Machine-learning approaches that combine predictive performance with model interpretability may improve lung cancer status classification. This study aimed to develop and internally evaluate an Explainable Precision Screening Framework for lung cancer risk classification using demographic, behavioral, and symptom-based variables from a publicly available dataset.

This retrospective cross-sectional study analyzed a publicly available Kaggle dataset containing 309 records, including 270 labeled as lung cancer and 39 as non-cancer. Six models—logistic regression, support vector machine (SVM), random forest, LightGBM, XGBoost, and a stacking ensemble—were compared using a stratified hold-out test set and repeated stratified five-fold cross-validation. Performance was assessed using classification metrics with bootstrap 95% confidence intervals (CIs). A separate Shapley additive explanations (SHAP) analysis was applied to the standalone SVM model for exploratory feature attribution.

Across all models, accuracy ranged from 85% to 92% (ROC-AUC: 0.93–0.95). The stacking ensemble achieved 0.92 accuracy (95% CI: 0.85–0.98), 0.94 sensitivity (95% CI: 0.88–1.00), 0.75 specificity (95% CI: 0.40–1.00), 0.96 precision (95% CI: 0.89–1.00), 0.95 F1 score (95% CI: 0.91–0.99), and 0.95 ROC-AUC (95% CI: 0.89–0.99). Its PR-AUC was 0.993 (95% CI: 0.981–0.999), and its Brier score was 0.074 (95% CI: 0.037–0.121). SHAP analysis identified smoking, yellow fingers, coughing, chest pain, wheezing, shortness of breath, and age as the features contributing most strongly to its predictions.

Within this public retrospective dataset, the stacking ensemble was among the highest-performing models, whereas separate SHAP analysis of the standalone SVM model identified the features contributing most strongly to its predictions. Given the marked class imbalance, the absence of a reported clinical reference standard for the source labels, the framework requires independent validation in clinically verified multicenter cohorts before clinical use.

Non-muscle-invasive bladder cancer (NMIBC) is characterized by a high recurrence rate and a substantial long-term surveillance burden. However, current detection and surveillance strategies rely largely on invasive cystoscopy and urine cytology, which are limited by patient discomfort, suboptimal adherence, and insufficient sensitivity, particularly for low-grade disease. This mini review examines the role of liquid biopsy in the detection, risk stratification, and surveillance of NMIBC. It summarizes current evidence on circulating tumor DNA, circulating tumor cells, exosomes and extracellular vesicles, urinary tumor DNA, and DNA methylation and protein biomarkers in blood or urine. For detection, urine-based molecular assays complement cystoscopy and cytology in the noninvasive assessment of patients with suspected bladder cancer. For risk stratification, molecular detection of residual disease and longitudinal biomarker changes help identify patients at increased risk of recurrence or progression. During surveillance, urine-based assays support earlier recurrence detection and, in selected settings, help reduce the frequency of cystoscopy. Overall, liquid biopsy is a promising minimally invasive complement to conventional NMIBC management although technical standardization and prospective clinical validation are required before routine implementation.

Hepatitis B virus (HBV) vertical transmission remains a major health challenge, and the characteristics of the placental immune microenvironment in chronic infection remain unclear. This study aimed to use mass cytometry to comprehensively analyze phenotypic changes in placental immune cell subsets.

We collected placental tissues from 20 pregnant women (6 healthy controls and 14 with chronic HBV infection). CD45+ leukocytes were detected using a 35-marker antibody panel. Unsupervised clustering identified 14 clusters, of which 13 immune clusters were analyzed.

HBV mainly caused functional remodeling of placental immune cells rather than changes in cell composition (P > 0.05 for all subsets). In natural killer (NK) cells, CD38 (P = 0.015) and CD16 (P = 0.0020) were notably upregulated and strongly correlated (ρ = 0.872, P < 0.001), suggesting potentially enhanced antibody-dependent cellular cytotoxicity (ADCC) function. T cells showed upregulation of CD27, CD38, and CXCR5. Basophils exhibited the most pronounced changes: 9 differential markers (including chemokine receptors CCR4 and CCR7) were consistently downregulated. Classical monocytes showed an M1 polarization tendency (CD38↑, CD163↓). All P-values were raw; no markers remained significant after false discovery rate (FDR) correction at an FDR threshold of < 0.1, indicating nominal significance. In addition, the coordinated expression patterns of markers within multiple cell subsets were weakened after infection.

