Primary mediastinal B-cell lymphoma is a rare subtype of non-Hodgkin lymphoma. Typical symptoms include cough, chest pain, and dyspnea; however, cardiac tamponade as the primary manifestation is exceedingly rare. We hereby present a case of a 83-year-old woman, who presented to our emergency department with dyspnea, cough and hypotension. On admission, echocardiography (transthoracic and transesophageal), computed tomography and cardiac magnetic resonance demonstrated a large 70 x 38 mm pericardial mass, with pericardial effusion and signs of cardiac tamponade. Positron emission tomography highlighted a marked hyperaccumulation of the tracer at the mass level, compatible with high metabolic activity. The patient underwent further workup with diagnostic and therapeutic pericardiocentesis, which demonstrated histopathology consistent with primary mediastinal B-cell lymphoma. This precise and complete diagnosis allowed the start of chemotherapy treatment with complete remission of the disease and regression of the mass in a few months. Our case highlights the importance of a complete and thorough workup for patients with chronic untraditional symptoms, like tamponade as the primary clinical presentation. Advanced multimodality imaging is crucial for early non-invasive assessment of primary cardiac tumors, helps guiding further investigations, treatment decision, assessing for potential complications, and allows documentation of therapeutic success.

Peptide-based immunotherapy targeting tumor-associated antigens presents a promising approach for prostate cancer intervention. In this study, we employed a preclinical approach to evaluate immunogenic epitope candidates derived from STEAP1 and PSMA, two well-characterized prostate cancer-associated antigens.

High-affinity cytotoxic T lymphocyte (CTL) epitopes restricted to HLA-A*02:01 were predicted and evaluated for antigenicity, conservation, and proteasomal processing. Molecular docking with HLA-A*02:01 was performed and peptides were synthesized for experimental validation. In-vitro assays including ELISA-based MHC binding, IFN-γ ELISpot, and intracellular cytokine staining (ICS) were conducted using splenocytes isolated from HLA-A*02:01 transgenic mice.

Four peptides (P1, P2, P3 and P4), demonstrated strong binding to HLA-A*02:01 in-silico and were structurally compatible with the MHC class I groove. ELISA confirmed high binding for P3 and P1 at lower concentrations, while P2 and P4 showed moderate affinity. ELISpot assays showed robust IFN-γ responses in peptide-stimulated splenocytes, particularly for P3 and P1. ICS confirmed CD8⁺ T cell activation and polyfunctional cytokine expression. A comparative Nano-immunogenicity profile revealed P3 as the most potent candidate.

This study provides preclinical evidence of antigenicity and MHC-I compatibility of four prostate cancer-derived CTL epitopes using a transgenic mouse model. These findings support the advancement of these peptides as candidates for peptide-based immunotherapy in prostate cancer.

W0180 is a humanised IgG1κ antagonistic monoclonal antibody against the V domain-containing immunoglobulin suppressor of T-cell activation (VISTA) designed to enhance antitumour activities by inhibiting the immunosuppressive role of VISTA in myeloid cells and T cells in solid tumours.

Preclinical experiments evaluated the pharmacodynamics and antitumour activity of W0180. A first-in-human phase 1 dose-escalation study investigated the maximum tolerated dose (MTD), safety/tolerability, preliminary efficacy, pharmacokinetics and pharmacodynamics of W0180, both as monotherapy and in combination with pembrolizumab (an anti-programmed cell death protein-1 (PD-1) therapy), with the aim of establishing a recommended dose for expansion (RDE). In the monotherapy arm, cohorts of patients with locally advanced/metastatic solid tumours received once-weekly W0180 at increasing doses (from 3.5 to 600 mg). In the combination therapy arm, patients with relapsed/refractory, advanced/metastatic solid tumours and ≥1 prior anti-PD (ligand)-1 therapy line received W0180 (60 or 300 mg)+pembrolizumab.

