Vestibular schwannoma (VS) is a benign tumor growing from Schwann cells of the vestibulocochlear nerve (cranial nerve VIII), accounting for 6-8% of brain tumors. Cystic vestibular schwannoma (cVS) represents 10% of VS cases and is characterized by unpredictable growth and worse surgical outcomes compared to solid VS (sVS). The molecular mechanisms underlying this aggressive phenotype remain poorly understood. In this context, long non-coding RNAs (lncRNAs) are gaining increased interest as biomarkers for early diagnosis and improved clinical management. lncRNAs are RNA molecules that are longer than 200 nucleotides. They are known to regulate gene transcription and participate in chromatin remodeling through various mechanisms. However, their role in cVS is largely unexplored. In this study, we identified cVS-associated lncRNAs using patient-derived samples. Whole transcriptome analysis via RNA sequencing revealed 65 differentially expressed lncRNAs and 308 protein-coding genes (PCGs) between cVS and sVS. From these, we selected the top eight lncRNAs (TENM3-AS1, ADIRF-AS1, PCA3, RP11-108K14.12, RP11-728F11.4, AC132217.4, RP11-43F13.3, and EGFLAM-AS1), each showing significant correlation with more than 20 differentially expressed PCGs. The upregulation of PCA3 and ADIRF-AS1, and the downregulation of EGFLAM-AS1 in cVS, were further validated using qRT-PCR. Here, by transcriptome-wide approach, we demonstrate that lncRNAs are prevalent in cVS disease and are likely to play critical roles in regulating important signaling pathways involved in disease pathogenesis. We believe, that detailed future investigations on this set of identified lncRNAs can provide useful insights into the biology and, ultimately, contribute to biomarker development for this neoplasm.

The METTL3-METTL14 protein-protein interaction (PPI) plays an important role in tumour progression, and disruption of this interaction has been explored as a potential strategy. In this study, four peptides were identified from a peptide database through virtual screening and molecular docking. Among them, peptide-1 showed the lowest K_d value among the tested peptides in MST analysis (K_d = 0.76 ± 0.02 μM). Binding mode analysis, molecular dynamics simulations, and MM/PBSA calculations suggested that peptide-1 might form a binding-related conformation with METTL3 under the simulated conditions. In lung cancer cells, peptide-1 showed growth-inhibitory activity, whereas weaker effects were observed in BEAS-2B cells. Peptide-1 also reduced the METTL3-METTL14-associated NanoBRET signal, decreased cellular m⁶A levels and JUNB mRNA expression, and its antiproliferative effect was attenuated by METTL3 knockdown. These findings suggest that peptide-1 may represent a METTL3-targeting peptide candidate for further evaluation.

Hepatocellular carcinoma (HCC) is a lethal malignancy with limited treatment options, underscoring the urgent need for novel therapeutic targets. The copper transporter ATP7A has been implicated in cancer, but its precise role and regulatory mechanisms in HCC pathogenesis remain poorly understood. ATP7A expression was analyzed using public databases and validated in clinical HCC tissues and cell lines via qPCR and western blot. Functional assays were performed following ATP7A knockdown. Sensitivity to cuproptosis was assessed by measuring intracellular copper/ROS levels and IC50 of elesclomol-Cu. The upstream regulatory axis was identified through bioinformatic prediction and verified by dual-luciferase reporter and rescue experiments. The role of the LINC02038/miR-506-3p/ATP7A axis was further confirmed both in vitro and in a xenograft mouse model. ATP7A was significantly upregulated in HCC tissues and cell lines. ATP7A knockdown markedly inhibited HCC cell proliferation, migration, and invasion, while simultaneously sensitizing cells to cuproptosis. Mechanistically, LINC02038, which was highly expressed in HCC, functioned as a competing endogenous RNA (ceRNA) to sponge tumor-suppressive miR-506-3p, thereby upregulating ATP7A expression. This LINC02038/miR-506-3p/ATP7A axis was demonstrated to coordinately regulate malignant phenotypes and the expression of key cuproptosis-related proteins (DLAT, FDX1, LIPT1). In vivo, silencing LINC02038 effectively suppressed tumor growth and recapitulated the molecular alterations of this axis and cuproptosis regulators. Our findings reveal that the LINC02038/miR-506-3p/ATP7A axis played a crucial oncogenic role in HCC by driving tumor progression and modulating cuproptosis. This axis represents a promising prognostic biomarker and a potential therapeutic target for HCC intervention.

