(1) Background: Hepatocellular carcinoma (HCC) is one of the most common cancers worldwide with limited treatment satisfaction. Finding new therapeutic targets has remained a major challenge. Ferroptosis is an iron-dependent cell death program that plays a regulatory role in HBV infection and HCC development. It is necessary to classify the roles of ferroptosis or ferroptosis-related genes (FRGs) in HBV-related HCC progression. (2) Methods: We conducted a matched case–control study from the TCGA database, retrospectively collecting demographic data and common clinical indicators from all subjects. The Kaplan–Meier curve, univariate and multivariate cox regression analysis of the FRGs were used to explore the risk factors for HBV-related HCC. The CIBERSORT algorithm and TIDE algorithm were executed to evaluate the functions of FRGs in the tumor-immune environment. (3) Results: A total of 145 HBV-positive HCC patients and 266 HBV-negative HCC patients were enrolled in our study. Four ferroptosis related genes (FANCD2, CS, CISD1 and SLC1A5) were positively correlated with the progression of HBV-related HCC. Among them, SLC1A5 was an independent risk factor for HBV-related HCC, and correlated with poor prognosis, advanced progression and an immunosuppression microenvironment. (4) Conclusions: Here, we revealed that a ferroptosis-related gene, SLC1A5, may be an excellent predictor of HBV-related HCC and may provide insight into the development of innovative possible therapeutic techniques.

Background: Prostate cancer remains one of the leading causes of cancer-related mortality in men worldwide. The treatment of it is currently based on surgical removal, radiotherapy, and hormone therapy. It is crucial to improve therapeutic prospects for the diagnosis and treatment of prostate cancer via drug target screening. Methods: We integrated eQTL data from the eQTLGen Consortium and pQTL data from UK Biobank Proteome Plasma Proteins (UKB-PPP) and deCODE health datasets. MR analyses (SMR, heterogeneity in dependent instruments (HEIDI), IVW, Wald ratio, weighted median, and MR-Egger) were used to screen candidate genes associated with prostate adenocarcinoma (PRAD) risk. Candidate genes were further verified through TCGA-based gene expression profile, survival analysis, and immune microenvironment evaluations. TIDE analysis was utilized to investigate gene immunotherapy response. Single-cell RNA sequencing data from the GSE176031 dataset were used to investigate the gene expression patterns. The Drug Bank, Therapeutic Target Database and Drug Signatures Database were utilized to predict targeted drugs for candidate genes. Results: MTHFD1 and LGALS4 were identified as promising therapeutic targets for PRAD, with evidence provided at multi-omics levels. LGALS4 was predominantly expressed in malignant cells and was correlated with enhanced immune checkpoint pathways, increased TIDE scores, and immunotherapy resistance. In contrast, MTHFD1was expressed in both tumor and microenvironmental cells and was associated with poor survival. Drug target prediction suggested that there are no currently approved drugs specifically targeting MTHFD1 and LGALS4. Conclusions: Our study identified MTHFD1 and LGALS4 as potential preventive targets for PRAD. However, future experiments are warranted to assess the utility and effectiveness of these candidate proteins.

N6-methyladenosine(m⁶A) is one of the most abundant modifications of mammalian cellular RNAs. m⁶A regulates various biological functions in epitranscriptomic ways, including RNA stability, decay, splicing, translation and nuclear export. Recent studies have indicated the growing importance of m⁶A modification in precancerous disease, influencing viral replication, immune escape, and carcinogenesis. Here, we review the role of m⁶A modification in HBV/HCV infection, NAFLD and liver fibrosis, and its function in liver disease pathogenesis. Our review will provide a new sight for the innovative treatment strategy for precancerous liver disease.

Breast cancer is a leading cause of cancer-related mortality worldwide, with drug resistance remaining a major therapeutic challenge. We integrated multi-omics data—including GWAS, eQTL, and pQTL—with Mendelian randomization to identify genes associated with breast cancer risk and therapy response. Our analyses revealed CTSF and GSTM3 as key candidates, showing consistent associations at both RNA and protein levels. Functional studies indicated that CTSF expression correlates with taxane resistance but cyclophosphamide sensitivity, while GSTM3 influences response across multiple regimens. Enrichment analyses suggest roles in immune and hormone signaling pathways. These findings highlight CTSF and GSTM3 as potential biomarkers and therapeutic targets for overcoming chemoresistance in breast cancer.

