Risk score development for pancreatic cancer in Chinese men: A population-based cohort study.

Advances in pyrimidine-like heterocyclic scaffolds: Innovative synthetic method for malic enzyme inhibition in pancreatic ductal adenocarcinoma (PDAC) - A comprehensive review.

tRF-Gly-CCC-012 enhances malignant process in pancreatic cancer via the HNRNPC/PHGDH axis.

Pancreatic cancer, known for its aggressive nature and poor prognosis, often eludes early detection and effective treatment. This study investigates the underexplored terrain of protein lactylation in pancreatic cancer to identify potential biomarkers and understand its immunological implications. Proteomic and transcriptomic analyses were conducted to profile lactylation changes, identifying 11 upregulated and 1 downregulated lactylation-related proteins. Intersection analysis between proteomics and transcriptomics highlighted four key genes (COQ9, GAA, LYST and TP53) with consistent expression trends, suggesting their central role in the lactylation pathway within pancreatic cancer. ROC curve analysis underscored the diagnostic potential of GAA and LYST, with AUCs over 0.9. Further, ssGSEA revealed significant correlations between these core genes and various immune cells, indicating an immune-modulatory role. Notably, most core lactylation-related genes were positively associated with immune checkpoint molecules, barring COQ9. GSEA of gene expression groups delineated three conserved upregulated KEGG pathways, with additional REACTOME pathway analysis uncovering 68 conserved pathways. These findings highlight lactylation's involvement in pancreatic cancer progression and its possible exploitation for diagnostic and therapeutic advancements.

Cancer-associated fibroblasts promote immune evasion in pancreatic cancer via miR-181b-5p/STING/LGALS1 pathway.

Tumor cell derived CCL20 exacerbates the immunosuppressive microenvironment by recruiting CCR6+ Tregs in pancreatic cancer.

The prognosis for patients diagnosed with pancreatic cancer has changed little over the past 4 decades. Fewer than 20 % of patients are diagnosed at a stage amenable to potentially curative surgery and therapeutic resistance remains widespread, compounded by a lack of therapeutic targets. Early detection of pancreatic cancer is notoriously difficult, due to non-specific symptoms that delay early diagnosis in addition to limited sensitivity of current imaging modalities. However, pancreatic cystic lesions (PCLs), such as intraductal papillary mucinous neoplasms (IPMNs), provide a unique opportunity for earlier disease intervention. Indeed, PCLs can be stratified by risk of malignant transformation, but current stratification guidelines remain highly contended within the field. Importantly, accumulating evidence suggests that inflammatory and immunogenetic mechanisms may influence both cyst development and malignant progression, yet these immunobiological factors are not currently integrated into PCL risk-stratification and management frameworks. In this review, we focus on the immunobiological dimension of PCLs, highlighting the interplay between chronic inflammation, immune dysregulation, and genetic alterations that may drive cystogenesis and malignant transformation. Furthermore, we assess the evidence to support integrating an immunobiological aspect to existing risk stratification guidelines to enhance identification of high-risk pre-malignant PCLs. Such integration may ultimately identify high-risk patients more accurately and inform surveillance and therapeutic intervention strategies to prevent late-stage pancreatic cancer.

Pancreatic cancer quality of care index trends, socioeconomic disparities, and future projections (1990-2035): A global epidemiological study.

Single-cell transcriptomic profiling of platelet-adherent circulating tumor cells using a microcavity-gel manipulation platform.