These exploratory findings suggest that HBV may reshape placental immunity through enhanced NK cell activation, broad basophil suppression, and disrupted marker coordination. The sample size was limited (n = 20), so the results need to be validated in larger cohorts. These findings provide new perspectives for understanding the mechanisms of mother-to-child transmission.

Estrogen receptor alpha, encoded by the ESR1 gene, is a major oncogenic driver in hormone receptor-positive/HER2-negative breast cancers. While endocrine therapies are effective in treating this subgroup, patients with advanced or metastatic disease may develop resistance associated with acquired somatic ESR1 mutations. This mini review summarizes recent clinical and technological advances in understanding ESR1 mutations, newly approved targeted therapies, and the use of liquid biopsy companion diagnostics, with a focus on their implications for pathologists.

We conducted a narrative review of PubMed-indexed literature and relevant regulatory and guideline sources related to ESR1 in breast cancer, with an emphasis on recent peer-reviewed studies of ESR1 mutations and clinical trials of emerging therapies.

This review describes the molecular features of ESR1 alterations and estrogen receptor pathway biology, the mechanisms and key trial data for recently approved ER-targeted therapies for ESR1-mutated breast cancer. Additionally, it evaluates liquid biopsy testing platforms for detecting ESR1 mutations, discusses the advantages and limitations of liquid biopsy in detection of treatment resistance, and considers the evolving role of pathologists in breast cancer care.

Acquired ESR1 mutations are major drivers of endocrine therapy resistance. Next-generation sequencing and liquid biopsy have increasingly informed the clinical management of breast cancer in the past decade. Pathologists can play an important role in implementing molecular testing, interpreting complex biomolecular data, and helping to guide timely treatment decisions in the era of precision oncology.

The IMbrave050 trial suggested that adjuvant immune checkpoint inhibitor therapy may benefit patients with hepatocellular carcinoma exceeding the “up-to-7” criterion. This study aimed to compare survival outcomes and safety between such patients receiving adjuvant programmed cell death protein 1 inhibitors and those undergoing active surveillance after curative resection.

Data were prospectively collected from patients at 13 medical centers in China between 2019 and 2024. The study was designed according to a target trial emulation framework, and propensity score matching was used to reduce confounding. The primary endpoint was recurrence-free survival; secondary endpoints included overall survival and incidence of treatment-related adverse events.

Median follow-up was 32.7 months (interquartile range, 20.9–47.5). Propensity score matching yielded 200 patients per group. Median recurrence-free survival was longer in the adjuvant group (28.0 months; 95% confidence interval [CI], 21.7–34.3) than in the surveillance group (14.4 months; 95% CI, 10.7–18.1; hazard ratio, 0.58; 95% CI, 0.45–0.74). Median overall survival was not reached in the adjuvant group and was 45.0 months (95% CI, 37.8–52.1) in the surveillance group (hazard ratio, 0.63; 95% CI, 0.45–0.89). The most frequent grade 3–4 treatment-related adverse events were hand–foot skin reaction (7.2%), elevated alanine aminotransferase (5.8%), and elevated aspartate aminotransferase (5.3%).

Adjuvant programmed cell death protein 1 inhibitors, with or without molecularly targeted agents, were associated with longer recurrence-free survival and acceptable safety in patients with hepatocellular carcinoma exceeding the “up-to-7” criterion.

Balloon-occluded transarterial chemoembolization (B-TACE) has emerged as a significant advancement in the locoregional treatment of hepatocellular carcinoma. This technique utilizes a balloon microcatheter selectively placed in target hepatic arteries to occlude blood flow and enhance drug accumulation within tumors while minimizing systemic exposure. The feasibility, safety, and effectiveness of the balloon occlusion technique have been verified. Recent studies have demonstrated that B-TACE achieves superior tumor response rates and potentially improves survival outcomes compared with conventional transarterial chemoembolization (C-TACE) techniques, particularly in cases with complex tumor vasculature or C-TACE-refractory disease. However, determining which patients would benefit from B-TACE requires comprehensive assessment. It remains to be determined in clinical practice whether this technique increases the risk of liver function impairment or is associated with specific complications. Further research is needed to better understand the technical conditions required for its clinical application, prognostic factors, and how it can be combined with other interventional techniques. This review summarizes the current literature on B-TACE, focusing on its technical principles, clinical efficacy, safety profile, and evolving role within the contemporary treatment landscape for advanced hepatocellular carcinoma, including its integration with systemic therapies.