Hepatitis B virus (HBV) infection and hepatitis C virus (HCV) infection are among the leading causes of chronic liver diseases worldwide. Through the same transmission routes, HBV/HCV coinfection is widespread and aggravates liver damage. In this study, we aimed to assess the safety and efficacy of sofosbuvir/velpatasvir (SOF/VEL) and the pre-treatment of tenofovir alafenamide fumarate (TAF) on HBV reactivation in HBV/HCV coinfected patients.

A multicenter, prospective, single-arm, open-label 12-week trial, followed by a 12/48-week observational clinical trial, was conducted. Ninety-six adults with chronic HBV/HCV coinfection were enrolled from May 2021 to December 2024 in thirteen centers in China. Seventy-seven non-cirrhotic patients were included in Group 1 and nineteen compensated cirrhotic patients in Group 2. All subjects were enrolled to receive SOF/VEL once daily for 12 weeks. Non-cirrhotic subjects received TAF once daily for 28 weeks, and compensated cirrhotic subjects received TAF once daily for 64 weeks simultaneously. Statistical significance was set at P < 0.05.

At the end of SOF/VEL treatment, the overall sustained virologic response was 97.9%, of which 100% was achieved in Group 2. HCV RNA, HBV DNA, and HBV RNA levels were substantially decreased in all patients. Alanine aminotransferase (ALT) (61.5 vs. 21.9, P < 0.001) and aspartate aminotransferase (AST) (50.8 vs. 25.7, P < 0.001) levels decreased, and albumin (ALB) (42.4 vs. 45.1, P < 0.001) level increased compared to pre-treatment in Group 1 at 12 weeks post-treatment. ALT (64.1 vs. 25.2, P < 0.001), AST (65.7 vs. 29.7, P < 0.001), alkaline phosphatase (ALP) (111.6 vs. 88.2, P < 0.05), and alpha-fetoprotein (AFP) (17.9 vs. 4.7, P < 0.05) levels decreased, and ALB (41.3 vs. 42.5, P = 0.051) and platelet count (PLT) (114.0 vs. 127.2, P = 0.052) levels showed a trend toward increase compared to pre-treatment in Group 2 at 48 weeks post-treatment. Liver stiffness measurement (LSM) (22.6 vs. 12.7, P < 0.01), aspartate aminotransferase to platelet ratio index (APRI) (1.6 vs. 0.6, P < 0.001), and fibrosis-4 index (FIB-4) (4.7 vs. 2.6, P < 0.05) significantly decreased after treatment in Group 2. Two patients in Group 1 with genotype 3 showed HBV reactivation and HCV relapse, respectively. No drug-related adverse events were observed in the study.

SOF/VEL effectively achieves a sustained virologic response and improves liver function, with an acceptable safety profile in chronic HBV/HCV coinfected patients, including those with compensated cirrhosis, who achieved modest improvement in non-invasive fibrosis indices. Pre-administration of TAF may mitigates the risk of HBV reactivation in this population.

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.

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.

Irinotecan is a camptothecin derivative that exerts its antitumor effects by metabolizing into the active metabolite 7-ethyl-10-hydroxycamptothecin (SN-38). It is widely used clinically for treating various advanced solid tumors. However, irinotecan frequently induces neutropenia, predisposing patients to infection and even death. This review aims to provide a theoretical basis for the clinical management of irinotecan-induced neutropenia (IIN). Irinotecan and SN-38 mainly induce hematopoietic stem cell damage and dysfunction by inhibiting topoisomerase I and triggering mitochondrial injury, which ultimately results in neutropenia. Notably, the risk factors of IIN include irinotecan dosage, gene polymorphism, individual baseline characteristics, and drug combination. And several strategies effectively prevent IIN, such as adjustment of drug dosage, genotype testing, oral alkalinizing drugs, supplement of granulocyte colony-stimulating factor, and regulation of intestinal microorganisms. In summary, this review systematically elaborates on the classification, epidemiology, pathogenesis, risk factors, and management strategies of IIN, with the goal of providing references for the clinical prevention and management of irinotecan-related adverse reactions.

Artificial intelligence (AI) is increasingly reshaping diagnostic pathology, with breast pathology representing one of the most advanced and clinically impactful areas of adoption. Despite rapid progress, many practicing pathologists remain unfamiliar with core AI concepts and their practical implications. This review provides a concise and accessible overview of AI in breast pathology, focusing on foundational principles, current clinical applications, and future directions.

