Baseline serum EV-miR-1-3p as a protective factor and biomarker for hepatocellular carcinoma development after HCV eradication
Background Direct-acting antiviral (DAA) therapy for chronic hepatitis C (CHC) achieves high sustained virologic response (SVR) rates; however, hepatocellular carcinoma (HCC) can still develop after viral eradication. Reliable biomarkers for predicting the post-SVR HCC risk are lacking. This study a...
Saved in:
| Published in | Journal of translational medicine Vol. 23; no. 1; pp. 722 - 15 |
|---|---|
| Main Authors | , , , , , , , |
| Format | Journal Article |
| Language | English |
| Published |
London
BioMed Central
01.07.2025
BioMed Central Ltd BMC |
| Subjects | |
| Online Access | Get full text |
| ISSN | 1479-5876 1479-5876 |
| DOI | 10.1186/s12967-025-06765-z |
Cover
| Abstract | Background
Direct-acting antiviral (DAA) therapy for chronic hepatitis C (CHC) achieves high sustained virologic response (SVR) rates; however, hepatocellular carcinoma (HCC) can still develop after viral eradication. Reliable biomarkers for predicting the post-SVR HCC risk are lacking. This study aimed to identify baseline serum extracellular vesicle microRNAs (EV-miRNAs) associated with HCC development following SVR.
Materials and methods
Eleven CHC patients who achieved SVR were retrospectively enrolled as a discovery cohort to identify candidate EV-miRNAs at SVR12 predictive of future HCC. An independent validation cohort of 89 CHC patients was also analyzed. HCC development was defined as the occurrence of HCC at ≥ 12 months after SVR. EV-miRNA profiles were assessed by small RNA sequencing and validated using a miRNA enzyme immunoassay (miREIA).
Results
In the discovery cohort, four EV-miRNAs (EV-miR-1-3p, EV-miR-148a-3p, EV-miR-223-3p, and EV-miR-4433b-5p) were significantly different between patients who later developed HCC and those who remained HCC-free at SVR12. In the 89-patient validation cohort, 51 (57.3%) developed HCC with a median disease-free survival (DFS) of 23.1 months, and 12 (13.5%) patients died during a median follow-up of 77 months. High baseline EV-miR-1-3p and EV-miR-148a-3p levels and low EV-miR-4433b-5p were associated with remaining HCC-free. Elevated EV-miR-1-3p and EV-miR-148a-3p levels were also correlated with longer DFS (
p
< 0.05). In multivariate analysis, EV-miR-1-3p was the only independent predictor of longer DFS (adjusted hazard ratio [HR] 0.459,
p
= 0.014) and improved overall survival (OS) (adjusted HR 0.390,
p
= 0.016) after SVR12. Among all biomarkers evaluated, baseline EV-miR-1-3p demonstrated the highest predictive accuracy for HCC occurrence (area under the curve [AUC] 0.843, vs. 0.769 for alpha-fetoprotein [AFP] and 0.755 for FIB-4;
p
< 0.001) and for OS (AUC 0.876, vs. 0.480 for AFP and 0.655 for FIB-4;
p
< 0.001). Furthermore, patients with high EV-miR-1-3p levels showed higher platelet counts and albumin, and a lower proportion with FIB-4 ≥ 3.25, suggesting that high EV-miR-1-3p reflects better preserved liver function and less advanced fibrosis.
Conclusions
Baseline serum EV-miR-1-3p serves as a protective biomarker for stratifying HCC risk and predicting survival in CHC patients after HCV eradication via DAA therapy. |
|---|---|
| AbstractList | Direct-acting antiviral (DAA) therapy for chronic hepatitis C (CHC) achieves high sustained virologic response (SVR) rates; however, hepatocellular carcinoma (HCC) can still develop after viral eradication. Reliable biomarkers for predicting the post-SVR HCC risk are lacking. This study aimed to identify baseline serum extracellular vesicle microRNAs (EV-miRNAs) associated with HCC development following SVR.BACKGROUNDDirect-acting antiviral (DAA) therapy for chronic hepatitis C (CHC) achieves high sustained virologic response (SVR) rates; however, hepatocellular carcinoma (HCC) can still develop after viral eradication. Reliable biomarkers for predicting the post-SVR HCC risk are lacking. This study aimed to identify baseline serum extracellular vesicle microRNAs (EV-miRNAs) associated with HCC development following SVR.Eleven CHC patients who achieved SVR were retrospectively enrolled as a discovery cohort to identify candidate EV-miRNAs at SVR12 predictive of future HCC. An independent validation cohort of 89 CHC patients was also analyzed. HCC development was defined as the occurrence of HCC at ≥ 12 months after SVR. EV-miRNA profiles were assessed by small RNA sequencing and validated using a miRNA enzyme immunoassay (miREIA).MATERIALS AND METHODSEleven CHC patients who achieved SVR were retrospectively enrolled as a discovery cohort to identify candidate EV-miRNAs at SVR12 predictive of future HCC. An independent validation cohort of 89 CHC patients was also analyzed. HCC development was defined as the occurrence of HCC at ≥ 12 months after SVR. EV-miRNA profiles were assessed by small RNA sequencing and validated using a miRNA enzyme immunoassay (miREIA).In the discovery cohort, four EV-miRNAs (EV-miR-1-3p, EV-miR-148a-3p, EV-miR-223-3p, and EV-miR-4433b-5p) were significantly different between patients who later