W0180 exhibited pH-independent blockade of the VISTA-ligand interaction in vitro and showed antitumour activity in a syngeneic preclinical murine model expressing human VISTA. In the phase 1 study, of the 33 patients in the monotherapy (n=24) or combination therapy (n=9) arms, 28 contributed to dose determination. Dose-limiting toxicities were Grade 2 cerebral infarction and Grade 3 infusion-related reaction (IRR; n=1 each). The study was terminated prematurely in the dose-escalation phase (due to a business decision by the sponsor) before the MTD/RDE was reached. Common related treatment-emergent adverse events were IRR and fatigue; most were of mild severity. No patients achieved Response Evaluation Criteria in Solid Tumours objective response; two had prolonged stable disease (SD; one from each arm). Biomarker analysis suggested a dose-dependent pharmacodynamic effect of W0180.

W0180 demonstrated manageable safety, preliminary signs of clinical activity with prolonged SD and dose-dependent pharmacodynamics consistent with preclinical data (even though MTD was not reached) in patients with locally advanced/metastatic tumours, both as monotherapy and in combination with anti-programmed cell death protein-1 therapy.

NCT04564417.

Merkel cell carcinoma (MCC) is a rare, aggressive cutaneous malignancy with substantial risks of mortality and vision-threatening morbidity when periocular. We aimed to characterize the clinicopathologic features, management strategies, ophthalmic outcomes, and survival of periocular MCC.

We conducted a retrospective cohort study of 18 periocular MCC cases treated at a tertiary center between January12010and February 1 2024. Demographic and tumor characteristics, treatment details, ocular complications, and survival endpoints were extracted from electronic records. Kaplan-Meier curves estimated overall survival (OS) and progression-free survival (PFS).

Eighteen patients (61% female; mean age ± SD, 71.6 ± 11.4 years) were included; 67% presented with upper-eyelid disease. Half of tumors were AJCC stage I (50.0%). Initial therapy was excision alone in 33%, excision plus radiation in 28%, and multimodal in the remainder; an average of 1.62 resections was required to achieve negative margins or functional reconstruction. Functional globe preservation was achieved in 78% of patients, with severe ocular complications in 11%. Median OS was 8.5 years (95% CI, 4.6-12.3) and the estimated 2-year OS rate was 88.9%. Median PFS was 6.4 years (95% CI, 0.1-12.8) with a 2-year PFS of 54.7%. Median follow-up was 17 months.

Periocular MCC in this single-center cohort was typically detected early and managed with eye-sparing surgery with acceptable morbidity, yielding favorable OS and PFS estimates; these site-specific benchmarks can guide counseling, reconstruction, and future multicenter validation.

Epidermal inclusion cysts are nonmalignant proliferations of squamous epithelium situated within the dermis. Their presence in the breast is uncommon and presents considerable diagnostic difficulty. This case report aims to elucidate the multimodal imaging findings and differential diagnosis of a rare breast epidermal inclusion cyst, highlighting its capacity to mimic malignant neoplasms. We present a case of a 38-year-old female with a palpable right breast nodule that had progressively increased over a period of 15 years. A clinical examination identified a firm mass in the upper inner quadrant of the right breast. Ultrasound revealed a heterogeneous solid nodule, whilst mammography detected a sizable, well-defined hyperdense mass (BI-RADS 4). Magnetic resonance imaging demonstrated a well-defined nodule with T2/STIR hyperintensity, characterized by a ring-like internal enhancement pattern and restricted diffusion, classified as BI-RADS 4. An ultrasound-guided core biopsy was performed, and histological analysis confirmed the diagnosis of an epidermal inclusion cyst. This case underscores the importance of considering epidermal inclusion cysts in the differential diagnosis of breast cancers with imaging features to avoid unnecessary invasive interventions.

The expression of Programmed Death-Ligand 1 (PD-L1) on tumor-infiltrating immune cells (TIICs), plays a crucial role in tumor progression and immune evasion, impacting both the natural immune response and immune-targeted therapeutic strategies. The neutrophil-to-lymphocyte ratio (NLR) has also gained attention as a potential predictive biomarker for immunotherapy efficacy, as it may correlate with treatment outcomes.