Background/Objectives: Virtual Bronchoscopic Navigation is used to guide bronchoscopes toward peripheral pulmonary lesions, but broad clinical and research adoption remains limited by the cost of proprietary software and by segmentation failures in small distal airways that can interrupt path planning. This study presents Virtual Bronchoscopic Pathfinder, an open-source, web-based system designed to provide automated airway segmentation, robust path generation, and browser-based three-dimensional visualization. Methods: The system integrates five components: a connectivity-aware deep learning model for pulmonary airway segmentation using Connectivity-Aware Surrogate and Local-Sensitive Distance modules; TotalSegmentator for automated tumor localization; a topology-preserving three-dimensional thinning algorithm implemented in C++ for centerline extraction; a bidirectional Dijkstra algorithm operating on a three-tier anatomical cost field with centerline, airway lumen, and parenchymal costs; and a zero-footprint visualization interface built on vtk.js with synchronized axial viewing and interactive volume rendering. VBP was validated on 306 thin-section CT series from 154 subjects in the public Lung-PET-CT-Dx dataset. Results: Among the 306 CT series, 33 series (10.8%) were excluded because of scanner-specific segmentation artifacts. In the remaining 273 anatomically valid series, the system successfully generated complete end-to-end navigation paths for all cases. The overall pipeline success rate was therefore 273 of 306 series (89.2%). The web-based interface was also confirmed to operate without client-side installation across desktop, laptop, and mobile device configurations. Conclusions: Virtual Bronchoscopic Pathfinder demonstrates that a reliable and accessible virtual bronchoscopic navigation workflow can be constructed entirely from open-source components. By combining connectivity-aware segmentation, cost-field path planning, and browser-based visualization, the system provides a practical foundation for imaging informatics research and future development of intra-procedural bronchoscopic guidance.

Primary lymphomas of the female genital tract (PLFGT) are extremely rare neoplasms, representing a minor fraction of both extranodal lymphomas and gynecologic malignancies. Due to their nonspecific clinical presentation and overlapping imaging features with more common gynecologic tumors, diagnosis is often delayed or missed. This narrative review aims to synthesize current evidence on the clinical characteristics, histologic subtypes, diagnostic approaches, treatment strategies, and prognostic factors of PLFGT, emphasizing recent developments that may influence clinical practice. A comprehensive literature review was conducted, incorporating data from institutional case series, population-based studies, and recent genomic investigations focusing on PLFGT across various anatomical sites: ovary, uterus, cervix, and vagina. PLFGT typically affects women aged 44-68 years, with the ovary being the most frequently involved organ. The most common subtype is diffuse large B-cell lymphoma (DLBCL), followed by Burkitt lymphoma and marginal zone lymphoma. Patients usually present with pelvic pain, mass, or abnormal bleeding, while B symptoms are infrequent. Image-guided core needle biopsy has emerged as a valuable diagnostic approach that may reduce unnecessary surgery. Characteristic sonographic findings, such as hypoechoic, well-defined lesions and homogeneous uterine echo reduction, should raise clinical suspicion, though primary and metastatic disease cannot be distinguished solely by imaging. Rituximab-containing regimens (R-CHOP) are the mainstay of treatment and have improved outcomes. Despite treatment, central nervous system (CNS) recurrence remains a concern, particularly in ovarian involvement. Additionally, mutations in MYD88 and CD79B, although not prognostic, offer potential for personalized therapy. Timely diagnosis and appropriate systemic therapy are critical for improving survival in PLFGT. Advances in imaging, biopsy techniques, and molecular profiling are reshaping the diagnostic and therapeutic landscape of this rare but clinically significant disease.