Background: Colorectal cancer (CRC) is a leading cause of cancer-related mortality worldwide. Identifying drug targets associated with CRC is crucial for developing targeted therapies. Methods: MR (IVW, Wald ratio, weighted median, and MR-Egger) and SMR analyses were used to screen candidate genes associated with CRC risk. Further validation was performed using The Cancer Genome Atlas (TCGA) to assess gene expression patterns and prognostic significance. Additionally, immune infiltration analysis was conducted to characterize the tumor immune microenvironment. Drug prediction was performed to explore potential therapeutic interventions. Results: Eight genes were identified associated with CRC. IGFBP3, CD72, SERPINH1, CHRDL2, LRP11, and SPARCL1 were linked to an increased risk of CRC, whereas DBI and HYAL1 were associated with a decreased risk of CRC. Notably, DBI exhibited a potentially favorable immune profile, negatively correlated with Tregs and MDSCs while positively associated with activated CD8⁺ and CD4⁺ T cells. Conclusions: Eight genes were identified as associated with CRC, among which DBI exhibited a potential protective role, correlating with improved patient survival, enhanced immune activation, and increased responsiveness to immunotherapy. The remaining proteins demonstrated diverse and complex functions within the tumor immune microenvironment, providing novel insights for the development of precision diagnostics and immunotherapeutic strategies.

Despite the success of the Expanded Program on Immunization (EPI) in reducing hepatitis B virus (HBV) prevalence, the long-term durability of vaccine-induced immunity and the precise trajectory of antibody decay in Chinese pediatric populations remain under-characterized. This study investigated the seroprevalence of hepatitis B surface antigen (HBsAg) and the kinetics of hepatitis B surface antibody (anti-HBs) in a large cohort of children in Wuhan to inform prime-boost vaccination strategies. We conducted a single-center, cross-sectional retrospective analysis of 58,169 children aged 0-17 years evaluated at Renmin Hospital of Wuhan University between January 2019 and November 2025. Serum HBsAg and anti-HBs levels were qualitative/quantified using chemiluminescence immunoassays (CLIA). Data were stratified by age, gender, and year. Statistical analyses utilized the Chi-square test for categorical variables and the Kruskal-Wallis test with Bonferroni‑corrected post-hoc pairwise comparisons for continuous variables. The overall HBsAg seroprevalence was 1.27% (723/56,956). However, this rate was heavily skewed by a high frequency of transient HBsAg reactivity in neonates aged 1-30 days (11.97%), likely attributable to vaccine-induced antigenemia and assay interference. After excluding infants < 1 year, the adjusted HBsAg prevalence was 0.47%, which declined significantly from 2019 (0.81%) to 2023 (0.27%). A secondary peak in HBsAg prevalence (1.16%) was observed in adolescents aged 13 years. Among 57,004 subjects assessed for immunity, 66.27% were seroprotected (anti-HBs ≥ 10 mIU/mL). Anti-HBs seropositivity peaked at 92.64% in infants aged 7-12 months but declined precipitously to 48.98% by age 3 years. From age 5 to 17 years, protective antibody rates stabilized at suboptimal levels (30-40%). While males exhibited a higher overall response rate than females (67.21% vs. 65.03%; P < 0.001), median titers in responders did not differ by sex. Although the HBsAg prevalence in Wuhan's pediatric population has decreased, the persistence of a 0.47% prevalence in children > 1 year and a resurgence of infection in early adolescence highlight gaps in the current elimination strategy. The rapid decay of anti-HBs titers by age 3 and the "juvenile pause" in immune surveillance suggest critical windows of vulnerability. These findings support the implementation of serological monitoring and targeted booster vaccination at ages 2-3 and 12-13 years to sustain population-level immunity and achieve the WHO 2030 elimination targets.