Pancreatic ductal adenocarcinoma (PDAC) is a highly lethal malignancy characterized by a dense desmoplastic stroma, profound immune suppression, and resistance to conventional therapeutics. Poor patient outcomes are driven by resistance to chemotherapy and immunotherapy arising from both tumor-intrinsic and microenvironmental mechanisms. Elucidating the molecular pathways underlying therapeutic failure is therefore critical. Transforming growth factor-β (TGF-β) is a central regulator of PDAC progression, promoting epithelial-mesenchymal-transition (EMT), stromal remodeling, immune exclusion, and checkpoint activation at advanced disease stages. The transcription factor Yin Yang 1 (YY1) is a critical downstream integrator and amplifier of TGF-β-driven signaling programs. YY1 reinforces EMT, metabolic adaptation, and immune evasion through transcriptional, epigenetic, and post-transcriptional regulations. Several key immune modulators of immune evasion include PD-L1, indoleamine 2,3-dioxygenase, FOXP3, and pro-tumoral chemokines. The coordinated TGF-β-YY1 signaling suppresses CD8 cytotoxic T-cell (CTL) and natural killer (NK) cell functions, promotes regulatory T (Treg) cells and myeloid-derived suppressor cells (MDSCs), and establishes an immune-cold, therapy-resistant tumor microenvironment. This review explores the mechanistic basis of the TGF-β-YY1 cross-talk regulation in the immune evasion of PDAC. It also discusses emerging therapeutic opportunities in targeting the TGF-β-YY1 axis to overcome immune escape and improve treatment outcomes in PDAC.

Decrypting the impact of ferroptosis and cuproptosis in development of pancreatic ductal adenocarcinoma.

Advanced pancreatic ductal adenocarcinoma (PDAC) often infiltrates or obstructs the superior mesenteric vein (SMV)/portal vein, leading to collateral vein (CV) formation. Although CVs are hypothesized to affect surgical outcomes, data regarding their clinical significance remain limited. This study aimed to evaluate the impact of CV formation on short-term outcomes in patients with PDAC who underwent portomesenteric venous resection (PVR). We retrospectively analyzed PDAC cases undergoing PVR at our institution between 2010 and 2023. CVs were identified using preoperative computed tomography, and patients were categorized based on the presence or absence of CVs. Short-term outcomes were assessed prospectively. A subgroup analysis was performed to evaluate the clinical relevance of proximal versus distal SMV involvement. Among 403 patients with PDAC undergoing PVR, 27 (6.7%) had CVs. The CV group exhibited significantly longer operative times (median: 618 vs. 517 minutes, p < 0.0001) and greater blood loss (median: 1500 vs. 590 mL, p < 0.0001). Postoperative complications (Clavien-Dindo classification ≥IIIa) were more frequent in the CV group (33.3% vs. 10.1%, p = 0.002). Multivariate analysis identified CV formation as the strongest predictor of blood loss ≥1000 mL (odds ratio: 6.63 [95% confidence interval 2.70-17.3], p < 0.0001). As expected, distal SMV involvement correlated with longer operative times but did not impact other outcomes. CV formation, a characteristic feature of advanced PDAC, was strongly associated with increased surgical difficulty and postoperative complications, highlighting the need for tailored strategies to optimize outcomes in PDAC cases undergoing PVR.

Markers of immune activation and immunotherapy responsiveness are increased in 3D Pancreatic cancer organoids when primed with photodynamic- and chemo-therapy.

ECM-responsive nanomedicine to enhance immunotherapy in pancreatic cancer.

Optical Flow-Guided Analysis of Intrafractional Anatomical Variations in Pancreatic Tumors and Organs at Risk During Magnetic Resonance-Guided Adaptive Radiation Therapy Under Abdominal Compression.

USP20-RAB8A signaling axis restricts pancreatic cancer progression by disrupting GLUT1 vesicular trafficking and inhibiting glucose uptake.

SLC5A11 mediates metformin-induced PD-L1 suppression to enhance cancer immunotherapy through AMPK-IRF1 signaling.

Emerging roles of non-coding RNAs in the tumor microenvironment of pancreatic cancer: Focusing on current challenges and future directions.

Modelling of dose-escalated proton beam therapy for Locally Advanced Pancreatic Cancer using simulated phantoms.

Analysis of eugenol macromolecular structure and anticancer effect using electrochemical sensor: Mechanisms of promoting apoptosis of pancreatic cancer cells via ROS pathway