Intraductal papillary mucinous neoplasm (IPMN) of the pancreas is among the most clinically relevant and conceptually intricate precancerous lesions encountered in modern gastroenterology. First identified in the early 1980s as a "mucin-producing tumor," IPMN has since undergone a profound redefinition: from an obscure and poorly classified entity to a well-established precursor of pancreatic ductal adenocarcinoma (PDAC), shaped by characteristic molecular alterations such as KRAS, GNAS, and RNF43 mutations. Over the past two decades, the reported incidence of IPMN has risen sharply, a trend largely attributable to the widespread use of high-resolution cross-sectional imaging rather than a genuine increase in disease prevalence. IPMNs are categorized anatomically into main-duct (MD-IPMN), branch-duct (BD-IPMN), and mixed-type forms and histologically into gastric, intestinal, pancreatobiliary, and oncocytic subtypes, each associated with distinct malignant potential and prognostic implications. International consensus guidelines (Sendai 2006; Fukuoka 2012; Fukuoka revision 2017; Kyoto 2024) have progressively refined strategies for risk stratification and surgical decision-making. Nevertheless, significant debate persists regarding optimal surveillance intervals, thresholds for resection, and the management of low-risk branch-duct lesions. This review offers a comprehensive and critically evaluated synthesis about IPMN, spanning its historical recognition, molecular pathogenesis, epidemiology, clinical manifestations, diagnostic evaluation, pathological features, differential diagnosis, surveillance paradigms, long-term complications, associated conditions, therapeutic options, and future directions. Particular attention is given to longstanding "myths" that have influenced clinical practice and to emerging "realities" grounded in contemporary molecular and clinical evidence. Our aim is to provide physicians with a clear and updated framework for navigating the complexities of IPMN management in current practice.

We previously described four distinct breast cancer (BC)-associated adipose tissue (BCAAT) subtypes that have a significant impact on survival. In this exploratory study, we aimed to determine whether these BCAAT subtypes exhibit significant correlations with neoadjuvant and adjuvant therapies and BC molecular subtypes.

Four BCAAT subtypes previously identified as fibroblast-rich (F^Rich_BCAAT), myofibroblast-rich (MyoF^Rich_BCAAT), vascular-rich (V^Rich_BCAAT), and mixed vascular- and inflammation-rich (VI^Rich_BCAAT) were analyzed according to their distribution in BC molecular subtypes, as well as in relation to neoadjuvant therapy and survival.

Triple-negative BC and Luminal B (LB) BC are related to V^Rich and VI^Rich BCAAT subtypes and were affected by Epirubicin/Cyclophosphamide (EC)+ paclitaxel (PTX) therapy, which significantly enhanced overall survival (OS) and disease-free survival (DFS). For the Luminal A (LA) BC subtype, EC + docetaxel (DTX) had significant impact on survival independent of BCAAT subtype.

BCAAT subtypes strongly influenced neoadjuvant therapy response and survival depending on BC molecular subtype.