Pertinent literature was reviewed. Personal experiences were also summarized and incorporated.

Key AI concepts, including algorithms, models, architectures, machine learning, deep learning, neural networks, and multimodal and foundational models, are introduced to establish a common framework. Important distinctions among generative, black-box, and explainable AI are highlighted, emphasizing the need for transparency and interpretability in clinical settings. The evolution of AI in breast pathology is reviewed, from early rule-based computer-assisted diagnostic systems to modern deep learning approaches leveraging large-scale whole-slide imaging datasets. Current applications span multiple domains, including detection of lymph node metastases, Nottingham grading, classification of benign and malignant lesions, and automated quantification of critical biomarkers. AI-based approaches to prognosis, risk stratification, prediction of treatment response, and analysis of the tumor microenvironment are also discussed. Finally, the review addresses challenges associated with real-world implementation, including data quality, bias, regulatory considerations, cost, infrastructure, and workflow integration.

As AI continues to evolve toward large-scale, multimodal, and explainable models, it is expected to function as an augmentative tool rather than a replacement for pathologists, supporting diagnostic accuracy, standardization, and personalized management in breast cancer care.

The current criterion of biochemical response to ursodeoxycholic acid in primary biliary cholangitis is an alkaline phosphatase (ALP) level of ≤1.67 × the upper limit of normal (ULN) after 12 months of treatment. However, a proportion of patients who meet this parameter may still progress to liver decompensation. This study aimed to optimize the clinical management of primary biliary cholangitis by (1) establishing ALP normalization as a core treatment target, (2) identifying early intervention windows, and (3) developing risk stratification criteria.

This multicenter retrospective study included an internal cohort and an external validation cohort. We assessed the prognostic impact of ALP normalization with Kaplan-Meier and Cox regression. Sankey diagrams and segmented Poisson regression analysis mapped dynamic risk transitions to identify critical intervention windows. Predictive performance (sensitivity/specificity/positive predictive value/negative predictive value (NPV)) of Mayo, Paris II, and Toronto criteria for 12-month ALP normalization was compared.

Patients achieving ALP normalization showed significantly higher complication-free survival versus those with ALP 1.0–1.67 × ULN (89.8% vs. 79.8%; P = 0.016). Segmented Poisson regression identified significant change points at 3.73 and 5.5 months for high-to-medium and medium-to-low risk transitions, respectively. Failure to meet the Toronto criteria at month 3 predicted non-normalization with 95% NPV, whereas Paris II criteria at month 6 provided optimal specificity (73%) for identifying patients who failed to achieve ALP normalization.

ALP normalization significantly improves clinical outcomes. Two subgroups demonstrate low normalization probability and warrant early intervention: (1) patients with ALP ≥ 1.67 × ULN after 3 months and (2) those not meeting Paris II criteria by month 6.

Acute-on-chronic liver failure (ACLF) lacks a universally accepted definition, and recent efforts have proposed consensus organ failure criteria. In this study, we aimed to compare the clinical validity of a recently proposed consensus ACLF framework with the outcome-calibrated A-TANGO classification.

We performed a multinational cohort study including 2,398 patients from the TIH cohort (India) and 2,568 from the CATCH-LIFE cohort (China) who were hospitalized with acute decompensation of cirrhosis. ACLF was defined using A-TANGO and an operationalized version of the 2025 consensus framework. Outcomes were 28- and 90-day mortality. Analyses assessed case capture, overlap, mortality risk, sensitivity, specificity, and net reclassification improvement (NRI).

ACLF prevalence differed substantially by definition. In TIH, A-TANGO classified 79.2% as ACLF versus 42.3% by the consensus definition; in CATCH-LIFE, the corresponding values were 31.4% versus 5.8%, respectively. Most consensus ACLF cases were captured by A-TANGO, which additionally classified 26%–37% of patients as having ACLF. These patients had substantial mortality (28-day: 18.1%–26.9%; 90-day: 33.2%–37.9%), significantly higher than those negative by both frameworks and comparable to established ACLF risk thresholds. A-TANGO showed higher sensitivity for 28-day mortality (TIH: 94.1% vs. 67.8%; CATCH-LIFE: 76.1% vs. 25.6%), whereas consensus criteria were more specific. Reclassification analyses showed improved discrimination with A-TANGO (NRI: 17.1% in TIH; 27.4% in CATCH-LIFE). Within the consensus non-ACLF group, A-TANGO further stratified patients into distinct risk groups with stepwise increase in mortality.

