Despite recent advances in the treatments of hepatocellular carcinoma (HCC), the prognosis of HCC patients remains controversial. The purpose of this study was to investigate the prognostic performance of pretreatment albumin to C-reactive protein ratio (ACR) in patients with HCC. This study included 409 initially diagnosed HCC patients retrospectively. The optimal cut-off points for distinguishing high and low ACR value was determined by the X-tile software. The chi-squared test was used for comparing the baseline clinicopathologic parameters in different groups and subgroups. The Cox regression with log-rank tests was used to analyze OS and DFS, and Kaplan-Meier curves was used to estimate the prognosis of HCC patients. Patients with lower ACR were significantly correlated with advanced clinical parameters, using a cut-off points of 5.4 (high ACR, n = 236 vs. low ACR, n = 173). Multivariate analysis demonstrated that ACR was associated with OS (HR = 0.544, 95% CI: 0.385–0.769, p = 0.001), with DFS (HR = 0.550, 95% CI: 0.392–0.772, p = 0.001). Treatment exposure (HR = 2.191; 95% CI: 1.533–3.132; p < 0.001), tumor size (HR = 1.973; 95% CI: 1.230–3.164; p = 0.005), serum AFP level (HR = 1.752; 95% CI: 1.277–2.403; p = 0.001), and TNM stage (HR = 0.470; 95% CI: 0.319–2.504; p < 0.001), were independent factors for OS in HCC patients. Treatment exposure (HR = 2.244; 95% CI: 1.590–3.166; p < 0.001), TNM stage (HR = 2.075; 95% CI: 1.436–3.000; p < 0.001), serum AFP level (HR = 1.819; 95% CI: 1.340–2.469; p = 0.001), tumor size (HR = 1.730; 95% CI: 1.113–2.689; p = 0.015), and ACR (HR = 0.550; 95% CI: 0.392–0.772; p = 0.001) were independent factors for DFS in HCC patients. Pretreatment ACR is a convenient and useful parameter for HCC patients predicting OS and DFS. Lower ACR was associated with advanced TNM stage, larger tumor size, and a high concentration of AFP. These results may help to design strategies to personalize management approaches among HCC patients.

The purpose of this work is to analyze preoperative serum aspartate aminotransferase (AST) levels and their effect on the prognosis of patients with non-small cell lung cancer (NSCLC) after surgical operation. These analyses were performed retrospectively in patients with NSCLC followed by surgery; participants were recruited between January 2004 and January 2008. All clinical information and laboratory results were collected from medical records. We explored the association between preoperative serum AST and recurrence-free survival (RFS), and the overall survival (OS) of NSCLC patients. Kaplan–Meier analysis and Cox multivariate analysis, stratified by the AST median value, were used to evaluate the prognostic effect. A chi-squared test was performed to compare clinical characteristics in different subgroups. A p-value of ≤0.05 was considered to be statistically significant. A total of 231 patients were enrolled. The median RFS and OS were 22 and 59 months, respectively. The AST levels were divided into two groups, using a cut-off value of 19 U/L: High AST (>19 U/L), n = 113 vs. low AST (≤19 U/L), n = 118. Multivariate analysis indicated that preoperative serum AST > 19 U/L (hazard ratio (HR) = 0.685, 95% confidence interval (CI): 0.493–0.994, p = 0.046 for RFS, HR = 0.646, 95% CI: 0.438–0.954, p = 0.028 for OS) was an independent prognostic factor for both RFS and OS. High preoperative serum AST levels may serve as a valuable marker to predict the prognosis of NSCLC after operation.

