American journal of cancer research最新文献

{"title":"Enhanced inhibitory effects of mianserin in combination with sorafenib on liver cancer growth through targeting the CCR9-AKT pathway.","authors":"Ya-Hui Huang, Chia-Jung Liao, Meng-Han Wu, Ming-Wei Lai, Yung-Hsin Yeh, Chau-Ting Yeh, Yang-Hsiang Lin, Kwang-Huei Lin","doi":"10.62347/CYDE4091","DOIUrl":"10.62347/CYDE4091","url":null,"abstract":"<p><p>Previously, our group showed that mianserin, an atypical antidepressant, exerts stronger cytotoxicity against liver cancer cells than normal hepatocytes, supporting its potential application as a therapeutic agent for liver cancer. However, the anti-tumor effects of mianserin <i>in vivo</i> and its mechanisms are yet to be established. In this study, we explored the inhibitory effects and mechanisms of mianserin and evaluated its efficacy in combination with sorafenib against liver cancer cells. Effects on cell viability were assessed via MTT and flow cytometry assays and antitumor activity evaluated using a xenograft model. Changes in the expression and distribution of specific proteins within cells were examined via immunoblot assay. Our results indicate that mianserin exerts cytotoxic effects by inhibiting cell viability through suppression of proliferation and induction of apoptosis. Therapeutic effects of mianserin were validated via intratumoral injection in the xenograft model. Mechanistically, our data indicate that mianserin-induced cytosolic HSP60 translocates to cell surface and participates in the downregulation of CCR9, leading to inactivation of the AKT-(β-catenin/NFκB) signaling pathway. Combination treatment with mianserin and sorafenib induced significant synergistic effects on cell viability, apoptosis, and <i>in vivo</i> tumor growth in both parental and sorafenib-resistant liver cancer cells. This study is the first to demonstrated that mianserin effectively limits the growth of liver cancer by downregulating CCR9, in turn, inactivating the AKT-(β-catenin/NFκB) pathway. Both <i>in vitro</i> and <i>in vivo</i> experiments highlight mianserin's potential as an adjuvant therapy to sorafenib, offering a promising strategy to overcome current challenges in liver cancer treatment.</p>","PeriodicalId":7437,"journal":{"name":"American journal of cancer research","volume":"15 6","pages":"2890-2904"},"PeriodicalIF":3.6,"publicationDate":"2025-06-25","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12256417/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144641498","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":"ESRP1 drives subtype-specific breast cancer progression through ER-regulated transcriptional programs and EMT-related splicing switch.","authors":"Xinyi Wang, Shuping Song, Weixuan Lin, Jiandi Huang, Wenchao Zhong, Donghang Li, Cainan Huo, Yongxuan Wang, Dingke Chen, Zhi Zhang, Yanqin Sun","doi":"10.62347/OXPE5390","DOIUrl":"10.62347/OXPE5390","url":null,"abstract":"<p><p>Epithelial Splicing Regulatory Protein 1 (ESRP1), an epithelial splicing regulator, influences the invasiveness and metastasis of breast cancer cells, yet its prognostic significance and interaction with estrogen receptors are not fully understood. Our findings indicate that ESRP1 is significantly up-regulated in breast cancer tissues and correlates positively with adverse clinical outcomes, particularly in estrogen receptor (ER) positive breast cancer. In vitro experiments with cells demonstrated a dual regulatory mechanism: in ER-positive breast cancer cells, reduced expression of ESRP1 suppresses tumor cell proliferation but does not significantly affect tumor cell invasion and migration; conversely, in ER-negative breast cancer cells, ESRP1 hinders tumor progression by regulating the alternative splicing of epithelial-mesenchymal transition (EMT)-related genes. To investigate whether the presence of ER is a decisive factor in ESRP1's role, we treated ER-positive breast cancer cells with an ER inhibitor to induce EMT, followed by the knockdown of ESRP1, which further promoted the EMT process and enhanced the cells' invasive and migratory abilities. This study demonstrates that ESRP1 is a potential breast cancer prognostic marker with subtype specificity and its value as a molecular target needs to be accurately assessed in the context of breast cancer subtypes, as ESRP1 function may be highly dependent on the ER background.