developed HCC and those who remained HCC-free at SVR12. In the 89-patient validation cohort, 51 (57.3%) developed HCC with a median disease-free survival (DFS) of 23.1 months, and 12 (13.5%) patients died during a median follow-up of 77 months. High baseline EV-miR-1-3p and EV-miR-148a-3p levels and low EV-miR-4433b-5p were associated with remaining HCC-free. Elevated EV-miR-1-3p and EV-miR-148a-3p levels were also correlated with longer DFS (p < 0.05). In multivariate analysis, EV-miR-1-3p was the only independent predictor of longer DFS (adjusted hazard ratio [HR] 0.459, p = 0.014) and improved overall survival (OS) (adjusted HR 0.390, p = 0.016) after SVR12. Among all biomarkers evaluated, baseline EV-miR-1-3p demonstrated the highest predictive accuracy for HCC occurrence (area under the curve [AUC] 0.843, vs. 0.769 for alpha-fetoprotein [AFP] and 0.755 for FIB-4; p < 0.001) and for OS (AUC 0.876, vs. 0.480 for AFP and 0.655 for FIB-4; p < 0.001). Furthermore, patients with high EV-miR-1-3p levels showed higher platelet counts and albumin, and a lower proportion with FIB-4 ≥ 3.25, suggesting that high EV-miR-1-3p reflects better preserved liver function and less advanced fibrosis.RESULTSIn the discovery cohort, four EV-miRNAs (EV-miR-1-3p, EV-miR-148a-3p, EV-miR-223-3p, and EV-miR-4433b-5p) were significantly different between patients who later developed HCC and those who remained HCC-free at SVR12. In the 89-patient validation cohort, 51 (57.3%) developed HCC with a median disease-free survival (DFS) of 23.1 months, and 12 (13.5%) patients died during a median follow-up of 77 months. High baseline EV-miR-1-3p and EV-miR-148a-3p levels and low EV-miR-4433b-5p were associated with remaining HCC-free. Elevated EV-miR-1-3p and EV-miR-148a-3p levels were also correlated with longer DFS (p < 0.05). In multivariate analysis, EV-miR-1-3p was the only independent predictor of longer DFS (adjusted hazard ratio [HR] 0.459, p = 0.014) and improved overall survival (OS) (adjusted HR 0.390, p = 0.016) after SVR12. Among all biomarkers evaluated, baseline EV-miR-1-3p demonstrated the highest predictive accuracy for HCC occurrence (area under the curve [AUC] 0.843, vs. 0.769 for alpha-fetoprotein [AFP] and 0.755 for FIB-4; p < 0.001) and for OS (AUC 0.876, vs. 0.480 for AFP and 0.655 for FIB-4; p < 0.001). Furthermore, patients with high EV-miR-1-3p levels showed higher platelet counts and albumin, and a lower proportion with FIB-4 ≥ 3.25, suggesting that high EV-miR-1-3p reflects better preserved liver function and less advanced fibrosis.Baseline serum EV-miR-1-3p serves as a protective biomarker for stratifying HCC risk and predicting survival in CHC patients after HCV eradication via DAA therapy.CONCLUSIONSBaseline serum EV-miR-1-3p serves as a protective biomarker for stratifying HCC risk and predicting survival in CHC patients after HCV eradication via DAA therapy. Background Direct-acting antiviral (DAA) therapy for chronic hepatitis C (CHC) achieves high sustained virologic response (SVR) rates; however, hepatocellular carcinoma (HCC) can still develop after viral eradication. Reliable biomarkers for predicting the post-SVR HCC risk are lacking. This study aimed to identify baseline serum extracellular vesicle microRNAs (EV-miRNAs) associated with HCC development following SVR. Materials and methods Eleven CHC patients who achieved SVR were retrospectively enrolled as a discovery cohort to identify candidate EV-miRNAs at SVR12 predictive of future HCC. An independent validation cohort of 89 CHC patients was also analyzed. HCC development was defined as the occurrence of HCC at [greater than or equal to] 12 months after SVR. EV-miRNA profiles were assessed by small RNA sequencing and validated using a miRNA enzyme immunoassay (miREIA). Results In the discovery cohort, four EV-miRNAs (EV-miR-1-3p, EV-miR-148a-3p, EV-miR-223-3p, and EV-miR-4433b-5p) were significantly different between patients who later developed HCC and those who remained HCC-free at SVR12. In the 89-patient validation cohort, 51 (57.3%) developed HCC with a median disease-free survival (DFS) of 23.1 months, and 12 (13.5%) patients died during a median follow-up of 77 months. High baseline EV-miR-1-3p and EV-miR-148a-3p levels and low EV-miR-4433b-5p were associated with remaining HCC-free. Elevated EV-miR-1-3p and EV-miR-148a-3p levels were also correlated with longer DFS (p < 0.05). In multivariate analysis, EV-miR-1-3p was the only independent predictor of longer DFS (adjusted hazard ratio [HR] 0.459, p = 0.014) and improved overall survival (OS) (adjusted HR 0.390, p = 0.016) after SVR12. Among all biomarkers evaluated, baseline EV-miR-1-3p demonstrated the highest predictive accuracy for HCC occurrence (area under the curve [AUC] 0.843, vs. 0.769 for alpha-fetoprotein [AFP] and 0.755 for FIB-4; p < 0.001) and for OS (AUC 0.876, vs. 0.480 for AFP and 0.655 for FIB-4; p < 0.001). Furthermore, patients with high EV-miR-1-3p levels showed higher platelet counts and albumin, and a lower proportion with FIB-4 [greater than or equal to] 3.25, suggesting that high