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At least 19 recordsLinked to original sources
PubMed2026

Liquid Biopsy Differentiation of Pancreatic Cancer From Non-Cancerous Pancreatic Disease Using Dielectrophoresis-Recovered Nanoparticles Carrying Cell-Free DNA and Protein Biomarkers.

Cancer-derived extracellular vesicle (EV) nanoparticles carry important biomarkers but are difficult to recover from plasma, making EV-based diagnostics a challenge for clinical settings. Here, we demonstrate nanoparticle-based detection of pancreatic cancer using dielectrophoresis (DEP) nanoparticle recovery technology, which purifies nanoparticles from undiluted plasma and quantifies associated biomarkers. We combined both nanoparticle recovery and biomarker quantification on a single device by simultaneously collecting cell-free DNA nanoparticles and EVs followed by on-chip biomarker fluorescent staining for DNA and Glypican-1. Using a blinded cohort, these biomarkers differentiated pancreatic cancer from benign pancreatic diseases, including cysts, pancreatitis, and precancerous low-grade intraductal papillary mucinous neoplasm (IPMN) lesions, with a sensitivity of 0.92, a specificity of 0.83, and an AUC of 0.93. The AUC increased to 0.97 for patients over 50 years old. This is higher than the standard invasive endoscopic ultrasound-guided fine needle aspiration tissue biopsy procedure (AUC 0.79). This study is among the first demonstrating a combined threshold of DNA and protein levels that can distinguish pancreatic cancer from its precursor IPMN lesions. We also demonstrated the detection of early-stage pancreatic cancer and high-grade in situ precancerous lesions. This DEP-based technique shows that multiple types of cancer-derived nanoparticles can be quickly and easily recovered from plasma making it promising for future clinical diagnostics.

Humans↗
PubMed2026

Machine learning-enabled multi-omics discovery of prognostic biomarkers and signaling targets in pancreatic cancer.

Pancreatic ductal adenocarcinoma (PDAC) remains difficult to subtype using single omics layers. We conducted an exploratory investigation integrating reverse-phase protein array (RPPA) and DNA methylation data from the cancer genome atlas (TCGA)- pancreatic adenocarcinoma (PAAD) to assess the feasibility of multi-omics subtyping, alongside a supervised machine learning analysis of a small gene expression omnibus (GEO) transcriptomic cohort (n = 26) to identify candidate diagnostic genes. RPPA-based K-means clustering suggested a weak, possible two-subtype structure (silhouette ≈ 0.16) that remained unassociated with overall survival (log-rank p = 0.113) and lacked independent prognostic value. An independently performed similarity network fusion (SNF) analysis integrating RPPA and methylation data showed low concordance with RPPA-derived subtypes (Adjusted Rand Index (ARI) = 0.014), indicating limited convergence between molecular modalities. Supervised machine learning analysis of the GEO cohort using a fully nested leave-one-out cross-validation pipeline achieved a mean (area under the curve) AUC of 0.896 across four classifiers and identified four-fold-stable candidate genes (ESCO2, COL17A1, BCL2L14, and SOWAHB). However, this gene panel demonstrated limited external validity across two independent PDAC cohorts (log-rank p = 0.438 for both GSE62452 and GSE28735), indicating limited generalizability despite robust internal performance. Collectively, these findings provide limited evidence for a robust, prognostically significant multi-omics subtype or a validated diagnostic gene signature; instead, this study serves as a hypothesis-generating resource and highlights the importance of rigorous cross-validation and independent external validation in small-sample transcriptomic biomarker discovery.

Humans↗
PubMed2023

Autophagy supports mitochondrial metabolism through the regulation of iron homeostasis in pancreatic cancer.

Pancreatic ductal adenocarcinoma (PDAC) cells maintain a high level of autophagy, allowing them to thrive in an austere microenvironment. However, the processes through which autophagy promotes PDAC growth and survival are still not fully understood. Here, we show that autophagy inhibition in PDAC alters mitochondrial function by losing succinate dehydrogenase complex iron sulfur subunit B expression by limiting the availability of the labile iron pool. PDAC uses autophagy to maintain iron homeostasis, while other tumor types assessed require macropinocytosis, with autophagy being dispensable. We observed that cancer-associated fibroblasts can provide bioavailable iron to PDAC cells, promoting resistance to autophagy ablation. To overcome this cross-talk, we used a low-iron diet and demonstrated that this augmented the response to autophagy inhibition therapy in PDAC-bearing mice. Our work highlights a critical link between autophagy, iron metabolism, and mitochondrial function that may have implications for PDAC progression.

Animals↗
PubMed1979

Non-operative differentiation between pancreatic cancer and chronic pancreatitis.

