Unexpected vascular lesions may complicate standard laparoscopic pancreatic procedures. We report a case of mucinous cystic neoplasm (MCN) treated with laparoscopic spleen-preserving distal pancreatectomy (LSPDP) in which unrecognized immunoglobulin G4 (IgG4)-related periarteritis of the splenic artery caused difficulty during vascular division. A 76-year-old woman underwent LSPDP for MCN. Preoperative computed tomography demonstrated circumferential soft-tissue thickening along the splenic artery. Intraoperatively, the splenic artery was deeply embedded within the pancreatic parenchyma, making the Kimura technique impractical; therefore, the Warshaw technique was selected. However, the splenic artery demonstrated marked circumferential wall thickening, precluding safe division with ligation or clipping alone. The artery was ultimately divided using a vascular stapler. Histopathological examination revealed low-grade MCN and IgG4-related periarteritis involving the splenic artery. This case highlights that IgG4-related periarteritis should be considered when unexplained perivascular soft-tissue thickening is identified preoperatively, as it may significantly alter intraoperative strategy during LSPDP.

Drug therapies targeting vasculature in metastatic cancer have not been highly effective and are therefore currently limited to an adjunctive role, such as in combination regimens. The development of novel, more effective therapeutic strategies with new mechanisms of action is therefore greatly needed. In a previous study, we reported a lipid nanoparticle (LNP)-based vascular-disrupting strategy utilizing cyclic RGD peptide-modified LNPs encapsulating small interfering RNA against Fas ligand (cRGD-LNP/siFasL). We combined this strategy for selective targeting of tumor endothelial cells with stimulator of interferon genes (STING) agonist-loaded LNPs (STING-LNPs). Here, we have demonstrated the potential of such combination therapy in treating lung metastases. We found that cRGD-LNPs accumulated in the vasculature within tumor colonies in the lung. A combination of cRGD-LNP/siFasL and STING-LNP induced significant antitumor effects in mouse models of Renca and 4T1 lung metastases. Moreover, this combination therapy reduced the vasculature within tumor colonies, with no obvious change in the surrounding normal lung tissue, indicating preferential vascular disruption. These findings demonstrate that the combination therapy exerts antitumor activity against lung metastases through tumor vascular disruption, indicating that such treatment is potentially a potent disrupter of the vascularity in metastatic tumors.

Glypican-3 (GPC-3) is a cell-surface glycoprotein, highly expressed in hepatocellular carcinoma (HCC) but largely absent in normal adult liver tissues, making it a clinically compelling biomarker and therapeutic target. Although monoclonal antibodies and antibody-drug conjugates have proven to be GPC-3-targeted therapies, their large molecular size, slow pharmacokinetics, and potential immunogenicity limit their diagnostic applications. Peptide ligands offer an attractive alternative owing to their low molecular weight, rapid tumor penetration, favorable clearance profiles, synthetic accessibility, and ease of chemical modification. This topical review highlights the development of linear and cyclic GPC-3-binding peptides over the past two decades, developed primarily via phage display, rational optimization, and structure-guided approaches, enabling PET, SPECT, and fluorescence imaging of HCC in preclinical models. Recent refinements, including albumin-binding modifications and cyclization strategies, have improved tumor-to-liver contrast and in vivo stability. This review summarizes the biological significance of GPC-3, compares peptides and peptide probes as targeting modalities, and critically analyzes recent advances in linear and cyclic peptide-based GPC-3 imaging probes. We also emphasized the importance, current challenges, and future opportunities in AI/ML-based design of peptide ligands for HCC theranostics.

This systematic review and meta-analysis evaluated the pooled outcomes and comparative evidence of balloon enteroscopy-assisted ERCP (BEA-ERCP) and EUS-guided biliary drainage (EUS-BD) for malignant biliary obstruction (MBO) in patients with surgically altered anatomy (SAA).