EV-miR-1-3p reflects better preserved liver function and less advanced fibrosis. Conclusions Baseline serum EV-miR-1-3p serves as a protective biomarker for stratifying HCC risk and predicting survival in CHC patients after HCV eradication via DAA therapy. Keywords: Hepatocellular carcinoma, Extracellular vesicle MiRNA, SVR12, Direct-acting antivirals Background Direct-acting antiviral (DAA) therapy for chronic hepatitis C (CHC) achieves high sustained virologic response (SVR) rates; however, hepatocellular carcinoma (HCC) can still develop after viral eradication. Reliable biomarkers for predicting the post-SVR HCC risk are lacking. This study aimed to identify baseline serum extracellular vesicle microRNAs (EV-miRNAs) associated with HCC development following SVR. Materials and methods Eleven CHC patients who achieved SVR were retrospectively enrolled as a discovery cohort to identify candidate EV-miRNAs at SVR12 predictive of future HCC. An independent validation cohort of 89 CHC patients was also analyzed. HCC development was defined as the occurrence of HCC at ≥ 12 months after SVR. EV-miRNA profiles were assessed by small RNA sequencing and validated using a miRNA enzyme immunoassay (miREIA). Results In the discovery cohort, four EV-miRNAs (EV-miR-1-3p, EV-miR-148a-3p, EV-miR-223-3p, and EV-miR-4433b-5p) were significantly different between patients who later developed HCC and those who remained HCC-free at SVR12. In the 89-patient validation cohort, 51 (57.3%) developed HCC with a median disease-free survival (DFS) of 23.1 months, and 12 (13.5%) patients died during a median follow-up of 77 months. High baseline EV-miR-1-3p and EV-miR-148a-3p levels and low EV-miR-4433b-5p were associated with remaining HCC-free. Elevated EV-miR-1-3p and EV-miR-148a-3p levels were also correlated with longer DFS ( p < 0.05). In multivariate analysis, EV-miR-1-3p was the only independent predictor of longer DFS (adjusted hazard ratio [HR] 0.459, p = 0.014) and improved overall survival (OS) (adjusted HR 0.390, p = 0.016) after SVR12. Among all biomarkers evaluated, baseline EV-miR-1-3p demonstrated the highest predictive accuracy for HCC occurrence (area under the curve [AUC] 0.843, vs. 0.769 for alpha-fetoprotein [AFP] and 0.755 for FIB-4; p < 0.001) and for OS (AUC 0.876, vs. 0.480 for AFP and 0.655 for FIB-4; p < 0.001). Furthermore, patients with high EV-miR-1-3p levels showed higher platelet counts and albumin, and a lower proportion with FIB-4 ≥ 3.25, suggesting that high EV-miR-1-3p reflects better preserved liver function and less advanced fibrosis. Conclusions Baseline serum EV-miR-1-3p serves as a protective biomarker for stratifying HCC risk and predicting survival in CHC patients after HCV eradication via DAA therapy. Direct-acting antiviral (DAA) therapy for chronic hepatitis C (CHC) achieves high sustained virologic response (SVR) rates; however, hepatocellular carcinoma (HCC) can still develop after viral eradication. Reliable biomarkers for predicting the post-SVR HCC risk are lacking. This study aimed to identify baseline serum extracellular vesicle microRNAs (EV-miRNAs) associated with HCC development following SVR. Eleven CHC patients who achieved SVR were retrospectively enrolled as a discovery cohort to identify candidate EV-miRNAs at SVR12 predictive of future HCC. An independent validation cohort of 89 CHC patients was also analyzed. HCC development was defined as the occurrence of HCC at ≥ 12 months after SVR. EV-miRNA profiles were assessed by small RNA sequencing and validated using a miRNA enzyme immunoassay (miREIA). In the discovery cohort, four EV-miRNAs (EV-miR-1-3p, EV-miR-148a-3p, EV-miR-223-3p, and EV-miR-4433b-5p) were significantly different between patients who later developed HCC and those who remained HCC-free at SVR12. In the 89-patient validation cohort, 51 (57.3%) developed HCC with a median disease-free survival (DFS) of 23.1 months, and 12 (13.5%) patients died during a median follow-up of 77 months. High baseline EV-miR-1-3p and EV-miR-148a-3p levels and low EV-miR-4433b-5p were associated with remaining HCC-free. Elevated EV-miR-1-3p and EV-miR-148a-3p levels were also correlated with longer DFS (p < 0.05). In multivariate analysis, EV-miR-1-3p was the only independent predictor of longer DFS (adjusted hazard ratio [HR] 0.459, p = 0.014) and improved overall survival (OS) (adjusted HR 0.390, p = 0.016) after SVR12. Among all biomarkers evaluated, baseline EV-miR-1-3p demonstrated the highest predictive accuracy for HCC occurrence (area under the curve [AUC] 0.843, vs. 0.769 for alpha-fetoprotein [AFP] and 0.755 for FIB-4; p < 0.001) and for OS (AUC 0.876, vs. 0.480 for AFP and 0.655 for FIB-4; p < 0.001). Furthermore, patients with high EV-miR-1-3p levels showed higher platelet counts and albumin, and a lower proportion with FIB-4 ≥ 3.25, suggesting that high EV-miR-1-3p reflects better preserved liver function and less advanced fibrosis. Baseline serum EV-miR-1-3p serves as a protective biomarker for stratifying HCC risk and predicting survival in CHC patients after HCV eradication via DAA