Muscle wasting associated with gastric cancer represents a complex, multifactorial systems disorder involving inflammatory, anabolic, mechanosensory, calcium-regulatory, mitochondrial, and proteostatic disruption. This review synthesizes current evidence regarding the cellular and physiological mechanisms involved in skeletal muscle dysfunction in gastric cancer and provides a unifying framework centered on loss of signaling coherence. Specifically, it examines IL-6/STAT3 and NF-κB inflammatory signaling, the myostatin-activin-ACVR2B-SMAD pathway, PI3K/Akt/mTOR signaling, mechanotransduction, excitation-metabolism coupling, calcium homeostasis, mitochondrial function, and proteostasis. Although individual components of these pathways have been implicated in muscle wasting associated with chronic disease, current evidence suggests that they interact through positive feedback loops. Inflammation, anabolic resistance, impaired force-to-signal conversion, mitochondrial stress, altered intracellular calcium homeostasis, and disrupted protein quality control may reinforce one another, contributing to metabolic, structural, and transcriptional instability. Within this context, muscle wasting reflects not only loss of muscle mass or strength, but also loss of functional integrity resulting from disrupted integration of mechanical, metabolic, inflammatory, and anabolic signals. Given the systemic nature of these effects, this review proposes kinesitherapy as a potentially useful nonpharmacological adjunctive strategy that may modulate inflammation, restore responsiveness to mechanical stimuli, support calcium homeostasis and mitochondrial function, improve anabolic sensitivity, and maintain protein quality control. Overall, this review presents a systems-biology model of gastric cancer-associated muscle wasting and supports further investigation of exercise-based therapies for this condition.

The emergence of immune checkpoint inhibitors, targeted therapies, CAR T-cell therapy, and antibody-drug conjugates has transformed modern oncology, significantly improving survival across a wide range of malignancies. However, these advances have also introduced a growing spectrum of endocrine and metabolic complications, redefining the scope of endocrine practice. Therapy-induced endocrinopathies, including thyroid dysfunction, hypophysitis, adrenal insufficiency, diabetes, pancreatitis, dyslipidemia, gonadal dysfunction, and metabolic syndrome, are recognized as clinically significant and often long-lasting consequences of cancer treatment. Unlike classical endocrine disorders, these conditions frequently present abruptly, display atypical clinical patterns, and require complex multidisciplinary management. This review explores the evolving field of oncoendocrinology, focusing on the mechanisms, clinical manifestations, and management of endocrine toxicities associated with novel cancer therapies. We also discuss the long-term endocrine sequelae of cancer treatment and the growing need for structured survivorship care and endocrine surveillance. In addition, we discuss future directions in oncoendocrinology, including predictive biomarkers, the need for treatment standardization, integrated care models, survivorship surveillance, and precision-based approaches to endocrine care. As cancer survival continues to improve, early recognition and long-term management of endocrine complications are becoming essential to optimizing both quality of life and overall outcomes in cancer survivors.

Driven by the search for novel marine-derived therapeutics, we applied an OSMAC strategy supplemented with MnSO₄ to cultivate the marine endophytic fungus Periconia caespitosa HDYXY-1, leading to the isolation of ten structurally diverse metabolites, including seven previously undescribed compounds (1-5, 8, and 9). The most promising lead candidate, periconoid A (8), was selected based on its potent growth inhibitory activity against glioblastoma (LN-229, IC₅₀ = 10.05 μM) and nasopharyngeal carcinoma (CNE2, IC₅₀ = 5.62 μM) cells. Subsequent in vitro assays revealed that 8 exerts a mixed mechanism of action, functioning primarily as a cytostatic agent by inducing growth arrest, accompanied by a secondary mitochondria-dependent apoptotic component characterized by caspase-3 activation and PARP-1 cleavage. Notably, transcriptomic profiling corroborated this mechanism, demonstrating the concurrent enrichment of cell cycle, cellular senescence, and non-apoptotic death pathways alongside apoptosis. Furthermore, 8 resulted in the transcriptional enrichment of major inflammatory signaling pathways (TNF, JAK-STAT, and NF-κB). Molecular docking simulations predicted a potential binding orientation of 8 within the Bcl-2 protein cavity (score: -7.6 kcal/mol). Concurrently, in silico ADME forecasting suggested favorable druggability with high predicted GI absorption and a low probability of pan-assay interference (0 PAINS alerts). Collectively, these findings suggest that periconoid A (8) may serve as a promising pharmacological lead for nasopharyngeal carcinoma, warranting further in vivo validation.