Oncology reports最新文献

{"title":"Liver metastasis of colorectal cancer: Mechanism and clinical therapy (Review).","authors":"Changjiang Yang, Long Zhao, Caihong Wang, Yingjiang Ye, Zhanlong Shen","doi":"10.3892/or.2025.8963","DOIUrl":"10.3892/or.2025.8963","url":null,"abstract":"<p><p>Liver metastasis is a common complication in colorectal cancer (CRC), with its presence and progression significantly shortening patient survival. Therefore, a deeper understanding of the underlying mechanisms driving liver metastasis in CRC is essential to identify more effective and actionable therapeutic targets and improve prognosis. Liver metastasis in CRC is a multifaceted and dynamic process. Tumor cells with invasive properties communicate with the surrounding microenvironment through mechanisms such as immune checkpoint molecules and cytokines, thereby establishing a supportive niche for their colonization and proliferation. Moreover, suppressive immune cells may enhance the invasiveness of tumor cells. The interplay between tumor cells and the microenvironment is an interdependent process. Targeting these interactions offers promising potential for novel therapeutic strategies. The present review outlined mechanisms of colorectal cancer liver metastasis, emphasizing the immune microenvironment's role, current treatment approaches, and future development prospects.</p>","PeriodicalId":19527,"journal":{"name":"Oncology reports","volume":"54 4","pages":""},"PeriodicalIF":3.9,"publicationDate":"2025-10-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12351159/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144799687","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":"[Corrigendum] Human chorionic gonadotropin β regulates epithelial‑mesenchymal transition and metastasis in human ovarian cancer.","authors":"Na Liu, Shu-Min Peng, Guang-Xi Zhan, Jing Yu, Wei-Min Wu, Hao Gao, Xiao-Feng Li, Xiao-Qing Guo","doi":"10.3892/or.2025.8948","DOIUrl":"10.3892/or.2025.8948","url":null,"abstract":"<p><p>Following the publication of the above article, an interested reader drew to the Editor's attention that, for the scratch‑wound assay experiments shown in Fig. 3 on p. 1468, the \"ES‑2 LV‑β‑hCG\" and \"ES‑2 siRNA‑β‑hCG\" data panels were apparently the same, suggesting that the same data panel had erroneously been included twice in this figure. Furthermore, β‑actin blots featured in Fig. 2C on p. 1467, and certain of the western blot data featured in Fig. 6A on p. 1470, were strikingly similar to western blot data that appeared in papers subsequently published by the same research group in the journals <i>Cell Cycle</i> and <i>Cancer Science</i>, respectively; finally, the same western blot data had been selected to represent β‑catenin and Slug protein bands in Fig. 6A. After having examined their original data, the authors realized that these figures had been inadvertently assembled incorrectly. The revised versions of Fig. 2 (showing all the correct β‑actin data in Fig. 2C), Fig. 3 (showing the correct data for the \"ES‑2 siRNA‑β‑hCG\" experiment) and Fig. 6 (showing the correct data for the \"Slug/ES‑2 siRNA‑β‑hCG\" and \"Slug/SKOV3 siRNA‑β‑hCG\" protein bands) are shown on the next two pages. Note that the revisions made to these figures do not affect the overall results and conclusions reported in the paper. The authors are grateful to the Editor of <i>Oncology Reports</i> for granting them the opportunity to publish this corrigendum, and all the authors agree with its publication; furthermore, they apologize to the readership of the journal for any inconvenience caused. [Oncology Reports 38: 1464‑1472, 2017; DOI: 10.3892/or.2017.5818].