therapy. Abstract Background Direct-acting antiviral (DAA) therapy for chronic hepatitis C (CHC) achieves high sustained virologic response (SVR) rates; however, hepatocellular carcinoma (HCC) can still develop after viral eradication. Reliable biomarkers for predicting the post-SVR HCC risk are lacking. This study aimed to identify baseline serum extracellular vesicle microRNAs (EV-miRNAs) associated with HCC development following SVR. Materials and methods Eleven CHC patients who achieved SVR were retrospectively enrolled as a discovery cohort to identify candidate EV-miRNAs at SVR12 predictive of future HCC. An independent validation cohort of 89 CHC patients was also analyzed. HCC development was defined as the occurrence of HCC at ≥ 12 months after SVR. EV-miRNA profiles were assessed by small RNA sequencing and validated using a miRNA enzyme immunoassay (miREIA). Results In the discovery cohort, four EV-miRNAs (EV-miR-1-3p, EV-miR-148a-3p, EV-miR-223-3p, and EV-miR-4433b-5p) were significantly different between patients who later developed HCC and those who remained HCC-free at SVR12. In the 89-patient validation cohort, 51 (57.3%) developed HCC with a median disease-free survival (DFS) of 23.1 months, and 12 (13.5%) patients died during a median follow-up of 77 months. High baseline EV-miR-1-3p and EV-miR-148a-3p levels and low EV-miR-4433b-5p were associated with remaining HCC-free. Elevated EV-miR-1-3p and EV-miR-148a-3p levels were also correlated with longer DFS (p < 0.05). In multivariate analysis, EV-miR-1-3p was the only independent predictor of longer DFS (adjusted hazard ratio [HR] 0.459, p = 0.014) and improved overall survival (OS) (adjusted HR 0.390, p = 0.016) after SVR12. Among all biomarkers evaluated, baseline EV-miR-1-3p demonstrated the highest predictive accuracy for HCC occurrence (area under the curve [AUC] 0.843, vs. 0.769 for alpha-fetoprotein [AFP] and 0.755 for FIB-4; p < 0.001) and for OS (AUC 0.876, vs. 0.480 for AFP and 0.655 for FIB-4; p < 0.001). Furthermore, patients with high EV-miR-1-3p levels showed higher platelet counts and albumin, and a lower proportion with FIB-4 ≥ 3.25, suggesting that high EV-miR-1-3p reflects better preserved liver function and less advanced fibrosis. Conclusions Baseline serum EV-miR-1-3p serves as a protective biomarker for stratifying HCC risk and predicting survival in CHC patients after HCV eradication via DAA therapy. Direct-acting antiviral (DAA) therapy for chronic hepatitis C (CHC) achieves high sustained virologic response (SVR) rates; however, hepatocellular carcinoma (HCC) can still develop after viral eradication. Reliable biomarkers for predicting the post-SVR HCC risk are lacking. This study aimed to identify baseline serum extracellular vesicle microRNAs (EV-miRNAs) associated with HCC development following SVR. Eleven CHC patients who achieved SVR were retrospectively enrolled as a discovery cohort to identify candidate EV-miRNAs at SVR12 predictive of future HCC. An independent validation cohort of 89 CHC patients was also analyzed. HCC development was defined as the occurrence of HCC at [greater than or equal to] 12 months after SVR. EV-miRNA profiles were assessed by small RNA sequencing and validated using a miRNA enzyme immunoassay (miREIA). In the discovery cohort, four EV-miRNAs (EV-miR-1-3p, EV-miR-148a-3p, EV-miR-223-3p, and EV-miR-4433b-5p) were significantly different between patients who later developed HCC and those who remained HCC-free at SVR12. In the 89-patient validation cohort, 51 (57.3%) developed HCC with a median disease-free survival (DFS) of 23.1 months, and 12 (13.5%) patients died during a median follow-up of 77 months. High baseline EV-miR-1-3p and EV-miR-148a-3p levels and low EV-miR-4433b-5p were associated with remaining HCC-free. Elevated EV-miR-1-3p and EV-miR-148a-3p levels were also correlated with longer DFS (p < 0.05). In multivariate analysis, EV-miR-1-3p was the only independent predictor of longer DFS (adjusted hazard ratio [HR] 0.459, p = 0.014) and improved overall survival (OS) (adjusted HR 0.390, p = 0.016) after SVR12. Among all biomarkers evaluated, baseline EV-miR-1-3p demonstrated the highest predictive accuracy for HCC occurrence (area under the curve [AUC] 0.843, vs. 0.769 for alpha-fetoprotein [AFP] and 0.755 for FIB-4; p < 0.001) and for OS (AUC 0.876, vs. 0.480 for AFP and 0.655 for FIB-4; p < 0.001). Furthermore, patients with high EV-miR-1-3p levels showed higher platelet counts and albumin, and a lower proportion with FIB-4 [greater than or equal to] 3.25, suggesting that high EV-miR-1-3p reflects better preserved liver function and less advanced fibrosis. Baseline serum EV-miR-1-3p serves as a protective biomarker for stratifying HCC risk and predicting survival in CHC patients after HCV eradication via DAA therapy. |
| ArticleNumber | 722 |
| Audience | Academic |
| Author | Chu, LiChieh Julie Lin, Yung-Chang Ku, Wei-Ting Lin, Po-Ting Liu, Hsuan Teng, Wei Lin, Chun-Yen Chen, Guan-Ting |