</p>","PeriodicalId":7437,"journal":{"name":"American journal of cancer research","volume":"15 6","pages":"2807-2825"},"PeriodicalIF":3.6,"publicationDate":"2025-06-25","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12256416/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144641501","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":"Resistance patterns of non-small cell lung cancer treated with third-generation epidermal growth factor receptor-tyrosine kinase inhibitors.","authors":"Nana Chen, Feng Zhao, Lu Yang, Xiaojing Tan, Dongfeng Wang, Xin Ye, Zhigang Wei","doi":"10.62347/ANQD9699","DOIUrl":"10.62347/ANQD9699","url":null,"abstract":"<p><p>The third-generation epidermal growth factor receptor (EGFR)-tyrosine kinase inhibitors (TKIs) are the preferred therapy for patients with EGFR mutant non-small cell lung cancer (NSCLC); however, the therapy faces resistance challenges. We aimed to clarify the resistance patterns of EGFR-TKIs in patients with EGFR mutant NSCLC. In this retrospective study, we analyzed 104 patients with advanced EGFR mutant NSCLC who experienced treatment failure of third-generation EGFR-TKIs. Resistance models were classified as 1) original site failure (OF), distant site failure (DF), and combined failure (ODF) based on the failure site or 2) oligo-progression (OP) and non-oligoprogression based on the disease progression (PD) pattern. Among the patients, 58.7% (n = 61 of 104) developed OF, while 25 (24.0%) and 18 (17.3%) developed DF and ODF, respectively. A high OP rate (76.9%, n = 80) was observed, with primary progression accounting for 30.8%. OF was related to sex (odds ratio = 3.961, 95% confidence interval: 1.629-9.631, P = 0.002). Over 50% of patients with third-generation EGFR-TKI treatment failure developed OF. Sex, central nervous system metastases, and disease stage influenced the resistance patterns of the EGFR-TKI therapy.</p>","PeriodicalId":7437,"journal":{"name":"American journal of cancer research","volume":"15 6","pages":"2843-2854"},"PeriodicalIF":3.6,"publicationDate":"2025-06-25","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12256412/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144641518","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":"Splicing factor 3b subunit 4 (SF3b4) is mediated by EP300 and CREBBP to promote colorectal cancer (CRC) proliferation by enhancing autophagy.","authors":"Tianhao Wu, Zhongxiang Xiao, Bowen Su, Zaihua Yan, Yv Zhao, Cheng Huang, Lu Zhou, Hongpeng Tian, Guangjun Zhang","doi":"10.62347/AHXI2343","DOIUrl":"10.62347/AHXI2343","url":null,"abstract":"<p><p>Splicing factor 3b subunit 4 (SF3b4) is closely associated with cancer development. As a core subunit of the SF3b complex, SF3b4 participates in regulating alternative splicing, and its abnormal expression is linked to the onset of malignant tumors. However, the role of SF3b4 in colorectal cancer (CRC) remains undefined. This study demonstrates that in CRC, E1A binding protein p300 (EP300) and CREB binding protein (CREBBP) regulate SF3b4 expression by activating Histone H3 lysine 27 acetylation (H3K27ac) on the SF3b4 promoter. Additionally, enhanced autophagy counteracts the proliferation-inhibitory effect of SF3b4 knockdown in CRC cells. Implications Statement: SF3b4 may promote CRC proliferation by enhancing cellular autophagy. SF3b4 acts as a potential oncogene in CRC tumorigenesis and progression. SF3b4 serves as a promising prognostic biomarker for CRC.</p>","PeriodicalId":7437,"journal":{"name":"American journal of cancer research","volume":"15 6","pages":"2826-2842"},"PeriodicalIF":3.6,"publicationDate":"2025-06-25","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12256420/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144641520","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":"Identification of CDK2 as a key apoptotic gene for predicting cervical cancer prognosis using bioinformatics and machine learning.","authors":"Miao-Miao Li, Min Song, Shu-Xia Wu, Xing-Ye Ren","doi":"10.62347/RUXJ3980","DOIUrl":"10.62347/RUXJ3980","url":null,"abstract":"<p><strong>Objectives: </strong>This study aimed to identify apoptosis - related genes with diagnostic and prognostic value in cervical cancer (CC) using integrated bioinformatics and machine learning approaches.