</p>","PeriodicalId":19527,"journal":{"name":"Oncology reports","volume":"54 4","pages":""},"PeriodicalIF":3.9,"publicationDate":"2025-10-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12308833/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144668058","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":"Chromosome 20q gene signature associated with colorectal cancer progression.","authors":"Jennifer Carter Jones, Apurva M Hegde, Yu-Jing Huang, Ganiraju Manyam, Vibhuti Srivastava, Jee Hoo Song, Yulan Cheng, Ralf Krahe, Warapen Treekitkarnmongkol, Stephen J Meltzer, Scott Kopetz, Stanley R Hamilton, Hiroshi Katayama, Subrata Sen","doi":"10.3892/or.2025.8954","DOIUrl":"10.3892/or.2025.8954","url":null,"abstract":"<p><p>Amplification of human chromosome 20q has been reported as the most frequently recurring genetic abnormality associated with large scale changes in mRNA and protein levels in sporadic colorectal carcinomas. While some studies have found 20q amplification to be consistent between primary and metastatic samples from the same patient with a role in the development of metastasis and worse patient prognosis, others have reported association with improved overall survival for a subset of these patients with colorectal cancer (CRC). To fine map the Minimal Common Regions (MCRs) of amplification on chromosome 20q and identify the candidate genes playing roles in progression of the disease, microarray comparative genomic hybridization analyses of two <i>in vitro</i> cultured CRC liver metastasis cell line model systems was utilized. Microarray expression analysis led to the identification of a candidate gene signature comprising of four genes, <i>BMP7, DNMT3B, UBE2C</i> and <i>YWHAB</i>, residing in the MCRs that were over expressed in CRC cells. By validating our results in a training set of 23 adenocarcinomas (tumors) and five adenomas (polyps) using reverse transcription‑quantitative PCR, as well as analyses of two larger colorectal cancer test data sets derived from 195 The Cancer Genome Atlas and 182 MD Anderson Cancer Center patients with colorectal adenocarcinoma patients, this gene signature was ascertained to be associated with lymph node spread and/or distant metastasis (P<0.05). Previously reported functional studies of the gene signature indicated their involvement in inflammatory and immune response pathways driving CRC progression.</p>","PeriodicalId":19527,"journal":{"name":"Oncology reports","volume":"54 4","pages":""},"PeriodicalIF":3.9,"publicationDate":"2025-10-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12308843/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144668060","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":"Zinc finger protein 695 facilitates the proliferation of colorectal cancer cells through activation of the NEK2 and PI3K/Akt/mTOR signaling pathways.","authors":"Xiaowei Li, Xubin Li, Jing Wang, Mei Xue, Mengqiao Zhang, Junfang Shuai, Jie Zhang, Danyang Ding, Ye Wang, Shiyang Hou, Xiaoqian Chi, Haiying Sun, Qiang Gao, Chunbo Kang","doi":"10.3892/or.2025.8949","DOIUrl":"10.3892/or.2025.8949","url":null,"abstract":"<p><p>Colorectal cancer (CRC) is the third most common malignant tumor and the second leading cause of cancer‑related deaths worldwide. Identifying driver genes in CRC development may provide clinical benefits for patients. Zinc finger protein 695 (ZNF695) is a nuclear protein with transcriptional regulatory activity, which has been implicated in tumor progression; however, the role of ZNF695 in CRC is unclear. The clinical relevance of ZNF695 and NIMA‑related kinase 2 (NEK2) in patients with CRC was analyzed based on The Cancer Genome Atlas database. Knockdown was performed by transfecting the cells with small interfering RNAs, whereas overexpression was induced by infecting the cells with a lentivirus. In addition, cell Counting Kit‑8, colony formation, cell cycle and apoptosis assays were carried out to assess the role of ZNF695 and NEK2 in CRC. Chromatin immunoprecipitation‑quantitative PCR (qPCR) and dual luciferase reporter assays were used to examine the transcriptional regulation of ZNF695 on the NEK2 gene. Reverse transcription‑qPCR and western blotting were applied to assess mRNA and protein abundance, respectively. The present study aimed to investigate the clinical relevance, contribution and downstream effects of ZNF695 in CRC. The results revealed that ZNF695 was upregulated in CRC tissues compared with that in non‑cancer tissues. CRC cells also expressed higher ZNF695 expression than normal cells. <i>In vitro</i>, knockdown of ZNF695 suppressed the proliferation of HCT‑8 cells; conversely, overexpression of ZNF695 promoted the malignancy of HT‑29 