| Author_xml | – sequence: 1 givenname: Wei surname: Teng fullname: Teng, Wei organization: Department of Gastroenterology and Hepatology, Chang Gung Memorial Hospital, Linkou Medical Center, College of Medicine, Chang Gung University, Liver Research Center, Chang Gung Memorial Hospital, Linkou Medical Center – sequence: 2 givenname: Wei-Ting surname: Ku fullname: Ku, Wei-Ting organization: Department of Gastroenterology and Hepatology, Chang Gung Memorial Hospital, Linkou Medical Center, Graduate Institute of Biomedical Sciences, College of Medicine, Chang Gung University – sequence: 3 givenname: Po-Ting surname: Lin fullname: Lin, Po-Ting organization: Department of Gastroenterology and Hepatology, Chang Gung Memorial Hospital, Linkou Medical Center, College of Medicine, Chang Gung University – sequence: 4 givenname: Guan-Ting surname: Chen fullname: Chen, Guan-Ting organization: Department of Gastroenterology and Hepatology, Chang Gung Memorial Hospital, Linkou Medical Center – sequence: 5 givenname: LiChieh Julie surname: Chu fullname: Chu, LiChieh Julie organization: Graduate Institute of Biomedical Sciences, College of Medicine, Chang Gung University, Molecular Medicine Research Center, Chang Gung University – sequence: 6 givenname: Hsuan surname: Liu fullname: Liu, Hsuan organization: Graduate Institute of Biomedical Sciences, College of Medicine, Chang Gung University, Molecular Medicine Research Center, Chang Gung University, Department of Cell and Molecular Biology, College of Medicine, Chang Gung University, Department of Pathology, Chang Gung Memorial Hospital, Linkou Medical Center – sequence: 7 givenname: Yung-Chang surname: Lin fullname: Lin, Yung-Chang organization: College of Medicine, Chang Gung University, Department of Hematology-Oncology, Chang Gung Memorial Hospital, Linkou Medical Center – sequence: 8 givenname: Chun-Yen surname: Lin fullname: Lin, Chun-Yen email: chunyenlin@gmail.com organization: Department of Gastroenterology and Hepatology, Chang Gung Memorial Hospital, Linkou Medical Center, College of Medicine, Chang Gung University |
| BackLink | https://www.ncbi.nlm.nih.gov/pubmed/40598241$$D View this record in MEDLINE/PubMed |
| BookMark | eNp9kk1rFTEUhgep2A_9Ay4k4MbN1MnXzGQl9VJtoSCIdhvOJGduU2eSazJzwS787eZ2aukFkSwSTp735ZzkPS4OfPBYFK9pdUppW79PlKm6KSsmy6pualnePSuOqGhUKdumPnhyPiyOU7qtKiakUC-KQ1FJ1TJBj4rfHyHh4DyShHEeyfl1ObqvJS35hkAiQDYxTGgmt0XSg5lCJOAt6VwYIf7ASPpcucENTMHgMMwDRGIgGuczQCxucQibEf1EoJ8yfrG6JhjBOgOTC_5l8byHIeGrh_2k-P7p_Nvqorz68vlydXZVGsn5VPYMsVVCUlQdN8ZWijELpmt72lUcesVt0-TZQPSy66QyLQoqLDTSUNlyxk-Ky8XXBrjVm-hy9790AKfvCyGuNcTJmQE12qYTtbWGGiVMU0NllJV1y5C1DYcue31YvDZzN6I1ebgIw57p_o13N3odtpoyxipJ2-zw7sEhhp8zpkmPLu2eDzyGOWnOWM2lUk2T0bcLuobcm_N9yJZmh-uzVtS8amu2o07_QeVlcXQmp6Z3ub4nePN0hsfm_wYjA2wBTAwpRewfEVrpXfr0kj6d06fv06fvsogvopRhv8aob8Mcff7Y_6n-ACIV3go |
| Cites_doi | 10.2147/IJN.S506542 10.1053/j.gastro.2018.11.053 10.7150/thno.30958 10.1016/j.jhep.2016.01.029 10.1038/cddis.2017.309 10.1016/j.jhep.2018.03.019 10.1111/j.1440-1746.2011.06785.x 10.3390/v16091485 10.1111/jvh.12745 10.1111/liv.13700 10.3389/fonc.2021.700649 10.3402/jev.v4.27066 10.1111/apt.14380 10.1111/jvh.13232 10.1016/j.jhep.2017.07.025 10.1111/jcmm.14045 10.1186/s10020-020-00259-y 10.1002/ijc.30521 10.3389/fcell.2021.652292 10.1111/jgh.15538 10.1245/s10434-017-6008-y 10.3390/biom10010150 10.1159/000343336 10.3390/ijms232415904 10.1016/j.jhep.2016.06.015 10.3322/caac.21660 10.3389/fgene.2022.865472 10.1111/jvh.12578 10.1007/s10620-022-07621-6 10.3390/pharmaceutics15092365 10.7326/0003-4819-158-5-201303050-00005 |
| ContentType | Journal Article |
| Copyright | The Author(s) 2025 2025. The Author(s). COPYRIGHT 2025 BioMed Central Ltd. The Author(s) 2025 2025 |
| Copyright_xml | – notice: The Author(s) 2025 – notice: 2025. The Author(s). – notice: COPYRIGHT 2025 BioMed Central Ltd. – notice: The Author(s) 2025 2025 |
| DBID | C6C AAYXX CITATION CGR CUY CVF ECM EIF NPM 7X8 5PM DOA |
| DOI | 10.1186/s12967-025-06765-z |
| DatabaseName | Springer Nature OA Free Journals CrossRef Medline MEDLINE MEDLINE (Ovid) MEDLINE MEDLINE PubMed MEDLINE - Academic PubMed Central (Full Participant titles) DOAJ Directory of Open Access Journals |
| DatabaseTitle | CrossRef MEDLINE Medline Complete MEDLINE with Full Text PubMed MEDLINE (Ovid) MEDLINE - Academic |
| DatabaseTitleList | MEDLINE - Academic MEDLINE |
| Database_xml | – sequence: 1 dbid: C6C name: Springer Nature OA Free Journals url: http://www.springeropen.com/ sourceTypes: Publisher – sequence: 2 dbid: DOA name: DOAJ Directory of Open Access Journals url: https://www.doaj.org/ sourceTypes: Open Website – sequence: 3 dbid: NPM name: PubMed url: https://proxy.k.utb.cz/login?url=http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?db=PubMed sourceTypes: Index Database – sequence: 4 dbid: EIF name: MEDLINE url: https://proxy.k.utb.cz/login?url=https://www.webofscience.com/wos/medline/basic-search sourceTypes: Index Database |
| DeliveryMethod | fulltext_linktorsrc |
| Discipline | Medicine |
| EISSN | 1479-5876 |
| EndPage | 15 |
| ExternalDocumentID | oai_doaj_org_article_ed7b46ddc1c94c76a0c9d5682e2873ab PMC12220518 A846308627 40598241 10_1186_s12967_025_06765_z |
| Genre | Journal Article |