In conclusion, the two frameworks identify fundamentally different populations. The consensus definition significantly reduces sensitivity and under-recognizes high-risk patients. Compared with consensus definitions, the outcome-calibrated framework better supports diagnosis, clinical decision-making, risk stratification, and trial design in ACLF.

Microbial resistance and oxidative stress are two significant health issues associated with chronic illnesses and therapy failures. The antioxidant and antibacterial properties of Euphorbia cuneata Vahl. aerial component extracts made with various polarity solvents were assessed in this work.

Disc diffusion and minimum inhibitory concentration (MIC) tests were used to evaluate the 1,1-diphenyl-2-picrylhydrazyl radical scavenging activity, total phenolic and flavonoid contents, and antimicrobial activity of n-hexane, toluene, ethanolic, and aqueous extracts against specific ESKAPE pathogens (Staphylococcus aureus, Escherichia coli, Pseudomonas aeruginosa, and Candida tropicalis). High-performance liquid chromatography and gas chromatography-mass spectrometry were used to further characterize the most active extract.

Compared to the aqueous (IC₅₀ = 51.61 µg/mL), toluene (IC₅₀ = 30.57 µg/mL), and n-hexane (IC₅₀ = 128.15 µg/mL) extracts, the ethanolic extract demonstrated the greatest 1,1-diphenyl-2-picrylhydrazyl radical scavenging activity (97.90 ± 0.8%; IC₅₀ = 28.52 µg/mL). Additionally, it has the highest levels of flavonoids (40.5 ± 1.5 mg luteolin equivalents/g) and phenolic (80.0 ± 0.2 mg gallic acid equivalents/g). While gas chromatography-mass spectrometry found methyl 12-hydroxy-9-octadecenoate (44.39%) as the main volatile molecule, high-performance liquid chromatography analysis identified caffeic acid, pyrogallol, rutin, and 7-hydroxyflavone as important ingredients. The ethanolic extract showed antifungal activity against C. tropicalis (MIC = 6.25 mg/mL) and moderate antibacterial activity with the lowest MIC values against S. aureus (450 µg/mL) and E. coli (500 µg/mL).

The ethanolic extract of Euphorbia cuneata demonstrated potent in vitro antioxidant activity and moderate antimicrobial effects, primarily attributable to its high phenolic and flavonoid content. These results support its potential as a natural source of bioactive compounds for further development.

Studies suggest that Yiguanjian (YGJ) may exert a therapeutic effect on liver fibrosis. However, the active components and molecular targets responsible for its action remain unclear. This study aimed to systematically evaluate the active ingredients and potential targets of YGJ in the treatment of liver fibrosis.

Active compounds and corresponding targets of YGJ were retrieved from the Traditional Chinese Medicine Systems Pharmacology Database and Analysis Platform (TCMSP) and the Encyclopedia of Traditional Chinese Medicine (ETCM) databases. Liver fibrosis-related datasets were obtained from the Gene Expression Omnibus (GEO) database and divided into training and validation sets. Differentially expressed genes (DEGs) from the training set were subsequently analyzed using network pharmacology, molecular dynamics simulations, and immune infiltration analysis. Three machine learning models were employed to screen for core targets, followed by Gene Set Enrichment Analysis (GSEA) and Mendelian randomization (MR) analysis. The validation set was used to assess the expression levels and diagnostic potential of core targets.

A total of 2,887 liver fibrosis-related targets and 1,198 YGJ-related targets were identified. Three hundred and three putative targets for YGJ in the treatment of liver fibrosis were identified. Three machine learning methods further narrowed these down to five core targets. Immune infiltration analysis revealed an increase in effector B cells, resting CD4+ memory T cells, γδ T cells, and M1 macrophages during liver fibrosis progression. MR analysis showed that all five core targets (FABP4, MDM2, AKR1B1, PDGFRB, and NR1H4) had odds ratios greater than 1, indicating that they function as risk factors. Expression analyses in both the training and validation sets consistently validated the MR results, demonstrating strong diagnostic potential. GSEA revealed that the core targets were enriched in key signaling pathways, including Wnt, PPAR, and MAPK. Molecular docking and molecular dynamics simulations showed that the active compounds of YGJ exhibited strong binding affinity and stability with the core targets.