Eighty-five of 186 patients investigated for suspected pancreatic cancer had an unequivocal final diagnosis of either pancreatic cancer (58 patients) or chronic pancreatitis (27 patients). They had been studied prospectively using ultrasonography, computerized tomography, radionuclide scanning, endoscopic retrograde cholangiopancreatography (ERCP), selective celiac and superior mesenteric angiography, duodenal drainage studies, cytologic studies, serum carcinoembryonic antigen assay, and pancreatic oncofetal antigen assay, The results were compared to determine which test would most frequently and reliably differentiate between pancreatic cancer and pancreatitis in a patient believed to have one or other disease. Criteria for interpreting results, first for highest rate of correct diagnoses, and second for highest accuracy were derived. Applying these criteria, ultrasonography achieved the highest rate of correct diagnoses (97% of patients diagnosed with 84% accuracy). ERCP, duodenal drainage studies, and cytology were the most accurate tests ((86% accuracy each test) but, with this accuracy, ERCP most frequently gave a diagnosis (diagnosis rate: ERCP--70%, duodenal drainage--32%, cytology--35%). The results suggest that ultrasonography is the best noninvasive test, and that a combination of ERCP, pancreatic juice assay and cytology in a single procedure may prove to be the best discriminating investigation.

Adult↗
PubMed1978

Endoscopic retrograde cholangio-pancreatography in pancreatic cancer and chronic pancreatitis. Differences in morphologic changes in the pancreatic duct and the bile duct.

The radiological findings in ERCP in 49 patients (ERP 49 patients and ERC 24 patients) with pancreatic diseases were evaluated blindly (24 patients with chronic pancreatitis and 25 patients with pancreatic cancer as a final diagnosis). Obstructions of the main pancreatic duct were found in 16 out of 24 patients with chronic pancreatitis and in 24 out of 25 patients with pancreatic cancer. Irregularity of obstructions was seen significantly more often in patients with cancer. Cholangiography demonstrated obstructions of the distal part of the common bile duct in both groups of patients, but irregularity of obstructions was exclusively seen in the cancer group. Though characteristic radiological features were demonstrated, a safe diagnosis must probably still rely on biopsy.

Adult↗
PubMed2026

Overcoming cancer resistance in pancreatic cancer: toward dynamic precision oncology.

Pancreatic ductal adenocarcinoma (PDAC) remains a highly lethal malignancy, largely because of its profound and evolving therapeutic resistance. Resistance is not determined by a single molecular alteration but arises from interconnected mechanisms, including intrinsic resistance, treatment-induced adaptive resistance, acquired resistance, genomic evolution, clonal selection, cancer stemness, phenotypic plasticity, metabolic adaptation, and tumor microenvironment-mediated effects. Emerging therapeutic approaches targeting KRAS/RAS signaling, stromal and immune components, metabolic dependencies, and DNA damage repair pathways offer opportunities to address these mechanisms, although durable efficacy remains limited by biological heterogeneity and adaptive responses. In this review, we examine therapeutic resistance as an evolutionary and multidimensional process and summarize emerging strategies for overcoming resistance. We further propose a Dynamic Precision Oncology (DPO) framework that extends conventional precision oncology beyond baseline molecular profiling by integrating longitudinal assessment of tumor genomics, circulating tumor DNA, CA19-9, imaging, radiomics, and clinical characteristics. This framework emphasizes iterative detection and characterization of emerging resistance, mechanism-informed treatment adaptation, and subsequent reassessment rather than automatic treatment modification based on a single biomarker. DPO may provide a conceptual framework for integrating evolving tumor biology into treatment decision-making, while prospective studies are needed to validate biomarkers, define actionable thresholds, and determine whether longitudinal resistance-guided strategies improve clinical outcomes in PDAC.

Humans↗
PubMed2026

The Association of Diabetes-Related Dietary Patterns with Pancreatic Cancer Risk in the European Prospective Investigation into Cancer and Nutrition Study.

BACKGROUND: Pancreatic cancer is relatively rare but remains one of the most lethal tumors. Identifying modifiable risk factors is a crucial step to reduce disease burden. Evidence suggests a potential role of type 2 diabetes mellitus in its pathogenesis. OBJECTIVES: The objective of this study is to examine the association between dietary patterns related to diabetes and pancreatic cancer risk in a European population. METHODS: A total of 367,395 participants from the European Prospective Investigation into Cancer and Nutrition study were included. After a median follow-up of 14.9 y, 926 incident cases were identified. The Diabetes Risk Reduction Diet (DRRD), the Empirical Dietary Index for Hyperinsulinemia (EDIH), and the Empirical Dietary Index for Insulin Resistance (EDIR) were estimated from food frequency questionnaires at recruitment. Hazard ratios (HRs) and 95% confidence intervals (CIs) for the association between dietary patterns and pancreatic cancer were calculated using multivariable Cox proportional hazards regression models, adjusted for relevant confounders. RESULTS: Adherence to DRRD showed no association with risk of pancreatic cancer (HRT3vsT1: 0.94; 95% CI: 0.79, 1.12). Higher adherence to EDIH was associated with a borderline 19% increased pancreatic cancer risk (HRT3vsT1: 1.19; 95% CI: 0.99, 1.44). No significant associations were observed in relation to EDIR. No heterogeneity was observed among the subgroups. CONCLUSIONS: Higher adherence to a hyperinsulinemic dietary pattern may contribute to risk of developing pancreatic cancer in our population. Further research is warranted to elucidate the potential role of dietary factors in cancer risk prevention.