| GeographicLocations | Taiwan |
| GeographicLocations_xml | – name: Taiwan |
| GrantInformation_xml | – fundername: Chang Gung Memorial Hospital, Linkou grantid: CMRPG3J1341, CMRPG3M1691 funderid: http://dx.doi.org/10.13039/501100005795 – fundername: Chang Gung Memorial Hospital, Linkou grantid: CMRPG3J1341, CMRPG3M1691 |
| GroupedDBID | --- 0R~ 29L 2WC 53G 5VS 6PF 7X7 88E 8FI 8FJ AAFWJ AAJSJ AASML AAWTL ABDBF ABUWG ACGFO ACGFS ACIHN ACIWK ACPRK ACUHS ADBBV ADUKV AEAQA AENEX AFKRA AFPKN AFRAH AHBYD AHMBA AHYZX ALMA_UNASSIGNED_HOLDINGS AMKLP AMTXH AOIJS BAPOH BAWUL BCNDV BENPR BFQNJ BMC BPHCQ BVXVI C6C CCPQU CS3 DIK DU5 E3Z EBD EBLON EBS ESX F5P FYUFA GROUPED_DOAJ GX1 HMCUK HYE IAO IHR INH INR ITC KQ8 M1P M~E O5R O5S OK1 OVT P2P PGMZT PHGZM PHGZT PIMPY PJZUB PPXIY PQQKQ PROAC PSQYO PUEGO RBZ RNS ROL RPM RSV SBL SOJ TR2 TUS UKHRP WOQ WOW XSB ~8M AAYXX ALIPV CITATION CGR CUY CVF ECM EIF NPM 7X8 5PM |
| ID | FETCH-LOGICAL-c533t-f2ee89451e9b3ccd0922dacb8f1b03af93d77454a4f5bb59c8e414da75c158323 |
| IEDL.DBID | C6C |
| ISSN | 1479-5876 |
| IngestDate | Wed Aug 27 01:24:49 EDT 2025 Thu Aug 21 18:33:32 EDT 2025 Tue Aug 26 08:57:55 EDT 2025 Wed Jul 16 16:53:06 EDT 2025 Tue Jul 15 03:51:54 EDT 2025 Sat Jul 05 01:30:50 EDT 2025 Thu Jul 03 08:27:16 EDT 2025 Sat Sep 06 07:28:34 EDT 2025 |
| IsDoiOpenAccess | true |
| IsOpenAccess | true |
| IsPeerReviewed | true |
| IsScholarly | true |
| Issue | 1 |
| Keywords | Hepatocellular carcinoma SVR12 Extracellular vesicle MiRNA Direct-acting antivirals |
| Language | English |
| License | 2025. The Author(s). Open Access This article is licensed under a Creative Commons Attribution-NonCommercial-NoDerivatives 4.0 International License, which permits any non-commercial use, sharing, distribution and reproduction in any medium or format, as long as you give appropriate credit to the original author(s) and the source, provide a link to the Creative Commons licence, and indicate if you modified the licensed material. You do not have permission under this licence to share adapted material derived from this article or parts of it. The images or other third party material in this article are included in the article’s Creative Commons licence, unless indicated otherwise in a credit line to the material. If material is not included in the article’s Creative Commons licence and your intended use is not permitted by statutory regulation or exceeds the permitted use, you will need to obtain permission directly from the copyright holder. To view a copy of this licence, visit http://creativecommons.org/licenses/by-nc-nd/4.0/. |
| LinkModel | DirectLink |
| MergedId | FETCHMERGED-LOGICAL-c533t-f2ee89451e9b3ccd0922dacb8f1b03af93d77454a4f5bb59c8e414da75c158323 |
| Notes | ObjectType-Article-1 SourceType-Scholarly Journals-1 ObjectType-Feature-2 content type line 23 |
| OpenAccessLink | https://doi.org/10.1186/s12967-025-06765-z |
| PMID | 40598241 |
| PQID | 3226359977 |
| PQPubID | 23479 |
| PageCount | 15 |
| ParticipantIDs | doaj_primary_oai_doaj_org_article_ed7b46ddc1c94c76a0c9d5682e2873ab pubmedcentral_primary_oai_pubmedcentral_nih_gov_12220518 proquest_miscellaneous_3226359977 gale_infotracmisc_A846308627 gale_infotracacademiconefile_A846308627 pubmed_primary_40598241 crossref_primary_10_1186_s12967_025_06765_z springer_journals_10_1186_s12967_025_06765_z |
| PublicationCentury | 2000 |
| PublicationDate | 2025-07-01 |
| PublicationDateYYYYMMDD | 2025-07-01 |
| PublicationDate_xml | – month: 07 year: 2025 text: 2025-07-01 day: 01 |
| PublicationDecade | 2020 |
| PublicationPlace | London |
| PublicationPlace_xml | – name: London – name: England |
| PublicationTitle | Journal of translational medicine |
| PublicationTitleAbbrev | J Transl Med |
| PublicationTitleAlternate | J Transl Med |
| PublicationYear | 2025 |
| Publisher | BioMed Central BioMed Central Ltd BMC |
| Publisher_xml | – name: BioMed Central – name: BioMed Central Ltd – name: BMC |
| References | RL Morgan (6765_CR3) 2013; 158 E Ogawa (6765_CR17) 2018; 47 X-P Tian (6765_CR11) 2019; 9 H Chen (6765_CR26) 2021; 9 6765_CR31 TM Carvalho (6765_CR23) 2022; 13 S Manthravadi (6765_CR4) 2017; 140 Z Lyu (6765_CR20) 2021; 11 H Shinkawa (6765_CR5) 2017; 24 GR Foster (6765_CR14) 2016; 64 W Teng (6765_CR6) 2017; 24 M Yanez-Mo (6765_CR10) 2015; 4 P Deng (6765_CR27) 2021; 27 6765_CR19 L Cheng (6765_CR21) 2017; 8 SA McDonald (6765_CR8) 2020; 27 WF Hsu (6765_CR15) 2021; 36 V Knop (6765_CR13) 2016; 23 F Conti (6765_CR16) 2016; 65 D Thabut (6765_CR9) 2019; 156 Y Deng (6765_CR22) 2019; 23 Q Jiang (6765_CR29) 2025; 20 SR Walter (6765_CR2) 2011; 26 HW Wang (6765_CR32) 2022; 12 H Sung (6765_CR1) 2021; 71 G Li (6765_CR28) 2012; 30 L Santangelo (6765_CR18) 2018; 38 R Waziry (6765_CR7) 2017; 67 European Association for the Study of the Liver (6765_CR12) 2018; 69 YC Liu (6765_CR30) 2023; 68 6765_CR25 6765_CR24 |