Background: Osteopontin (OPN), a phosphorylated glycoprotein encoded by SPP1, critical in hepatic inflammation and fibrosis, requires further investigation for its role on hepatocellular carcinoma (HCC) and predictive value for anti-programmed cell death ligand 1 (anti-PD-L1) immunotherapy responses. Methods: Publicly available datasets were utilized to explore OPN expression in HCC. A retrospective cohort study involving 316 participants, recruited from January 2015 to March 2017. Serum OPN levels were measured by enzyme-linked immunosorbent assay. Diagnostic performance was assessed using receiver operating characteristic (ROC) curves, a logistic regression model was developed for early HCC diagnosis. Prospective follow-up was conducted from 2017 to 2024 to evaluate overall survival (OS) and disease-free survival (DFS) using Kaplan-Meier analyses. The survival benefit of anti-PD-L1 immunotherapy for patients with OPN patterns was investigated. Results: Serum OPN levels were significantly elevated in HCC compared to chronic liver disease and healthy individuals (both p < 0.001). The area under the curve (AUC) for OPN was 0.903, with 88.2% sensitivity and 83.3% specificity, significantly superior to AFP alone (AUC: 0.707). A combined diagnostic model integrating OPN with alpha-fetoprotein (AFP) and aspartate aminotransferase (AST) enhanced accuracy further (AUC: 0.941). High OPN levels indicated higher tumor burden and predicted worse clinical outcomes (mean OS: 49.1 vs 75.1 months; mean DFS: 37.7 vs 60.9 months, respectively; both log-rank p < 0.001). Anti-PD-L1 immunotherapy significantly prolonged survival (OS: 62.9 vs 38.0 months, p = 0.009; DFS: 48.7 vs 28.6 months, p = 0.033) in patients with OPN high pattern. Conclusion: Serum OPN demonstrates standalone diagnostic value for HCC and enhances conventional biomarker panels when combined with AFP and AST. OPN high pattern identify patients likely to benefit from anti-PD-L1 immunotherapy, suggesting its dual utility as a diagnostic and predictive biomarker.

Background: Esophageal squamous cell carcinoma (ESCC) is a common malignant tumor in China, with a poor five-year survival rate due to the lack of effective early diagnostic methods. This study aimed to identify potential non-invasive biomarkers and clarify their underlying mechanisms. Methods: We employed an integrative approach combining serum proteomic profiling, bulk RNA sequencing, and single-cell RNA-seq (scRNA-seq) analyses. Quantitative proteomics was conducted on 15 serum samples of treatment-naive early-stage ESCC patients and 5 from healthy controls. Differentially expressed proteins (DEPs) were cross-referenced with differentially expressed genes (DEGs) from the GSE53624 dataset, and a diagnostic model was developed using LASSO regression. Cross-validation was performed using scRNA-seq data. The enzyme-linked immunosorbent assay (ELISA) was utilized to validate FTL in 155 serum samples from two centers. In silico FTL knockouts were conducted using scTenifoldKnk, followed by GO, KEGG, and PPI network analyses. Results: Proteomic profiling identified a total of 129 DEPs. Intersection with GSE53624 DEGs yielded 8 overlapping genes, and a 6-biomarker (TF, CHAD, CSRP1, FCGR3A, RCN1, FTL) diagnostic model was built, with AUC 0.882–1.0 across validation cohorts. scRNA-seq intersection analysis identified FTL as the only overlapping DEG, exhibiting high expression levels in ESCC epithelial cells and macrophages. FTL demonstrated strong standalone diagnostic performance, with AUC values ranging from 0.872 to 0.970 across three GEO datasets. ELISA validation yielded an AUC of 0.75 (95% CI: 0.674–0.816) and 0.838 (95% CI: 0.751–0.905) for early-stage ESCC, surpassing the performance of CEA and SCCA. The combination of FTL with SCCA further enhanced discriminatory efficacy. Mechanistically, FTL was associated with altered immune cell infiltration, characterized by increased resting dendritic cells and M2 macrophages and decreased follicular helper T cells, as well as activation of the ferroptosis pathway. In silico FTL knockouts revealed DEGs enriched in stress and metabolic biological processes, extracellular vesicles (cellular component), transcriptional regulation (molecular function, CHOP-ATF3 complex), IL-17/TNF pathways, and lipid/ROS-related pathways. Protein-protein interaction hubs included FOS, ATF3, NFKBIA, and CXCL8, with FTL linked to NFE2L2, TFRC, and TXNRD1. Conclusions: FTL represents a credible non-invasive serum diagnostic biomarker for ESCC. Computational analyses suggest it is a candidate molecule requiring further mechanistic and therapeutic investigation.