To examine the expression of PD-L1 on TIICs and assess the influence of PD-L1 and NLR on immunotherapy outcomes following biliary tract cancers (BTC) recurrence.

From January 1, 2017, to January 1, 2020, this study enrolled 239 patients from the Department of Pancreaticobiliary Surgery at Sun Yat-sen University Cancer Center. Immunohistochemical analysis of PD-L1 on TIICs was conducted on pathological tissue sections from these patients. Clinical data, including overall survival (OS), disease-free survival (DFS), and pathological findings, were collected during follow-up. Statistical analyses were performed to assess outcomes related to the study objectives. Furthermore, data from The Cancer Genome Atlas (TCGA) were utilized to examine PD-L1 expression profiles and related information.

Tumor stage did not differ significantly (P = 0.173), while metastasis stage approached significance (P = 0.093), with a higher proportion of M0 cases in the PD-L1 low group. Univariate analysis revealed vascular tumor thrombus, tumor differentiation, node stage, and preoperative CA199 levels as factors associated with DFS. Notably, vascular tumor thrombus (HR = 1.791, P = 0.002), moderate tumor differentiation (HR = 0.537, P = 0.002), and elevated preoperative CA199 levels (>35, HR = 1.624, P = 0.009) emerged as significant risk factors. Elevated NLR demonstrated a significant association with reduced DFS (HR = 1.54, p = 0.017 one week prior; HR = 1.70, p = 0.007 one month after) and diminished OS (HR = 2.30, p < 0.001 one week prior; HR = 1.94, p = 0.005 one month after). Exploratory analysis in a limited immunotherapy subgroup (n=35) suggested patients exhibiting high PD-L1 levels on TIICs may be associated with worse OS following immunotherapy after recurrence (HR = 3.03, p = 0.036). High NLR, both one month before recurrence (HR = 2.23, p = 0.015) and one month after recurrence (HR = 2.10, p = 0.027), correlated with decreased OS.

PD-L1 expression on TIICs and dynamic NLR may be indicative of prognosis in BTC and could provide insights into immune status and response to immunotherapy after recurrence. These findings highlight the potential value of integrating local immune contexture with systemic inflammatory markers, but further validation in larger and prospective cohorts is warranted.

This study aimed to evaluate the knowledge, attitudes, and clinical decision-making of healthcare professionals in hyperbaric oxygen therapy (HBOT) units and oncology specialties regarding HBOT as an adjunctive cancer treatment.

A cross-sectional survey was conducted between February, 2024 and February, 2025. Data were collected using a structured questionnaire, which included sections on demographic characteristics and assessed participants' knowledge, attitudes, and practices (KAP) related to hyperbaric oxygen-assisted cancer therapy. The KAP scores were calculated to quantify the respondents' familiarity with and perspectives on the treatment.

Of 202 valid questionnaires, 58.91% were physicians. The majority (63.86%) had over 15 years of clinical experience, and 79.70% reported prior HBOT training in oncology. The mean scores were 52.87 ± 12.21 for knowledge, 41.24 ± 5.92 for attitudes, and 22.40 ± 2.38 for decision-making. Analysis indicated that knowledge positively influenced attitudes (β=0.393, P = 0.013) and decision-making (β = 0.159, P = 0.018), while attitudes significantly impacted decision-making (β = 0.318, P = 0.012). Knowledge indirectly affected decision-making via attitude (β = 0.125, P = 0.004).

Healthcare professionals working in HBOT units and oncology-related specialties demonstrated a generally adequate level of knowledge, positive attitudes, and a proactive approach toward the use of HBOT as an adjunctive cancer treatment, with attitude emerging as a key mediator linking knowledge to clinical decision-making. These findings highlight the importance of targeted educational interventions aimed at strengthening both knowledge and attitudes, which may in turn enhance evidence-based clinical decision-making and support the broader integration of HBOT into oncologic care pathways.