| References_xml | – volume: 20 start-page: 4319 year: 2025 ident: 6765_CR29 publication-title: Int J Nanomed doi: 10.2147/IJN.S506542 – volume: 156 start-page: 997 issue: 4 year: 2019 ident: 6765_CR9 publication-title: Gastroenterology doi: 10.1053/j.gastro.2018.11.053 – volume: 9 start-page: 1965 issue: 7 year: 2019 ident: 6765_CR11 publication-title: Theranostics doi: 10.7150/thno.30958 – volume: 64 start-page: 1224 issue: 6 year: 2016 ident: 6765_CR14 publication-title: J Hepatol doi: 10.1016/j.jhep.2016.01.029 – volume: 8 start-page: e2916 issue: 7 year: 2017 ident: 6765_CR21 publication-title: Cell Death Dis doi: 10.1038/cddis.2017.309 – volume: 69 start-page: 182 issue: 1 year: 2018 ident: 6765_CR12 publication-title: J Hepatol doi: 10.1016/j.jhep.2018.03.019 – volume: 26 start-page: 1757 issue: 12 year: 2011 ident: 6765_CR2 publication-title: J Gastroenterol Hepatol doi: 10.1111/j.1440-1746.2011.06785.x – ident: 6765_CR31 doi: 10.3390/v16091485 – volume: 24 start-page: 1160 issue: 12 year: 2017 ident: 6765_CR6 publication-title: J Viral Hepat doi: 10.1111/jvh.12745 – volume: 38 start-page: 1741 issue: 10 year: 2018 ident: 6765_CR18 publication-title: Liver Int doi: 10.1111/liv.13700 – volume: 11 start-page: 700649 year: 2021 ident: 6765_CR20 publication-title: Front Oncol doi: 10.3389/fonc.2021.700649 – volume: 4 start-page: 27066 year: 2015 ident: 6765_CR10 publication-title: J Extracell Vesicles doi: 10.3402/jev.v4.27066 – volume: 12 start-page: 3164 issue: 7 year: 2022 ident: 6765_CR32 publication-title: Am J Cancer Res – volume: 47 start-page: 104 issue: 1 year: 2018 ident: 6765_CR17 publication-title: Aliment Pharmacol Ther doi: 10.1111/apt.14380 – volume: 27 start-page: 270 issue: 3 year: 2020 ident: 6765_CR8 publication-title: J Viral Hepat doi: 10.1111/jvh.13232 – volume: 67 start-page: 1204 issue: 6 year: 2017 ident: 6765_CR7 publication-title: J Hepatol doi: 10.1016/j.jhep.2017.07.025 – volume: 23 start-page: 1415 issue: 2 year: 2019 ident: 6765_CR22 publication-title: J Cell Mol Med doi: 10.1111/jcmm.14045 – volume: 27 start-page: 9 issue: 1 year: 2021 ident: 6765_CR27 publication-title: Mol Med doi: 10.1186/s10020-020-00259-y – volume: 140 start-page: 1042 issue: 5 year: 2017 ident: 6765_CR4 publication-title: Int J Cancer doi: 10.1002/ijc.30521 – volume: 9 start-page: 652292 year: 2021 ident: 6765_CR26 publication-title: Front Cell Dev Biol doi: 10.3389/fcell.2021.652292 – volume: 36 start-page: 2884 issue: 10 year: 2021 ident: 6765_CR15 publication-title: J Gastroenterol Hepatol doi: 10.1111/jgh.15538 – volume: 24 start-page: 3196 issue: 11 year: 2017 ident: 6765_CR5 publication-title: Ann Surg Oncol doi: 10.1245/s10434-017-6008-y – ident: 6765_CR24 doi: 10.3390/biom10010150 – volume: 30 start-page: 1481 issue: 6 year: 2012 ident: 6765_CR28 publication-title: Cell Physiol Biochem doi: 10.1159/000343336 – ident: 6765_CR25 doi: 10.3390/ijms232415904 – volume: 65 start-page: 727 issue: 4 year: 2016 ident: 6765_CR16 publication-title: J Hepatol doi: 10.1016/j.jhep.2016.06.015 – volume: 71 start-page: 209 issue: 3 year: 2021 ident: 6765_CR1 publication-title: CA Cancer J Clin doi: 10.3322/caac.21660 – volume: 13 start-page: 865472 year: 2022 ident: 6765_CR23 publication-title: Front Genet doi: 10.3389/fgene.2022.865472 – volume: 23 start-page: 994 issue: 12 year: 2016 ident: 6765_CR13 publication-title: J Viral Hepat doi: 10.1111/jvh.12578 – volume: 68 start-page: 323 issue: 1 year: 2023 ident: 6765_CR30 publication-title: Dig Dis Sci doi: 10.1007/s10620-022-07621-6 – ident: 6765_CR19 doi: 10.3390/pharmaceutics15092365 – volume: 158 start-page: 329 issue: 5 Pt 1 year: 2013 ident: 6765_CR3 publication-title: Ann Intern Med doi: 10.7326/0003-4819-158-5-201303050-00005 |
| SSID | ssj0024549 |
| Score | 2.4336095 |
| Snippet | Background
Direct-acting antiviral (DAA) therapy for chronic hepatitis C (CHC) achieves high sustained virologic response (SVR) rates; however, hepatocellular... Direct-acting antiviral (DAA) therapy for chronic hepatitis C (CHC) achieves high sustained virologic response (SVR) rates; however, hepatocellular carcinoma... Background Direct-acting antiviral (DAA) therapy for chronic hepatitis C (CHC) achieves high sustained virologic response (SVR) rates; however, hepatocellular... Abstract Background Direct-acting antiviral (DAA) therapy for chronic hepatitis C (CHC) achieves high sustained virologic response (SVR) rates; however,... |
| SourceID | doaj pubmedcentral proquest gale pubmed crossref springer |
| SourceType | Open Website Open Access Repository Aggregation Database Index Database Publisher |
| StartPage | 722 |
| SubjectTerms | Aged Analysis Antiviral agents Biomarkers, Tumor - blood Biomedical and Life Sciences Biomedicine Carcinoma, Hepatocellular - blood Carcinoma, Hepatocellular - genetics Carcinoma, Hepatocellular - virology Care and treatment Control Diagnosis Direct-acting antivirals Disease-Free Survival Dosage and administration Extracellular vesicle MiRNA Extracellular Vesicles - genetics Extracellular Vesicles - metabolism Female Genetic aspects Hepacivirus - physiology Hepatitis C virus Hepatitis C, Chronic - blood Hepatitis C, Chronic - complications Hepatitis C, Chronic - drug therapy Hepatocellular carcinoma Hepatoma Humans Identification and classification ImmunoVirology and ImmunoOncology Liver Neoplasms - blood Liver Neoplasms - genetics Liver Neoplasms - virology Male Medicine/Public Health MicroRNAs - blood MicroRNAs - genetics Middle Aged Protective Factors RNA sequencing ROC Curve SVR12 |