PubMed, Web of Science, and the Cochrane Library were searched up to January 2026. The primary outcome was the pooled technical success rate. Secondary outcomes included the clinical success rate, adverse event rate, recurrent biliary obstruction (RBO) rate, and mean procedure time. Subgroup analyses compared outcomes in studies directly comparing the two procedures. A random-effects model was used.

Thirteen studies were included, comprising nine studies investigating BEA-ERCP (394 patients) and seven investigating EUS-BD (206 patients), including three comparative studies. Pooled technical and clinical success rates were 75% and 72% for BEA-ERCP and 97% and 92% for EUS-BD, respectively. Pooled adverse event rates were 11% for BEA-ERCP and 17% for EUS-BD, and pooled RBO rates were 26% and 23%, respectively. In subgroup analyses of the three comparative studies, technical success rates (risk ratio [RR], 0.74; 95% confidence interval [CI], 0.67-0.82) and clinical success rates (RR, 0.70; 95% CI, 0.61-0.80) were significantly lower with BEA-ERCP than with EUS-BD, with no significant differences in adverse event rates, RBO rates, or procedural times.

In the three comparative studies, EUS-BD achieved higher technical and clinical success rates than BEA-ERCP for MBO in patients with SAA, with no significant difference in adverse events. These non-randomized findings are preliminary, and large-scale prospective comparative studies are warranted.

Cigarette smoke-induced chronic inflammation (CI) potentiates development of non-small cell lung cancer (NSCLC) by mediating genetic and epigenetic events. Using normal lung organoids (LOs), we define how chronic cigarette smoke condensate (CSC) exposure drives two separate stem cell populations to evolve premalignant states harboring progressive epigenetic and linked transcriptomic abnormalities in the absence of major driver mutations. These dynamics facilitate evolution of an immune evasive state with downregulation of inflammatory pathways and accompanying death signals mediated by epigenetic silencing of PANoptosis regulator, Zbp1. The stem cell populations evolve through distinct trajectories to respond differently to subsequent introduction of oncogenic mutations, Kras^G12V and loss of Tp53, to induce one step transformation of CSC exposed organoids resulting in two major NSCLC subtypes. Kras mutations drive tumorigenesis primarily in a bronchioalveolar stem cell-derived state producing adenocarcinomas while TP53 loss drives tumorigenesis in a basal stem cell-derived state resulting in squamous cell carcinomas. CSC-induced downregulation of Zbp1 and interferon signaling is further potentiated in tumors with mutation-specific changes marked by decreased expression in Kras-mutant contexts. Our findings define unique transcriptomic profiles in CI-induced stem cell states and reveal a key role for cell death pathway-associated genes in potentiating oncogenic drivers to promote NSCLC. Together, our data suggest strategies to predict cancer risk and enable early interception.

Esophageal squamous cell carcinoma (ESCC) is a highly aggressive malignancy with an unfavorable prognosis, and the molecular mechanisms underlying its metastatic progression remain incompletely defined. Here, we investigated the functional role of ephrin type-B receptor 1 (EPHB1), a member of the ephrin receptor family, in ESCC metastasis. Integrated analyses of RNA-sequencing data and publicly available databases demonstrated that EPHB1 expression is significantly upregulated in ESCC tissues and is positively associated with advanced tumor grade and poor patient survival. Gain- and loss-of-function assays revealed that EPHB1 knockdown markedly inhibited ESCC cell migration, invasion, and epithelial-mesenchymal transition (EMT), whereas EPHB1 overexpression exerted the opposite effects. Consistently, in vivo metastasis assays further confirmed that EPHB1 promotes lung metastasis of ESCC cells. Mechanistically, we identified SRY-box transcription factor 2 (SOX2) as a critical upstream regulator that directly binds to the EPHB1 promoter and transcriptionally activates its expression. Rescue experiments demonstrated that SOX2-induced EMT and invasive capacity are largely mediated through EPHB1. Collectively, these findings uncover a previously unrecognized SOX2/EPHB1 signaling axis that drives ESCC metastasis and suggest EPHB1 as a potential therapeutic target for ESCC.