Vasohibin-1 (VASH-1) is an endothelial protein that serves as a negative feedback regulator of angiogenesis. Through its microtubule carboxypeptidase activity, VASH-1 plays a key role in vascular homeostasis. While previous studies have investigated its involvement in vascular regulation, most have focused on isolated functions or specific disease models, without systematically addressing its multi-dimensional regulatory mechanisms, tissue-specific functional paradoxes, and translational potential. This review provides a comprehensive analysis of VASH-1's biological characteristics: its expression is induced by pro-angiogenic factors, and it forms a functional complex with SVBP. In pathological contexts, VASH-1 exhibits paradoxical expression patterns-downregulated in neuroendocrine tumors but upregulated in bladder cancer-and demonstrates tissue-specific functions that either inhibit or promote angiogenesis. Clinically, VASH-1 serves both as a diagnostic marker (e.g., serum biomarker and tissue-based prognostic indicator) and a therapeutic target (such as improving renal disease or promoting tumor vascular normalization). This review aims to elucidate the complex physiological and pathological roles of VASH-1, providing a foundation for future precision intervention strategies targeting VASH-1 in disease diagnosis and therapy.

Dendritic cells (DCs) are central orchestrators of antitumor immunity, but their functions are markedly curtailed by glycolysis-dominated metabolic constraints in the tumor microenvironment (TME). This review focuses on two interconnected dimensions: tumor-derived metabolic stressors that suppress DC activation and the intrinsic metabolic programs of DC subsets that define their immunogenic potential. Lactate accumulation, hypoxia, adenosine signaling, and lipid overload disrupt antigen cross-presentation, type I interferon (IFN-I) production, and DC migration, collectively biasing DCs toward tolerogenic or checkpoint-high states. At the same time, subset-specific metabolic wiring-such as reliance on oxidative phosphorylation (OXPHOS) and fatty acid oxidation (FAO) in conventional type 1 DCs (cDC1s), glycolysis-dependent Th17-skewing capacity in conventional type 2 DCs (cDC2s), and pronounced hypoxia sensitivity in plasmacytoid DCs-creates distinct vulnerabilities that can be therapeutically exploited. We further summarize emerging strategies to restore DC metabolic fitness, including blockade of tumor glycolysis, intrinsic DC metabolic rewiring, modulation of immunometabolites and redox balance, use of natural products and nanomaterials, and rational combinations with radiotherapy or immune checkpoint blockade. Finally, we outline translational priorities such as single-cell and spatial mapping of DC metabolic heterogeneity, development of metabolism-linked biomarkers, and integration of DC-targeted interventions into existing immunotherapy frameworks. Together, these insights position DC metabolism as a critical lever to reprogram the TME and to enable more durable antitumor immunity.

Polycystic ovary syndrome (PCOS) is a well-known hormonal and metabolic condition linked to immune system irregularities and persistent inflammatory responses. Cytokines play a central role in PCOS, contributing to insulin resistance (IR), ovarian dysfunction, and systemic inflammation. Metformin (Met), a first-line treatment for IR, exhibits immunomodulatory properties beyond its glucose-lowering effects. This review critically evaluates the molecular mechanisms by which Met modulates pro- and anti-inflammatory cytokines in PCOS, synthesizing preclinical and clinical evidence while highlighting inconsistencies and therapeutic implications. Met suppresses inflammation by reducing pro-inflammatory cytokines such as IL-6, IL-1, IL-17, TNF-α, and others. Met also regulates TGF-β signaling, mitigating ovarian fibrosis while promoting follicular development and oocyte maturation through increased expression of TGF-β family members such as GDF-9 and BMP-15. These effects highlight Met's dual role in modulating inflammation and fibrosis. Additionally, Met influences inflammatory chemokines such as CXCL13, fractalkine, and others, further regulating immune responses and reducing inflammation. Moreover, combining Met with anti-inflammatory agents, such as resveratrol and probiotics, shows synergistic benefits in PCOS management. Understanding Met's immunomodulatory mechanisms offers new insights into its therapeutic potential beyond glucose metabolism. Future large-scale, phenotype-stratified clinical trials are warranted to validate these mechanisms and translate the immunomodulatory potential of metformin into tailored therapeutic strategies for PCOS.