</p><p><strong>Methods: </strong>Gene expression datasets were obtained from the National Center for Biotechnology Information Gene Expression Omnibus (GEO) and the Cancer Genome Atlas (TCGA), with GSE192897 used as the training set. A total of 451 differentially expressed genes (DEGs) were identified, including 221 upregulated and 230 downregulated genes. Eleven apoptosis - related upregulated DEGs were selected for further analysis using three machine learning algorithms: random forest, logistic regression, and support vector machine. Validation was performed using GSE192897, GSE166466, and TCGA-CESC datasets.</p><p><strong>Results: </strong>Among the evaluated genes, cyclin-dependent kinase 2 (CDK2) consistently achieved an AUC > 0.8 in all three validation datasets and had a weighted sum rank > 10, meeting stringent selection criteria. In a CC mouse model, CDK2 expression was significantly elevated and positively correlated with squamous cell carcinoma antigen, carcinoembryonic antigen, vascular endothelial growth factor, and heparanase. siRNA-mediated knockdown of CDK2 reduced cell proliferation and migration while promoting apoptosis. Mice with high CDK2 expression showed significantly lower 4-week survival rates, indicating poor prognosis.</p><p><strong>Conclusions: </strong>This study identified CDK2 as a key apoptosis - related gene with strong diagnostic and prognostic value in cervical cancer. CDK2 promotes tumor progression and is associated with poor survival, suggesting its potential as a biomarker and therapeutic target for personalized treatment strategies in CC.</p>","PeriodicalId":7437,"journal":{"name":"American journal of cancer research","volume":"15 6","pages":"2750-2764"},"PeriodicalIF":3.6,"publicationDate":"2025-06-25","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12256406/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144641462","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":"Are they all the same? Different effects of opioid types on survival in metastatic NSCLC receiving nivolumab.","authors":"Onur Yazdan Balçık, İsmail Beypınar, Semiha Urvay, Müslih Ürün, Berrak Erçek, Canan Yıldız, Murat Araz, Ahmet Oruç, Yusuf İlhan, Arif Hakan Önder, Hacer Demir","doi":"10.62347/VHDF3303","DOIUrl":"10.62347/VHDF3303","url":null,"abstract":"<p><p>The aim of this study was to evaluate the effects of concurrent opioid analgesic (OA) use and types of OA on progression-free survival (PFS) and overall survival (OS) in non-small cell lung cancer (NSCLC) patients receiving nivolumab. This observational, retrospective study included patients with pathologically confirmed, driver mutations negative metastatic NSCLC at five different hospitals in Turkey between 2018 and 2024. A total of 209 patients were included in this study. Of these patients, 113 (54.1%) used OA. 86 (41.1%) patients were using tramadol, and 48 (23.4%) were using fentanyl. The median survival of the group without OA was significant in the univariate analysis compared to that of the group with OA PFS (7 vs. 4 months, P = 0.006) an OS (8 vs. 14 months, P = 0.003). The group with bone metastases had worse OS than the group without bone metastases [7 vs. 15 months, HR (95% CI) = 1.810 (1.064-3.079), (P = 0.029)]. In the group without bone metastases, patients on tramadol had worse PFS than patients not on tramadol [5 vs. 8 months, HR (95% CI) = 2.260 (1.097-4.655), (P = 0.027)]. In conclusion, OA use was associated with poor PFS and OS. Fentanyl use led to worse OS in the group with bone metastases, whereas tramadol use led to worse PFS in the group without bone metastases. The prognostic impact of OA may differ according to the site of metastasis; therefore, prospective studies that include the type of OA are needed.