Advances in therapy have transformed multiple myeloma (MM) into a chronic relapsing-remitting disease, resulting in a growing population of survivors requiring long-term, comprehensive care. Five-year relative survival for.

Breast cancer is the most common cancer among females globally. While treatment is life-saving and essential, it can significantly affect physical health, psychological well-being, quality of life, and body image.

To systematically review and synthesize the evidence on the impact of breast cancer and its treatment on body image in females.

Systematic review and meta-analysis.

Four major databases were searched for relevant peer-reviewed studies published until 2025. A total of 41 studies were included in the systematic review, of which 24 were eligible for the meta-analysis. Standardized mean differences with 95% confidence intervals were calculated using a restricted maximum likelihood model, with analyses conducted in JAMOVI and heterogeneity assessed via Q and I² statistics.

Females with breast cancer reported significantly lower body image scores than healthy controls (ES = -1.02). Furthermore, body image scores declined from pre-treatment to during treatment (ES = -0.45). Mastectomy was associated with poorer body image compared to breast-conserving therapy (ES = -1.11).

Although medically essential, breast cancer treatment can adversely affect body image. Integrating body image support into treatment plans is crucial for promoting the overall health and quality of life of females diagnosed with breast cancer.

PROSPERO No. CRD42024503033.

Pneumonia is a leading cause of mortality for children under five worldwide and is often diagnosed using WHO clinical criteria. In resource-limited settings, accurate diagnosis remains challenging. Lung ultrasound (LUS) is an effective, low-cost diagnostic tool, however, its performance in smaller regional hospitals remains underexplored. We conducted a prospective observational study to evaluate the diagnostic yield of LUS among children hospitalized with WHO-defined pneumonia in Eastern Uganda. All children received a systematic 12-zone LUS by a trained operator using a linear probe in the sagittal plane. LUS was remotely interpreted by two blinded reviewers. Chest X-ray (CXR) was performed when feasible. We enrolled 46 patients with a total of 523 lung zones reviewed. The average age was 22 months (± 26.8 months); 67% of patients demonstrated hypoxemia. LUS was adequate in 42/46 (91%) children. LUS identified pneumonia in 25/42 (59%), bronchiolitis in 2/42 (5%), and normal lung in 15/42 (36%). CXR was completed in 40/46 (87%) children and showed pneumonia in 18/40 (45%). For the 36 children with both LUS and CXR, four (11%) demonstrated pneumonia on CXR but not LUS, compared to 11 (30%) who had pneumonia on LUS but not CXR. Our study demonstrated that LUS is feasible and identified features of pneumonia is 59% of LUS studies. While the overall diagnostic yield of LUS is comparable to CXR, a substantial proportion of children had pulmonary findings detected by only one imaging modality. These findings suggest a complementary rather than redundant role for LUS and CXR.

US health care spending growth has long outpaced economic growth. However, during the period 2014-19 (before the COVID-19 pandemic), growth in per capita health care spending relative to per capita gross domestic product growth fell by 21 percent compared with 2007-14. We examined spending growth domestically and internationally to determine the causes of this slowdown. We decomposed spending growth by source of funds, compared four drivers of growth over time within the US and relative to fifteen Organization for Economic Cooperation and Development countries, and conducted a US-specific breakdown of utilization. We found that declining growth in health care prices and utilization were major drivers of the slowdown of health care spending. Slower growth did not appear to have been driven by across-the-board reductions in disease burden and input costs, although certain metrics fell. Utilization reduction was a major driver through technology allowing the use of alternative sites of care; greater use of preventive care that reduces costs; ongoing expansion of Medicare Advantage, managed Medicaid, and high-deductible health plans; and increased utilization management. This slowdown suggests the need to monitor trends more closely for signs of additional major shifts in spending growth.