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Original Article Open Access
Analysis of MIR142 Gene Mutations in Primary Diffuse Large B-cell Lymphoma of the Central Nervous System: A Cross-sectional Study
Elena Voropaeva, Olga Seregina, Maria Voytko, Tatyana Babaeva, Vladimir Maksimov, Yuriy Orlov, Tatyana Pospelova
Published online April 28, 2026
Gene Expression. doi:10.14218/GE.2025.00089
Abstract
The pathogenic role of MIR142 genetic abnormalities in the development of primary diffuse large B-cell lymphoma (DLBCL) of the central nervous system (CNS) is unexplored. The objective [...] Read more.

The pathogenic role of MIR142 genetic abnormalities in the development of primary diffuse large B-cell lymphoma (DLBCL) of the central nervous system (CNS) is unexplored. The objective of this study was to investigate the frequency, spectrum, and functional significance of mutations in the MIR142 gene in primary CNS DLBCL.

Direct Sanger sequencing of the MIR142 gene was performed in tumor tissue from 35 patients with primary DLBCL of the CNS. In silico prediction of microRNA (miRNA)–target interactions, enrichment analysis of target gene ontologies, and prediction of the secondary structure and minimum free energy of the miRNA hairpin were performed.

The mutation frequency was 37.1% (95% confidence interval: 23.2–53.7%). The vast majority of the identified single-nucleotide variants were located outside the regions encoding mature miRNA chains. In silico analysis showed that the n.29A>G mutation located in the seed sequence of miR-142-5p resulted in a significant reduction in the number of potential targets and alterations to the interaction spectrum. All single-nucleotide variants identified in the study patients caused a change in minimum free energy and affected the shape and length of the hairpin stem of pri-miRNA. The results indicate the fragility of the pri-miR-142 hairpin.

The frequency of gene mutations in primary DLBCL of the CNS significantly exceeds that reported for systemic DLBCL.

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Original Article Open Access
GSTM3 Knockdown Promotes Liver Fibrosis Reversal by Inhibiting Hepatic Stellate Cell Activation via PPARγ Signaling
Chenxue Hou, Bingqing Yang, Yuanying Zhao, Hao Chang, Tong Bu, Qi Wang, Yue Li
Published online May 25, 2026
Journal of Clinical and Translational Hepatology. doi:10.14218/JCTH.2025.00658
Abstract
Liver fibrosis is a pivotal and reversible stage in the progression of chronic liver disease. However, the mechanisms underlying fibrosis reversal remain unclear, and effective [...] Read more.

Liver fibrosis is a pivotal and reversible stage in the progression of chronic liver disease. However, the mechanisms underlying fibrosis reversal remain unclear, and effective diagnostic biomarkers are lacking in clinical practice. In this study, we aimed to elucidate the role and molecular mechanisms of glutathione S-transferase Mu 3 (GSTM3) in liver fibrosis reversal, and preliminarily determine whether GSTM3 can serve as a novel biomarker for liver fibrosis reversal.

Carbon tetrachloride-induced mouse models of liver fibrosis and spontaneous reversal were established. Proteomic analysis was used to identify proteins shared between liver tissue and serum that were continuously downregulated during fibrosis reversal. The expression of GSTM3 was evaluated in the livers of mice undergoing fibrosis reversal and in clinical samples from patients with liver fibrosis. Hepatic stellate cells (HSCs) were transfected with Gstm3-silencing RNA or an overexpression plasmid to assess the effects on fibrosis markers. RNA sequencing analyses were performed, and the underlying molecular mechanisms were investigated.

Proteomic analysis revealed significantly decreased GSTM3 levels in both hepatic tissue and serum in mice undergoing fibrosis reversal, and its expression was negatively correlated with the extent of reversal. GSTM3 levels were markedly increased in the hepatic tissue and serum of patients with liver fibrosis. GSTM3 expression was upregulated in transforming growth factor-β-stimulated HSCs. GSTM3 knockdown inhibited the expression of fibrosis markers, such as collagen type I α1 and tissue inhibitor of metalloproteinase 1, whereas its overexpression promoted their expression. Mechanistic studies indicated that GSTM3 knockdown activated peroxisome proliferator-activated receptor γ (PPARγ) signaling and downregulated its downstream targets, cluster of differentiation 36 and fatty acid-binding protein 4, thereby suppressing HSC activation.

GSTM3 knockdown promotes liver fibrosis reversal via PPARγ signaling-mediated inhibition of HSC activation. Therefore, GSTM3 is a promising therapeutic target and diagnostic biomarker for liver fibrosis.

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Reviewer Acknowledgement Open Access
2025 Reviewer Acknowledgement
Editorial Office of Exploratory Research and Hypothesis in Medicine
Published online December 30, 2025
Exploratory Research and Hypothesis in Medicine. doi:10.14218/ERHM.2025.000RA
Consensus Open Access
Chinese Consensus on Early Screening and Surveillance for Pancreatic Cancer in High-risk Individuals (2026 Revision, Nanjing)
Pancreatic Disease Collaborative Group, Chinese Society of Digestive Endoscopy
Published online May 27, 2026
Cancer Screening and Prevention. doi:10.14218/CSP.2026.00004
Abstract
Pancreatic cancer remains a highly lethal malignancy owing to the difficulty of early detection. In 2021, the Chinese Consensus on Early Screening and Surveillance for Pancreatic [...] Read more.

Pancreatic cancer remains a highly lethal malignancy owing to the difficulty of early detection. In 2021, the Chinese Consensus on Early Screening and Surveillance for Pancreatic Cancer in High-risk Individuals was first established. However, the evidence landscape has evolved rapidly, necessitating an updated, evidence-based framework tailored to the Chinese healthcare context. This revised consensus aims to standardize the early screening and surveillance process for high-risk populations in China. A multidisciplinary expert panel comprising 53 specialists from 17 provincial-level regions systematically reviewed the literature using the GRADE (Grading of Recommendations Assessment, Development and Evaluation) methodology. A modified Delphi process was employed, with consensus predefined as ≥75% agreement. The panel formulated 26 evidence-based recommendations covering screening objectives, the definition of high-risk populations (hereditary susceptibility, new-onset diabetes, chronic pancreatitis, and pancreatic cystic neoplasms), age at screening initiation, surveillance intervals, imaging modalities (magnetic resonance imaging/magnetic resonance cholangiopancreatography, endoscopic ultrasound, computed tomography), surgical indications, and lifestyle modifications. Of these recommendations, 14 are strong and 12 are weak, supported by evidence levels ranging from A to D. Implementation of this consensus in clinical practice will help improve the early diagnosis of stage I pancreatic cancer and high-grade precursor lesions, thereby advancing standardized multidisciplinary care and ultimately improving patient outcomes in China.

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