cells. Moreover, ZNF695 accelerated cell cycle progression and inhibited apoptosis in CRC cells. Mechanistically, it was revealed that ZNF695 upregulated the expression of NEK2 at both the mRNA and protein levels. Luciferase reporter assay demonstrated that ZNF695 enhanced the transcriptional activity of the NEK2 promoter. Furthermore, knockdown of NEK2 reversed the oncogenic function of ZNF695. Additionally, ZNF695 activated the PI3K/Akt/mTOR signaling pathway in CRC cells. Inhibition of this pathway with rapamycin resulted in higher cytotoxicity to CRC cells with ZNF695 overexpression, suggesting that elevated ZNF695 levels may increase the sensitivity of CRC cells to rapamycin. In summary, the current study identified ZNF695 as a tumor‑promoting protein in CRC through activation of the NEK2 and PI3K/Akt/mTOR signaling pathways. Targeting the NEK2 and PI3K/Akt/mTOR signaling pathways may therefore be a promising strategy for the treatment of patients with CRC and high ZNF695 expression.</p>","PeriodicalId":19527,"journal":{"name":"Oncology reports","volume":"54 4","pages":""},"PeriodicalIF":3.9,"publicationDate":"2025-10-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12308799/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144668064","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":"PTP4A1 promotes intrahepatic cholangiocarcinoma development and progression by interacting with PTEN and activating the PI3K/AKT/GSKα axis.","authors":"Ou Li, Yuhuai Peng, Jinhui Che, Yubin Liu","doi":"10.3892/or.2025.8958","DOIUrl":"10.3892/or.2025.8958","url":null,"abstract":"<p><p>Intrahepatic cholangiocarcinoma (ICC) is a highly aggressive biliary cancer originating within the liver with a high incidence, high degree of malignancy and extremely poor prognosis. Protein tyrosine phosphatase 4A1 (PTP4A1) plays a carcinogenic role in numerous tumors. However, the role of PTP4A1 in the progression of ICC has not been fully elucidated. The aim of the present study was to clarify the function of PTP4A1 in ICC. Cell Counting Kit‑8 assay, 5‑ethynyl‑2'‑deoxyuridine staining and a cell colony formation assay were performed to detect cell proliferation and viability. Wound healing and Transwell assays were used to analyze cell migration and invasion. The interaction of PTP4A1 with phosphatase and tensin homolog (PTEN) was validated by immunofluorescence and co‑immunoprecipitation assays. Reverse transcription‑quantitative PCR, western blotting and immunohistochemistry were used to evaluate the mRNA and protein expression levels. The present study demonstrated that PTP4A1 was highly expressed and associated with invasive pathological features in ICC. Furthermore, PTP4A1 promoted ICC cell proliferation, migration and invasion both <i>in vitro</i> and <i>in vivo</i>. Mechanistically, PTP4A1 interacts with PTEN, contributes to the suppression of PTEN phosphorylation and promotes the activation of the PI3K/AKT/glycogen synthase kinase 3 alpha pathway. In addition, the present results demonstrated that the promotion of cell proliferation, migration and invasion by PTP4A1 was dependent on the regulation of the PTEN/PI3K/AKT/GSk3α pathway in ICC. Collectively, these data revealed that PTP4A1 is a promising target for ICC therapeutics.</p>","PeriodicalId":19527,"journal":{"name":"Oncology reports","volume":"54 4","pages":""},"PeriodicalIF":3.9,"publicationDate":"2025-10-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12340664/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144760666","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":"[Corrigendum] Highly sensitive detection of leukemia cells based on aptamer and quantum dots.","authors":"Yating Yu, Siliang Duan, Jian He, Wei Liang, Jing Su, Jianmeng Zhu, Nan Hu, Yongxiang Zhao, Xiaoling Lu","doi":"10.3892/or.2025.8962","DOIUrl":"10.3892/or.2025.8962","url":null,"abstract":"<p><p>Following the publication of the above article, the authors drew to the Editor's attention that, concerning the histological images shown in Fig. 5B on p. 890, two pairs of the data panels showed overlapping sections, such that these data were derived from the same original source where the panels were intended to