| SummonAdditionalLinks | – databaseName: DOAJ Directory of Open Access Journals dbid: DOA link: http://utb.summon.serialssolutions.com/2.0.0/link/0/eLvHCXMwrV09b9YwELZQB8SC-CZQkJGQGCBqHOfDHtuq1SukMiBadbPOZ0ft0LzV-7F04Ldz5ySlKRIsrLEHx3e-e86-e06Ij-QjUMUGciy5hVlbQA4YNcU8LdaoIJTpMufkW7M4rb6e1-d3Wn1xTthADzxs3F4Mra-aEFChrbBtoEAb6saUkbC-Bs_Wt7DFFExNLHsU9kwlMqbZW5NXI4PArVvJOjd1fjNzQ4mt_0-bfMcp3U-YvPdqmpzR8RPxeESRcn9Y_VPxIPbPxMOT8Z38ufh5AKnQPErSsO2VPDrLry6_UxynryWsJciRnoFMnRw67kjog-RafE7XWUmCsvKCPNVmyTf7nKoqkbsO9TRBht-JRjL1GJeLwzMZVxDGC8AX4vT46MfhIh87LeRIcG-Td2WMxla1itZrxFDYsgyA3nTKFxo6qwPBxLqCqqu9ry2aWKkqQEvirMkm6Jdip1_28bWQGk1juoJUg6niuggtUAAOBgqvVRcwE5-njXfXA6GGS4GIadwgJkdicklM7iYTByyb25lMhp0-kIq4UUXcv1QkE59Yso6PLIkPYaw8oAUz-ZXbJwymObRrM7E7m0lHDWfDHybdcDzE-Wl9XG7XjswiITdLYDoTrwZduV0zQWJrCChlwsy0aPZT85H-8iIxfauS66CVycSXSeHcaGPWf9m1N_9j196KR2U6MJyavCt2NqttfEcAbOPfp7P2C4wZLvQ priority: 102 providerName: Directory of Open Access Journals |
| Title | Baseline serum EV-miR-1-3p as a protective factor and biomarker for hepatocellular carcinoma development after HCV eradication |
| URI | https://link.springer.com/article/10.1186/s12967-025-06765-z https://www.ncbi.nlm.nih.gov/pubmed/40598241 https://www.proquest.com/docview/3226359977 https://pubmed.ncbi.nlm.nih.gov/PMC12220518 https://doaj.org/article/ed7b46ddc1c94c76a0c9d5682e2873ab |
| Volume | 23 |
| hasFullText | 1 |
| inHoldings | 1 |
| isFullTextHit | |
| isPrint | |
| link | http://utb.summon.serialssolutions.com/2.0.0/link/0/eLvHCXMwlV1LaxsxEB6aBEovpe9smhoVCj20S1erlVZ7jI2DKSQU0wTTi5iVtCSHrIMflxz62zOS10k2LYVefLBkWO-8vpFmvgH4RDHCcq8wtXkYYVZmmKL1gnKe0krL0eXxMOfkVE3Oiu8zOetockIvzMP7e67VtyXFIzLlMHSV_KqS6c0O7ElyvEGbR2p0z6tHic62Keavv-sFnsjP_6cXfhCGHpdIPronjeHn-AU873AjO9oI-iU88e0reHrS3Yy_ht9DjK3lnpFOra_Y-Dy9upxS5iauGS4Zso6QgZwb28zYYdg6FrrvQ4HOghF4ZRcUm1bzcJYfilOZDXOGWtrA3H1pEYtTxdlkdM78Al135PcGzo7HP0eTtJutkFoCeKu0yb3XVSG5r2phrcuqPHdoa93wOhPYVMIRMJQFFo2sa1lZ7QteOCxJgJK8gHgLu-289fvAhNVKNxkpQyCHazyWSCk3asxqwRtnE_iyffHmekOhYWLqoZXZiMmQmEwUk7lJYBhkc7cz0F_HL0grTGdNxruyLpRzltuqsKXCzFZOKp17SgAF1gl8DpI1wUhJfBa7XgN64EB3ZY4IdYmQzJUJHPZ2knHZ3vLHrW6YsBQq0lo_Xy8NOULCahXB5wTebXTl7pkJBFeaoFECuqdFvT_VX2kvLyK3N89D5zPXCXzdKpzpvMryH2_t4P-2v4dneTSNUHZ8CLurxdp_IHC1qgewU87KAewNx6c_poNoY4N4UEGf0-GvWy9nI5I |
| linkProvider | Springer Nature |
| linkToHtml | http://utb.summon.serialssolutions.com/2.0.0/link/0/eLvHCXMwlV1Lb9QwEB5BkYAL4k2ggJGQOEBEHCeOc2xXrRbo9oDaqjdrYjtqD81W-7j00N_eGW-2bQpC4rp2pGzm9Y098w3AZ4oRTgaNqct5hFmVYYouKMp5Klc6iT6PhzmTfT0-LH4el8c9TQ73wty-v5dGf59TPCJT5qGr5Fd1mV7chwd8c8k8-SM9uuHVo0Rn3RTz1-cGgSfy8__phW-FobslknfuSWP42X0KT3rcKLZWgn4G90L3HB5O-pvxF3C5jbG1PAjSqeWZ2DlKz05_U-amzgXOBYqekIGcm1jN2BHYecHd91ygMxMEXsUJxabFlM_yuThVOJ4z1NEG4W9Ki0ScKi7GoyMRZuj7I7-XcLi7czAap_1shdQRwFukbR6CqYtShrpRzvmsznOPrjGtbDKFba08AcOywKItm6asnQmFLDxWJMCSvIB6BRvdtAtvQChntGkzUgYmh2sDVkgpNxrMGiVb7xL4uv7w9nxFoWFj6mG0XYnJkphsFJO9SGCbZXO9k-mv4w-kFba3Jht81RTaeyddXbhKY-ZqX2qTB0oAFTYJfGHJWjZSEp_DvteAXpjpruwWoS7FyVyVwOZgJxmXGyx_WuuG5SWuSOvCdDm35AgJq9UEnxN4vdKV63cmEFwbgkYJmIEWDf7UcKU7PYnc3jLnzmdpEvi2Vjjbe5X5P77a2__b_hEejQ8me3bvx_6vd_A4j2bCJcibsLGYLcN7AlqL5kO0sCt1ayH8 |
| linkToPdf | http://utb.summon.serialssolutions.com/2.0.0/link/0/eLvHCXMwlV1Lb9QwEB5BK1VcEO8GChgJiQNETeI4sY_b0tWy0AoBrXqzJrZDe2h2tZu99MBvZ-xk26YgJK7xRHIyr2_seQC8JR9hUldgbDI_wqxMMEbjOMU8pREmRZuFw5zDo2JynE9PxemNKv6Q7b6-kuxqGnyXpqbdndu6U3FZ7C7JS5GC-1GsZG0LEV_ehU0plKLwa3M0mn6fXvfbowBoXSzz1zcHDin07f_TOt9wT7dTJ2_dnwa3NH4A93s8yUadADyEO655BFuH_Y35Y_i1h6Hk3DGStdUFOziJL86_UUTH5wyXDFnfqIGMHutm7zBsLPNV-T5xZ8EI1LIz8lntzJ_x-6RVZvz8oYYImL1OOWJh2jib7J8wt0DbHwU-gePxwY_9SdzPXIgNAb82rjPnpMpF6lTFjbGJyjKLppJ1WiUca8UtAUaRY16LqhLKSJenucWSGCvIOvCnsNHMGrcNjBtZyDohIfFN42qHJVIojhKTiqe1NRG8X_94Pe9aa-gQkshCd2zSxCYd2KQvI9jzvLmi9G2xw4PZ4qfutUw7W1Z5Ya1JjcpNWWBilBWFzBwFhhyrCN55zmqvvMQ-g30NAm3Yt8HSI0Jj3Ad5ZQQ7A0pSOjNYfrOWDe2XfKZa42arpSYDSRiOJJFonnWycrVnAsdKEmSKQA6kaPBRw5Xm_Cz0_E4zXxGdygg-rAVO99Zm-Y-_9vz_yF_D1tePY_3l09HnF3AvC1riM5N3YKNdrNxLwl9t9apXsd8YJiu6 |
| openUrl | ctx_ver=Z39.88-2004&ctx_enc=info%3Aofi%2Fenc%3AUTF-8&rfr_id=info%3Asid%2Fsummon.serialssolutions.com&rft_val_fmt=info%3Aofi%2Ffmt%3Akev%3Amtx%3Ajournal&rft.genre=article&rft.atitle=Baseline+serum+EV-miR-1-3p+as+a+protective+factor+and+biomarker+for+hepatocellular+carcinoma+development+after+HCV+eradication&rft.jtitle=Journal+of+translational+medicine&rft.au=Teng%2C+Wei&rft.au=Ku%2C+Wei-Ting&rft.au=Lin%2C+Po-Ting&rft.au=Chen%2C+Guan-Ting&rft.date=2025-07-01&rft.pub=BioMed+Central&rft.eissn=1479-5876&rft.volume=23&rft_id=info:doi/10.1186%2Fs12967-025-06765-z&rft_id=info%3Apmid%2F40598241&rft.externalDocID=PMC12220518 |
| thumbnail_l | http://covers-cdn.summon.serialssolutions.com/index.aspx?isbn=/lc.gif&issn=1479-5876&client=summon |
| thumbnail_m | http://covers-cdn.summon.serialssolutions.com/index.aspx?isbn=/mc.gif&issn=1479-5876&client=summon |
| thumbnail_s | http://covers-cdn.summon.serialssolutions.com/index.aspx?isbn=/sc.gif&issn=1479-5876&client=summon |