a HNSCC cell line. Gene set enrichment analysis (GSEA) was performed using data from The Cancer Genome Atlas. ANGPTL4 expression (≥7.7%) in patients with OPSCC was significantly associated with improved OS and DFS. Multivariate analysis confirmed that low ANGPTL4 expression was an independent prognostic factor for OS [hazard ratio (HR)=3.676, 95% confidence interval (CI)=1.678‑8.056; P=0.001) and DFS (HR=2.959, 95% CI=1.533‑5.713; P=0.001)]. FaDu cells with <i>ANGPTL4</i> knockdown demonstrated significantly increased proliferation compared with negative controls in the CellTiter‑Glo 2.0 assay (P=0.010), accompanied by a significant increase in Ki‑67 expression as revealed by immunofluorescence staining (P=0.021). The relative <i>ANGPTL4</i> mRNA expression levels decreased to 38%, whereas those of <i>MKI67</i> increased significantly. GSEA revealed significant enrichment of cell cycle progression signatures in cases with low <i>ANGPTL4</i> expression. ANGPTL4 expression was significantly associated with a favorable prognosis in OPSCC, and its knockdown increased proliferative activity in FaDu cells. Thus, ANGPTL4 may serve as a prognostic biomarker in OPSCC. Further <i>in vivo</i> studies are warranted to clarify causality and assess the therapeutic potential of <i>ANGPTL4</i> targeting in OPSCC.</p>","PeriodicalId":19527,"journal":{"name":"Oncology reports","volume":"55 6","pages":""},"PeriodicalIF":3.9,"publicationDate":"2026-06-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC13122131/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"147777693","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"[Expression of Concern] Metformin inhibits growth and sensitizes osteosarcoma cell lines to cisplatin through cell cycle modulation.","authors":"Irene Quattrini, Amalia Conti, Laura Pazzaglia, Chiara Novello, Stefano Ferrari, Piero Picci, Maria Serena Benassi","doi":"10.3892/or.2026.9116","DOIUrl":"10.3892/or.2026.9116","url":null,"abstract":"<p><p>Following the publication of the above paper, it was drawn to the Editor's attention by a concerned reader that, regarding the flow cytometric plots shown in Fig. 3 on p. 372, the C/U2OS and 48 h/U2OS, C/143B and 48 h/143B, and C/MG63 and 72 h/143B data panels, respectively, were strikingly similar, suggesting that this figure has been assembled incorrectly, and that these data were derived from a smaller number of original sources. The authors have been contacted by the Editorial Office to offer an explanation for the apparent duplication of these data panels within this figure, and we are waiting their response. Owing to the fact that the Editorial Office has been made aware of potential issues surrounding the scientific integrity of this paper, we are issuing an Expression of Concern to notify readers of this potential problem while the Editorial Office continues to investigate this matter further. [Oncology Reports 31: 370‑375, 2014; DOI: 10.3892/or.2013.2862].</p>","PeriodicalId":19527,"journal":{"name":"Oncology reports","volume":"55 6","pages":""},"PeriodicalIF":3.9,"publicationDate":"2026-06-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC13107149/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"147639482","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}