</p>","PeriodicalId":7437,"journal":{"name":"American journal of cancer research","volume":"15 6","pages":"2794-2806"},"PeriodicalIF":3.6,"publicationDate":"2025-06-25","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12256418/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144641489","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":"METTL3-mediated m⁶A methylation of lncRNA PVT1 promotes the progression of oral squamous cell carcinoma via the miR-185-5p/SERPINB4 axis.","authors":"Cheng Chen, Jun Li, Bingwu Yang, Li Kong, Di Zhang, Jianran Guo, Longxun Zhou, Guangliang Bai, Huaqiang Zhao, Zhen Meng","doi":"10.62347/HERV8396","DOIUrl":"10.62347/HERV8396","url":null,"abstract":"<p><p>Oral squamous cell carcinoma (OSCC) is one of the most common malignant tumors of the head and neck region. Plasmacytoma variant translocation 1 (PVT1), a long non-coding RNA (lncRNA), has been found to be overexpressed in multiple cancers, including OSCC. However, the upstream and downstream regulatory mechanisms through which PVT1 influences the malignant progression of OSCC remain to be further explored. In this study, PVT1 was confirmed to be overexpressed in OSCC tissues, and its roles in promoting OSCC cell proliferation, migration and invasion were identified. RNA-sequencing was used to screen the candidate target genes of PVT1, among which serpin family B member 4 (SERPINB4) was the most downregulated. SERPINB4 promoted OSCC cell proliferation, migration and invasion. In addition, mechanistic investigations demonstrated that PVT1 regulates SERPINB4 by sponging miR-185-5p in OSCC cells. Furthermore, SERPINB4 overexpression or miR-185-5p knockdown partly restores the decrease of OSCC cell proliferation and metastasis induced by PVT1 knockdown. Additional studies revealed that methyltransferase-like 3 (METTL3)-mediated N6-methyladenosine (m⁶A) modification induced the upregulation of PVT1 by stabilizing its RNA transcript. In conclusion, elevated expression of PVT1 in OSCC is associated with poor prognosis and promotes tumor development. METTL3 promotes PVT1 stability through m⁶A deposition and upregulates its expression in OSCC, which could upregulate SERPINB4 by sponging miR-185-5p, and ultimately promoting OSCC growth and metastasis. These findings suggest that PVT1 could serve as a potential biomarker and therapeutic target for OSCC.</p>","PeriodicalId":7437,"journal":{"name":"American journal of cancer research","volume":"15 6","pages":"2872-2889"},"PeriodicalIF":3.6,"publicationDate":"2025-06-25","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12256411/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144641469","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":"Erratum: MiR-1205 functions as a tumor suppressor by disconnecting the synergy between KRAS and MDM4/E2F1 in non-small cell lung cancer.","authors":"Hong Yan, Xiaoying Chen, Yu Li, Lei Fan, Yusi Tai, Yang Zhou, Yuxiang Chen, Xinming Qi, Ruimin Huang, Jin Ren","doi":"10.62347/XVNE7528","DOIUrl":"https://doi.org/10.62347/XVNE7528","url":null,"abstract":"<p><p>[This corrects the article on p. 312 in vol. 9, PMID: 30906631.].</p>","PeriodicalId":7437,"journal":{"name":"American journal of cancer research","volume":"15 6","pages":"2908-2910"},"PeriodicalIF":3.6,"publicationDate":"2025-06-25","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12256402/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144641500","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":"Impact of clinicopathological features of meibomian gland adenocarcinoma on the outcomes of surgical resection combined with eyelid reconstruction.","authors":"Huiqin Zhan, Hanyan Mao, De Wu, Jilin Zhou","doi":"10.62347/QRFV7325","DOIUrl":"10.62347/QRFV7325","url":null,"abstract":"<p><p>This study aims to investigate the clinical and pathological characteristics of meibomian gland carcinoma (MGC) and their impact on the outcomes of surgical resection combined with eyelid defect reconstruction. A retrospective study was conducted on 128 patients diagnosed with MGC between December 2020 and January 2022. Demographic, clinical, pathological, surgical, and postoperative follow-up data were collected from the medical records. Patients were divided