show the results from differently performed experiments. Upon examining their original data, the authors realized that inadvertent errors were made in assembling the data in this figure. The corrected version of Fig. 5, now showing replacement data for the liver and lung images in Fig. 5B, is shown on the next page. Note that this error did not affect the overall conclusions reported in the paper. All the authors agree with the publication of this corrigendum, and are grateful to the Editor of <i>Oncology Reports</i> for allowing them the opportunity to publish this. They also apologize to the readership for any inconvenience caused. [Oncology Reports 36: 886‑892, 2016; DOI: 10.3892/or.2016.4866].</p>","PeriodicalId":19527,"journal":{"name":"Oncology reports","volume":"54 4","pages":""},"PeriodicalIF":3.9,"publicationDate":"2025-10-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12329636/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144760662","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":"Visfatin facilitates esophageal cancer migration by suppressing miR‑3613‑5p expression and promoting VEZF1/VCAN production.","authors":"Chang-Lun Huang, Shubham Suresh Ghule, Yu-Hsiang Chang, Hsiao-Chi Tsai, Ming-Yu Lien, Jeng-Hung Guo, Chun-Lin Liu, Po-I Liu, Chih-Hsin Tang","doi":"10.3892/or.2025.8961","DOIUrl":"10.3892/or.2025.8961","url":null,"abstract":"<p><p>Esophageal cancer, one of the most prevalent types of cancer worldwide, frequently exhibits distant metastases. The adipokine visfatin is implicated in cancer progression and metastasis. However, the mechanisms by which visfatin regulates motility in esophageal cancer remain unclear. Bioinformatics analysis showed levels of visfatin were higher in patients with metastatic esophageal cancer than in those with primary esophageal cancer. Cell motility assay revealed that visfatin stimulation enhanced the migration and invasion of esophageal cancer cells. Treatment with or without visfatin (30 ng/ml) in KYSE410 cells followed by miRNA sequencing, revealed that miR‑3613‑5p controlled visfatin‑induced cell motility. Further cell migration, invasion, qPCR and western blot assay shows that visfatin promoted esophageal cancer cell migration by decreasing miR‑3613‑5p expression and subsequently increasing vascular endothelial zinc finger 1/versican production. Thus, the visfatin/miR‑3613‑5p axis may be a promising target for inhibiting esophageal cancer cell migration and invasion.</p>","PeriodicalId":19527,"journal":{"name":"Oncology reports","volume":"54 4","pages":""},"PeriodicalIF":3.9,"publicationDate":"2025-10-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12329650/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144760668","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":"TRPML3‑mediated lysosomal Ca²⁺ release enhances drug sequestration and biogenesis, promoting osimertinib resistance in non‑small cell lung cancer.","authors":"Mi Seong Kim, Min Seuk Kim","doi":"10.3892/or.2025.8946","DOIUrl":"10.3892/or.2025.8946","url":null,"abstract":"<p><p>Lysosomes and lysosomal Ca²⁺ play crucial roles in cellular homeostasis and drug resistance. The lysosomal Ca²⁺ channel transient receptor potential mucolipin 3 (TRPML3; also known as mucolipin‑3 or MCOLN3) is a key regulator of autophagy and membrane trafficking; however, its role in tyrosine kinase inhibitor (TKI) resistance remains unclear. The contribution of TRPML3 to osimertinib resistance in non‑small cell lung cancer (NSCLC) was therefore assessed. Using publicly available RNA sequencing data, including profiles from clinical samples before and after osimertinib treatment, <i>TRPML3</i> expression was measured in lung adenocarcinoma (LUAD) tissues. Additionally, two‑dimensional cell culture of, and three‑dimensional spheroids derived from, NSCLC cell lines were used to elucidate roles of TRPML3 in drug resistance. <i>TRPML3</i> expression was significantly upregulated in both LUAD tissues from patients with residual disease after osimertinib treatment, as well as in osimertinib‑resistant NSCLC cells. <i>TRPML3</i> knockdown in resistant PC9 cells restored sensitivity to osimertinib and multiple TKIs; this was replicated in spheroid models. Mechanistically, osimertinib induced intracellular Ca²⁺ oscillations in PC9 cells via lysosomal Ca²⁺ release through TRPML3 rather than through TRPML1. In summary, the present findings suggest that elevated TRPML3 expression compensates for TRPML1 to maintain lysosomal acidity and biogenesis during TKI treatment, facilitating drug sequestration and resistance and identifying <i>TRPML3</i> as a potential target for overcoming osimertinib resistance in NSCLC.