YGJ exerts its potential antifibrotic effects by downregulating or antagonizing the risk-associated targets (FABP4, MDM2, AKR1B1, PDGFRB, and NR1H4). These findings provide new insights into the potential of YGJ for treating liver fibrosis, while offering a scientific reference for the prevention and treatment of chronic liver diseases.

Hepatic myelopathy, a rare neurological complication of decompensated chronic liver disease, profoundly impairs quality of life. While liver transplantation represents the only curative treatment for hepatic myelopathy, we report a case in which progressive and severe spastic paraparesis was markedly improved following embolization of a paraspinal vein shunt.

Hepatocellular carcinoma (HCC) remains a leading cause of cancer-related mortality, underscoring the need for effective therapies. Although miR-125b-5p shows therapeutic potential, its efficacy in metabolic dysfunction-associated steatotic liver disease (MASLD)-related HCC and the underlying mechanisms remain unclear. In this study, we aimed to develop a magnetic resonance imaging (MRI)-trackable miR-125b-5p-engineered MSC platform for HCC therapy and to determine whether MASLD attenuates its antitumor efficacy through metabolic reprogramming.

Bone marrow mesenchymal stem cells (MSCs) were genetically engineered to coexpress miR-125b-5p (a therapeutic gene) and ferritin heavy chain (Fth; a MRI reporter gene), enabling sustained delivery and real-time tracking. Orthotopic HCC models with or without MASLD were established to evaluate therapeutic outcomes. In vivo MRI, histological analyses, and bioinformatics approaches were used to assess efficacy and mechanisms.

Transplantation of miR-125b-5p-Fth-MSCs significantly suppressed HCC growth in vivo over an extended period. However, MASLD attenuated this therapeutic effect. Mechanistically, miR-125b-5p directly targeted hexokinase 2 (HK2), inhibiting HCC proliferation and migration through suppression of the PI3K/AKT/mTOR pathway. Fatty acid-induced lipotoxicity upregulated HK2 expression and counteracted the antitumor effects of miR-125b-5p.

Multigene-modified MSCs enable effective, MRI-monitored HCC therapy. MASLD diminishes the efficacy of miR-125b-5p through HK2 upregulation. These findings establish a multimodal theranostic framework for HCC and provide mechanistic insights into MASLD-associated therapeutic resistance.

Primary liver cancer is one of the most common malignant tumors in China, which seriously threatens people’s lives and health. In recent years, with the advancement of basic and clinical research, the diagnosis and treatment methods for primary liver cancer have been continually enriched. Traditional Chinese medicine (TCM) has played an important role in the diagnosis and treatment of primary liver cancer, but there is no unified standard for differentiation and treatment, and efficacy evaluation. In order to further standardize the TCM diagnosis and treatment of primary liver cancer, according to the requirements of TCM standardization and related technical guidance documents, the drafting team compiled this guideline through literature research, expert interviews, questionnaire surveys, consensus meetings, etc., for reference by clinicians. This guideline is approved and issued by the China Association of Chinese Medicine, standard number: T/CACM 1575-2024.

Hepatic encephalopathy (HE) is a neurologic complication of advanced liver disease (e.g., cirrhosis) resulting in impaired functioning and reduced quality of life. This condition is associated with a substantial burden for patients and their caregivers and carries a poor prognosis and increased risk of hospitalization and mortality. This narrative review discusses the burden of HE, precipitating risk factors, and clinical considerations for reducing the risk of overt HE (OHE) recurrence in adults with cirrhosis. Key precipitating factors include certain medications, constipation, dehydration, uncontrolled diabetes mellitus, electrolyte imbalances, gastrointestinal bleeding, infection, and sarcopenia, among others. Identification and treatment of precipitating factors are critical steps in the management of HE. Components of ongoing care include patient and caregiver education, nutritional supplementation and sleep management, pharmacotherapy, and nonpharmacologic interventions (e.g., spontaneous portosystemic shunt embolization and liver transplantation in appropriate patients). Clinical guidelines recommend lactulose therapy as secondary prophylaxis after an initial episode of OHE. Rifaximin is recommended as add-on therapy to lactulose when an additional OHE episode occurs. Polyethylene glycol has been investigated as an alternative to lactulose in patients with acute HE and in those with chronic HE and a poor response to lactulose. Oral L-ornithine-L-aspartate may reduce the risk of OHE recurrence in patients with cirrhosis. Investigational agents include nitazoxanide, fecal microbiota transplantation, and the use of artificial intelligence, app-based technology, and wearable devices to facilitate acute and prophylactic management of HE.

