Biliary duct invasion (BDI) is an underrecognized growth pattern of colorectal cancer (CRC) liver metastases that can mimic intrahepatic cholangiocarcinoma or intraductal papillary neoplasm of the bile duct. Its prevalence and clinicopathologic associations remain unclear. This study aimed to determine the prevalence of BDI and its clinicopathologic associations in surgically resected CRC liver metastases.

We retrospectively analyzed 133 consecutive patients who underwent hepatic resection for CRC liver metastases. Clinicopathologic variables, including age, sex, resection type, tumor differentiation, lymphovascular invasion (LVI), tumor budding, surgical margin status, and primary tumor characteristics, were compared between BDI-positive and BDI-negative cases. Categorical variables were analyzed using the chi-square, Fisher exact, or Fisher-Freeman-Halton exact test, as appropriate; continuous variables were analyzed using the Mann-Whitney U test.

BDI was identified in 19 of 133 cases (14.3%). Male sex showed the strongest numerical trend toward BDI (84.2% vs. 61.4%, P = 0.096), and LVI showed a nonsignificant numerical trend toward higher BDI rates (26.3% vs. 12.3%, P = 0.149). No clinicopathologic variable in the primary cohort analysis reached statistical significance after Bonferroni correction (α = 0.0050).

BDI occurs in approximately 14% of surgically resected CRC liver metastases in this cohort. Male sex and LVI show nonsignificant numerical trends toward higher BDI rates, but these findings should be interpreted cautiously given the limited sample size. Accurate histopathologic recognition of BDI and its distinction from intrahepatic cholangiocarcinoma remain important for correct pathologic diagnosis. Further prospective studies are warranted to clarify the clinicopathologic and prognostic significance of BDI.

Endovascular embolization is a cornerstone treatment for intracranial aneurysms, and transfemoral access (TFA) has traditionally been the default vascular route. Transradial access (TRA) is increasingly used in neurointervention because it may reduce clinically important access-site complications, improve postprocedural comfort, and facilitate earlier ambulation. This narrative review aims to summarize direct and indirect evidence comparing TRA and TFA for intracranial aneurysm embolization, with attention to technical feasibility, access conversion, puncture-site complications, neurological events, radiation exposure, procedure duration, recovery, and cost considerations. Direct comparative evidence specific to aneurysm embolization remains limited and is mainly observational; some supporting data come from diagnostic cerebral angiography, mixed therapeutic neurointervention, and cardiovascular access literature. Available data suggest that TRA may be a safe and feasible option for selected patients when performed by experienced operators, particularly when radial anatomy is favorable and the intended device strategy is compatible with upper-extremity access. TFA remains essential for complex anatomy, large-bore device requirements, or insufficient TRA expertise. Access selection should therefore be individualized rather than based on a presumption of universal superiority. Well-designed multicenter studies are needed to define aneurysm-specific outcomes, long-term angiographic durability, patient-reported outcomes, and cost-effectiveness.

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.

Colorectal cancer is a major cause of cancer morbidity and mortality worldwide, including in China. Screening can facilitate earlier detection and reduce disease burden, while primary healthcare institutions are central to population outreach, risk assessment, referral, and follow-up. However, resource constraints, limited public awareness, low screening adherence, and fragmented coordination continue to hinder implementation in community and rural settings. This mini review summarizes the epidemiological and health-economic rationale for colorectal cancer screening in primary healthcare and discusses organizational models, risk-stratified screening and referral, workforce training, quality control, data management, and information sharing. Available evidence supports coordinated pathways that link noninvasive initial screening to timely colonoscopy and follow-up, supported by clear governance, trained personnel, and traceable data systems. The ongoing Yazhou District program is included briefly as a descriptive example of how these components may be organized in practice. Future research should evaluate uptake, positivity, colonoscopy completion, lesion detection, adverse events, costs, and longer-term outcomes in diverse primary-care settings.

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.

Since their first inception, neuroendocrine neoplasms of the breast have undergone many iterations of classification and definition. Taken together with their extremely low incidence, the ever-evolving landscape has made diagnosis, treatment, and research exceedingly challenging.

Our patient is a 45-year-old female who had a breast mass with clinical workup favoring a breast primary. A diagnosis of small cell carcinoma was established after an extensive clinical and pathologic workup. The mass did not respond to traditional neoadjuvant platinum-based chemotherapy, and she underwent a total mastectomy. Shortly thereafter, imaging revealed widely metastatic disease involving the brain, chest, abdomen, and pelvis. She received whole-brain radiation and, given the previous lack of response to chemotherapy, was recommended to try off-label tarlatamab. To date, with a short-term follow-up of 5 months, after whole-brain radiotherapy administered concurrently with the first cycle of tarlatamab, subsequent imaging showed near-complete radiographic resolution of extracranial metastatic disease, while the brain lesions also showed radiographic resolution on follow-up MRI.

We report the novel and preliminary use of tarlatamab in a patient with small cell neuroendocrine carcinoma of the breast, with short-term follow-up. We also discuss the most critical challenges associated with this rare pathologic diagnosis and the important elements to consider to ensure that metastatic disease is excluded.

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.