Metabolic dysfunction-associated steatotic liver disease (MASLD) is increasingly prevalent worldwide and is frequently encountered in patients undergoing liver transplantation and hepatic surgery. Although hepatic steatosis was once considered a relatively benign condition, accumulating evidence indicates that MASLD is associated with reduced tolerance to ischemic stress and increased susceptibility to ischemia–reperfusion injury, which may contribute to graft dysfunction and postoperative liver injury. In this mini review, we used the concept of hepatic resilience, referring to the ability of the liver to maintain homeostasis during stress and recover after injury. We discussed how MASLD may reduce hepatic resilience through mechanisms involving lipotoxicity, mitochondrial dysfunction, oxidative stress, inflammatory activation, regulated cell death, and impaired regeneration. MASLD represents a heterogeneous disease spectrum, and susceptibility to ischemia–reperfusion injury may differ according to disease stage and phenotype, particularly in the presence of progressive inflammation and fibrosis. We further summarized strategies aimed at improving hepatic resilience, including metabolic optimization, mitochondrial protection, modulation of reperfusion-associated inflammation, and enhancement of tissue repair. However, current evidence remains limited by the paucity of human studies and validated approaches for assessing hepatic resilience. Further investigation of these mechanisms may help develop individualized strategies to protect the liver in patients with MASLD during hepatic surgery and transplantation.

CXC chemokine receptor 2 (CXCR2) expression has been observed in normal neuroendocrine cells, but its role in neuroendocrine neoplasms is less well established. We aimed to evaluate CXCR2 expression with somatostatin receptor type 2 (SSTR2) expression in pancreatic neuroendocrine tumors (PanNETs) and small intestinal neuroendocrine tumors (SI-NETs).

This was a cross-sectional study. Pathology archives were searched for PanNETs with ≥2 resected liver metastases and SI-NETs with resected liver metastases, mesenteric tumor deposits (MTDs), and/or peritoneal metastases. Immunohistochemistry for CXCR2 was performed on de-identified tissue microarrays containing PanNETs and SI-NETs. SSTR2 and CXCR2 immunohistochemistry was also performed on tumor blocks from primary and metastatic PanNETs and SI-NETs. Based on H-scores, expression was scored as negative (<50), weak (50–100), moderate (>100–200), or strong (>200). Marker expression was descriptively reported among primary tumors, liver metastases, MTDs, and peritoneal metastases.

Among 12 primary PanNETs and 38 liver metastases, mean CXCR2 H-scores were 269.6 ± 36.7 and 254.6 ± 75.5, respectively, and mean SSTR2 H-scores were 261.5 ± 61.9 and 259.3 ± 70.9, respectively. All 84 SI-NET lesions showed moderate/strong CXCR2 expression, whereas 12 showed negative/weak SSTR2 expression. CXCR2 H-scores were 284.0 ± 26.5 in primary tumors, 272.5 ± 28.7 in MTDs, 269.6 ± 42.8 in liver metastases, and 265.0 ± 51.5 in peritoneal metastases. SSTR2 expression appears to be lower in MTDs than in primary tumors (182.2 ± 76.5 vs 235.9 ± 55.9).

CXCR2 is moderately/strongly expressed in most sampled PanNETs and all sampled SI-NETs. In SI-NETs, moderate/strong CXCR2 expression is less heterogeneous than SSTR2 expression.

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.

Standardized pathologic sampling and reporting are essential for pancreatic cancer staging, prognosis assessment, and comparable clinical data. This guideline aimed to develop evidence-based recommendations for standardized pathologic sampling and diagnostic reporting of pancreatic cancer in China. Literature searches were conducted in English and Chinese databases, guideline websites, Google, and reference lists for records published before December 31, 2023. Two investigators screened and extracted the evidence; methodological quality and certainty were assessed using AMSTAR/AGREE II and GRADE, respectively; and recommendations were formulated through two rounds of modified Delphi consultations, with an agreement threshold of ≥ 75% for consensus. The final guideline includes 11 recommendations, including six strong and five weak recommendations, addressing margin and surface assessment, sampling methods, histologic classification and grading, lymphovascular and perineural invasion, TNM staging, tumor regression grading after neoadjuvant therapy, background lesions, and structured reporting. These recommendations provide a standardized framework for pathologic assessment and reporting of pancreatic cancer resection specimens and may support more consistent prognostic evaluation and clinical decision-making.

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.

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.

Hepatic sinusoidal obstruction syndrome (SOS) is characterized by hepatic sinusoidal endothelial cell injury and detachment, hepatic sinusoidal congestion, and hepatic cell necrosis. Currently, limited data exist concerning changes during the recovery period, especially histopathological changes. The purpose of this study was to investigate the evolution of pathology in patients with pyrrolizidine alkaloid (PA)-induced SOS and in a monocrotaline-induced SOS rat model.

Patients diagnosed with PA-induced SOS who underwent liver biopsy after achieving clinical remission were consecutively enrolled in this retrospective study. To compare the clinical and pathological differences between patients with acute and convalescent SOS, a 2:1 matched analysis was performed based on age, sex, treatment regimen, and baseline Drum Tower Severity Scoring (DTSS) during the acute phase. Additionally, an animal model of PA-induced SOS was established through the administration of monocrotaline.

Fourteen consecutive patients with SOS who had adequate liver biopsy specimens obtained during recovery were identified. During convalescence, most laboratory and imaging findings, such as the map-like enhancement observed on computed tomography, also disappeared. However, histopathological analysis revealed a distinct shift from hepatic sinusoidal endothelial cell injury in the acute phase to portal tract abnormalities, primarily characterized by portal vein stricture, in the recovery phase. These pathological changes were corroborated in our animal model.

Our study suggests that both patients with PA-induced SOS and rats in the convalescent stage may exhibit porto-sinusoidal vascular disease-like changes. Regular follow-up and dynamic pathological assessment are therefore recommended to facilitate the early detection of potential signs of portal hypertension.