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.

EWSR1 fusions are recurrent genetic alterations in a wide spectrum of mesenchymal tumors and are often associated with specific clinicopathologic entities. However, the presence of an EWSR1 rearrangement does not always indicate a functional or disease-defining fusion.

We report a case of undifferentiated pleomorphic sarcoma with high-grade morphologic features harboring an EWSR1 rearrangement detected by fluorescence in situ hybridization. It was subsequently characterized by RNA sequencing as a likely nonfunctional fusion of EWSR1 exon 1 and NF2 intron 1. Histologically, the tumor was composed of pleomorphic spindle cells with brisk mitotic activity and lacked a specific line of differentiation. Immunohistochemically, the tumor showed diffuse cytoplasmic S100 positivity, with nuclear staining in a subset of tumor cells, while the overall immunophenotype did not support a specific line of differentiation. The EWSR1::NF2 fusion was inferred to have a tail-to-tail configuration, and additional KRAS and TP53 alterations were detected.

This case highlights that an EWSR1 rearrangement detected by fluorescence in situ hybridization should be interpreted cautiously and does not necessarily represent a functional or disease-defining fusion. Comprehensive molecular evaluation is important for the accurate interpretation and classification of sarcomas with atypical EWSR1 rearrangements.

Head, thoracic, abdominal, and pelvic polytrauma is clinically complex and requires coordinated multidisciplinary care, creating an urgent need for standardized guidance. This guideline aims to provide an evidence-based foundation and clinical pathway for the diagnosis, assessment, damage control, surgical timing, and acute-phase management of patients with head, thoracic, abdominal, and pelvic polytrauma. Led by the Senior Department of Neurosurgery, Chinese PLA General Hospital, a multidisciplinary working group comprising experts in thoracic surgery, general surgery, orthopedics, critical care medicine, anesthesiology, radiology, emergency medicine, nursing, and related disciplines developed the guideline through systematic review of the relevant literature, consideration of the characteristics of trauma care in China’s military and civilian medical systems, and two rounds of expert voting and consensus decision-making. The guideline addresses 22 key clinical questions covering imaging assessment, damage-control resuscitation, prioritization of craniocerebral and torso injury management, anticoagulation and hemostatic management, intensive care, and early rehabilitation. A total of 22 recommendations were formulated by integrating evidence quality, clinical feasibility, and implementability, together with corresponding implementation points and quality-control indicators. The guideline emphasizes stabilization of vital signs, damage-control principles, multidisciplinary collaboration, standardized clinical pathways, and a tiered trauma-care system. Implementation of these recommendations may improve the consistency and timeliness of multidisciplinary care and provide a framework for reducing early mortality while preserving neurological and functional outcomes.

Hepatitis B virus (HBV) reactivation is a well-recognized complication in patients with lymphoma receiving immunosuppressive therapy, particularly rituximab-containing regimens. We describe a 58-year-old man with diffuse large B-cell lymphoma and an atypical baseline HBV serological profile: hepatitis B surface antibody (anti-HBs) positivity (102.00 U/L), antibody to hepatitis B core antigen negativity, a low-level hepatitis B surface antigen (HBsAg) result (0.35 COI, reported as negative by the local laboratory), and undetectable HBV DNA. Thirteen days after initiation of the fourth cycle of modified R-CHOP (rituximab, cyclophosphamide, pirarubicin, vinorelbine and dexamethasone) chemoimmunotherapy, the anti-HBs titer had decreased to 1.31 S/CO, the HBsAg level to 0.02 S/CO, and HBV DNA was not reassessed until reactivation. Approximately 16 weeks after treatment completion, the patient developed fatigue, anorexia, and jaundice. HBsAg increased from 28.66 S/CO to 8048.30 IU/mL, hepatitis B e antigen became positive, and HBV DNA increased to 1.94 × 109 IU/mL. Despite treatment with tenofovir alafenamide fumarate and plasma exchange, the patient died of refractory liver failure and hepatic encephalopathy. These findings suggest that atypical serological profiles may not reliably indicate a low risk of severe HBV reactivation during intensive immunosuppressive therapy. Comprehensive pretreatment risk assessment and long-term monitoring of anti-HBs titers, HBsAg, and HBV DNA during and after therapy may facilitate earlier detection and intervention.

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.

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.