into two groups based on their total aesthetic outcome score: the satisfied group (score ≥27, n=87) and the dissatisfied group (score <27, n=41). Additionally, patients were categorized into recurrence (n=29) and non-recurrence groups (n=99) based on postoperative recurrence status. Results showed that age (OR=1.080, 95% CI: 1.015~1.149, P=0.015), tumor size (OR=1.625, 95% CI: 0.681~0.887, P<0.001), and tumor stage (OR1=0.007, 95% CI: 0.001~0.070; OR2=0.019, 95% CI: 0.003~0.145, P<0.001) significantly influenced aesthetic outcomes following surgical resection combined with eyelid defect reconstruction. Recurrence analysis indicated that tumor size (HR=1.224, 95% CI: 1.091~1.374, P<0.001) and stage (HR1=0.008, 95% CI: 0.001~0.084; HR2=0.051, 95% CI: 0.011~0.242, P<0.001) were significant factors affecting the recurrence. Receiver operating characteristic (ROC) curve analysis demonstrated that the combined prediction of clinical and pathological features had the highest efficacy in predicting aesthetic outcomes and tumor recurrence following surgical resection and reconstruction (aesthetic outcome: Z=5.544, 3.110, 4.527; recurrence: Z=3.319, 2.986; all P<0.05). The Kaplan-Meier survival curve revealed significant differences in disease-free survival rates across different stages of tumors (χ²=29.275, P=0.005). In conclusion, the surgical treatment of MGC should consider clinical and pathological characteristics such as patient age, tumor size and stage, and individualized surgical and reconstruction plans should be developed accordingly. The combined prediction of aesthetic outcomes and recurrence risk can enhance surgical efifcacy and improve patient prognosis.</p>","PeriodicalId":7437,"journal":{"name":"American journal of cancer research","volume":"15 6","pages":"2765-2778"},"PeriodicalIF":3.6,"publicationDate":"2025-06-25","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12256423/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144641465","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":"GDF15 promotes gallbladder cancer progression by activating the NF-κB mediated Vascular Endothelial Growth Factor A (VEGFA) expression.","authors":"Mina Joo, Hyo Jin Lee, Jin-Man Kim","doi":"10.62347/NAZM2261","DOIUrl":"10.62347/NAZM2261","url":null,"abstract":"<p><p>Growth differentiation factor 15 (GDF15) has been found to be elevated in several different types of cancer, thus demonstrating its potential for use as a biomarker. Although its physiological and pathophysiological roles in cancer are increasingly understood, the specific functions and molecular mechanisms of GDF15 in gallbladder cancer remain unclear and require further investigation. Immunohistochemical staining was performed to evaluate the expression of GDF15 in tissue samples from 57 patients with gallbladder cancer. The biological function of GDF15 and the molecular mechanism underlying this were further elucidated through knockdown experiments in NOZ and OCUG-1 gallbladder cancer cell lines. Our results demonstrate that there was a significant correlation be-tween high GDF15 expression and poor survival indicating a poor prognosis in individuals with gallbladder cancer. NanoString analysis results showed that VEGFA, a key angiogenic factor, was significantly upregulated in the GDF15 high-expression group. Moreover, GDF15 knockdown significantly reduced cell motility, as well as migration and invasion. Additionally, GDF15 knockdown in gallbladder cancer cells decreased VEGFA expression via the AKT/NF-κB pathway. Taken together, these results suggest that GDF15 contributes to the aggressive behavior of gallbladder cancer by promoting activation of the AKT/NF-κB pathway. These findings suggest that the GDF15 signaling pathway may represent a promising therapeutic target for gallbladder cancer treatment.</p>","PeriodicalId":7437,"journal":{"name":"American journal of cancer research","volume":"15 6","pages":"2779-2793"},"PeriodicalIF":3.6,"publicationDate":"2025-06-25","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12256407/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144641503","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}