</p>","PeriodicalId":19527,"journal":{"name":"Oncology reports","volume":"54 3","pages":""},"PeriodicalIF":3.8,"publicationDate":"2025-09-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12284468/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144668057","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":"[Retracted] SMAD specific E3 ubiquitin protein ligase 1 promotes ovarian cancer cell migration and invasion via the activation of the RhoA/ROCK signaling pathway.","authors":"Wei Wang, Han Du, Huiping Liu, Fangfang Hu, Guangzhi Liu","doi":"10.3892/or.2025.8938","DOIUrl":"10.3892/or.2025.8938","url":null,"abstract":"<p><p>Following the publication of this paper, it was drawn to the Editor's attention by a concerned reader that a pair of the data panels shown for the Transwell migration assay experiments in Fig. 1B on p. 671, and two further pairs of data panels showing the results of invasion and migration assay experiments in Fig. 2A and B on p. 672 respectively, contained overlapping sections of data, such that the affected panels, which were intended to show the results of differently performed experiments, had all apparently been derived from the same original sources. Owing to the identification of these duplicated data panels in this paper, the Editor of <i>Oncology Reports</i> has decided that it should be retracted from the Journal on account of a lack of confidence in the presented 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 41: 668‑676, 2019; DOI: 10.3892/or.2018.6836].</p>","PeriodicalId":19527,"journal":{"name":"Oncology reports","volume":"54 3","pages":""},"PeriodicalIF":3.8,"publicationDate":"2025-09-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12236145/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144560712","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":"[Retracted] Expression of α‑fetoprotein in gastric cancer AGS cells contributes to invasion and metastasis by influencing anoikis sensitivity.","authors":"Sumei Lu, Yongmei Ma, Tao Sun, Rui Ren, Xiaoning Zhang, Wanshan Ma","doi":"10.3892/or.2025.8945","DOIUrl":"10.3892/or.2025.8945","url":null,"abstract":"<p><p>Following the publication of this paper, it was drawn to the Editor's attention by a concerned reader that several instances of duplicated data existed within several of the figures in this article; specifically: i) two pairs of data panels in the four‑panel Fig. 2B (so affecting all the panels in this figure part, which showed the results from migration and invasion assay experiments) were overlapping; ii) a pair of data panels for the fluorescence experiments shown in Fig. 4 were also found to be overlapping; and iii) one set of protein bands in the western blots featured in Fig. 5 (for the caspase‑3 data) had also been included in a paper submitted to and published in <i>Oncology Reports</i> a few months earlier, with the author Tao Sun held in common between these papers. Owing to the number of cases of data duplication that were identified in this paper, the Editor of <i>Oncology Reports</i> has decided that it should be retracted from the Journal on account of a lack of confidence in the presented data. After contacting the authors, they accepted the decision to retract the paper. The Editor apologizes to the readership for any inconvenience caused. [Oncology Reports 35: 2984‑2990, 2016; DOI: 10.3892/or.2016.4678].</p>","PeriodicalId":19527,"journal":{"name":"Oncology reports","volume":"54 3","pages":""},"PeriodicalIF":3.9,"publicationDate":"2025-09-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12284458/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145001080","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}