Cannabinoid hyperemesis syndrome is an underrecognized cause of recurrent vomiting, weight loss, and abdominal pain in adolescents, often overlooked due to its nonspecific presentation and overlap with other gastrointestinal conditions. This case report highlights a 13-year-old female who presented with significant weight loss and postprandial bilious vomiting initially attributed to superior mesenteric artery syndrome. Persistent symptoms, despite surgical removal of an incidental ovarian dermoid cyst, prompted reevaluation after nondiagnostic imaging and lack of improvement. Further history two weeks later revealed daily cannabis use, confirmed by a positive urine toxicology screen for tetrahydrocannabinol. Following supportive care and cannabis cessation, her symptoms resolved. This case illustrates how incomplete social histories and incidental findings can delay the identification of cannabinoid hyperemesis syndrome and lead to unnecessary procedures. Early use of urine toxicology screening and validated substance use tools (CRAFFT, BSTAD, S2BI) in adolescents with persistent vomiting and abdominal pain can facilitate timely recognition, reduce hospital length of stay, and improve outcomes.

Chikungunya fever, caused by the Chikungunya virus (CHIKV), has re-emerged as a significant global health concern in recent decades. A notable event was the largest-ever local outbreak in China in 2025, marking a critical juncture in its epidemiology. Although conventional treatment remains predominantly supportive, the integration of traditional Chinese medicine (TCM) offers promising complementary strategies for alleviating both acute symptoms and chronic polyarthralgia. This narrative review aims to consolidate current knowledge on the etiology, pathogenesis, clinical manifestations, and management of Chikungunya fever, with a particular focus on the evidence-based application of TCM. By integrating molecular virology with clinical and epidemiological insights, this review offers a comprehensive perspective on the challenges posed by CHIKV and underscores the strategic imperatives essential for its future management. In conclusion, addressing the expanding threat of CHIKV necessitates a multi-pronged public health strategy that integrates standard clinical and preventive measures with evidence-based TCM therapies, highlighting the urgent need for rigorous clinical trials to globally validate these integrative treatments.

Chronic hepatitis B (CHB) remains a major global public health challenge. Current therapies based on nucleos(t)ide analogues and interferon mainly achieve long-term viral suppression, whereas only a small proportion of patients attain a functional cure, defined as sustained hepatitis B surface antigen loss with hepatitis B virus (HBV) DNA below the limit of quantification for at least 24 weeks after treatment discontinuation, with or without anti-HBs seroconversion. Emerging evidence from the gut–liver axis indicates that gut microbiota–derived metabolites, particularly short-chain fatty acids (SCFAs) and bile acids (BAs), modulate the HBV life cycle and immune regulation in CHB, thereby offering therapeutic targets to overcome immune tolerance. This review summarizes the biological characteristics of SCFAs and BAs and their mechanistic roles across different stages of HBV infection, with emphasis on translational relevance. In vitro and animal studies suggest that butyrate and related SCFAs suppress HBV gene expression by inhibiting histone deacetylases and remodeling covalently closed circular DNA minichromatin. SCFAs may also enhance antiviral immunity, although they may reinforce immune tolerance in certain contexts. For BAs, the farnesoid X receptor, Takeda G protein–coupled receptor 5, and the HBV entry receptor sodium taurocholate cotransporting polypeptide form a key signaling hub with dual effects on viral replication and host responses. Early-phase studies suggest that farnesoid X receptor agonists, pegylated interferon-α, or nucleos(t)ide analogues are associated with hepatitis B surface antigen reductions, though larger trials are needed. This review proposes biomarker-guided stratification and multi-target combination strategies to improve functional cure rates in CHB.

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.