Humans↗
PubMed2026

Chinese expert consensus on precision testing and molecular diagnosis of pancreatic cancer (2025).

This consensus by the CSCO Pancreatic Cancer Expert Committee establishes evidence-based guidelines for molecular testing in pancreatic ductal adenocarcinoma. It details recommendations for biomarkers (e.g., KRAS, BRCA, MSI), liquid biopsy, and precision imaging to direct targeted therapies and immunotherapy, aiming to standardize diagnosis and optimize individualized patient care. Pancreatic ductal adenocarcinoma (PDAC) is the most common pathological type of primary pancreatic malignancy, accounting for ~95% of cases and generally referred to as pancreatic cancer [1]. Its prognosis is extremely poor and its incidence continues to rise [2]. According to the most recent global cancer statistics, the incidence of pancreatic cancer ranks 12th among all cancers, and its mortality ranks 6th, making it one of the deadliest malignancies worldwide [3]. Approximately 57% of patients have metastatic disease at diagnosis and require systemic therapy, for which chemotherapy remains the standard first-line option [1]. However, the overall response rate to currently available systemic regimens is low, and the 5-year survival rate for patients with metastatic disease remains below 5% [3]. Although most pancreatic cancers harbor canonical driver mutations, they exhibit marked heterogeneity at the molecular level. Whole-genome sequencing (WGS) and integrative genomic analyses have identified molecular subtypes of PDAC with potential clinical relevance [4-9]. With the increasing implementation of precision oncology, the Chinese Society of Clinical Oncology (CSCO) Guidelines for the Diagnosis and Treatment of Pancreatic Cancer give a level 1 recommendation to perform genetic and other molecular testing on tissue or cytologic specimens as part of the pathological diagnostic work-up, in order to guide individualized treatment, including targeted therapy and immunotherapy [10]. To further promote the use of genetic and molecular testing in the precision treatment of pancreatic cancer, the CSCO Pancreatic Cancer Expert Committee convened a multidisciplinary panel to develop the present Chinese Expert Consensus on Precision Testing and Molecular Diagnosis of Pancreatic Cancer (2025), aiming to provide clinicians with an authoritative reference for precision diagnostics and treatment decision-making.

Humans↗
PubMed1979

Assessment of the clinical usefulness of serum ribonuclease assays: an indicator for the detection of pancreatic cancer.

To evaluate diagnostic usefulness for pancreatic cancer, serum ribonuclease (RNase) level was determined in three groups of subjects; 1) normal volunteers as control, 2) patients with histologically determined pancreatic cancer, and 3) patients with miscellaneous diseases other than pancreatic cancer. A small increase of RNase values was recognized with age in the normal subjects and in the patients with nonpancreatic diseases, if renal function was normal. The mean RNase level in the control subjects was 97 +/- 41.2 units. A marked elevation of serum RNase level was demonstrated in the patients with pancreatic cancer (p less than 0.001) and in the patients with renal dysfuction, but no significant rise was noticed in the patients with pancreatitis. Mean values of RNase in the patients with pancreatic cancer and renal dysfuncton were 368 +/- 146 units and 342 +/- 78.1 units respectively. RNase values above 300 units were recognized in 15(71%) out of 21 patients with pancreatic cancer. Seven cases with elevated RNase over 300 units other than non-pancreatic malignancy and renal dysfunction were noticed in 6 instances of obstructive jaundice and in one instance of early gastric cancer (an 84-year-old male). The above-stated findings indicate that serum RNase determinations can be utilized as a diagnostic indicator for pancreatic cancer.

Adult↗
PubMed1977

Detection of bacterial infection of the pancreatic ducts in patients with pancreatitis and pancreatic cancer during endoscopic cannulation of the pancreatic duct.

Bacterial infections of the pancreas and bacteremia may occur during episodes of pancreatitis. Detection of bacterial infections of the pancreas in the past has required laparotomy. The present study was undertaken to determine whether bacterial infection of the pancreas occurred during nonsuppurative pancreatitis. During endoscopic cannulation of the main pancreatic duct, secretin was administered intravenously and pancreatic juice aspirated from within the duct was cultured. Bacterial infections were detected in 11 of 35 patients with pancreatitis and 3 of 5 with pancreatic cancer. The pancreatic juice was sterile in 25 controls. Cultures from the common bile duct in 9 controls were also sterile whereas 4 of 6 with pancreatitis showed infected bile. The infecting organisms were principally gram-negative and the infections were usually polymicrobial. Antibiotics, where used, successfully eradicated the infecting organisms but did not appear to affect the patient's clinical course.

Adult↗
PubMed1979

A study of secretory proteins, cytology and tumor site in pancreatic cancer.

Pure pancreatic fluid was aspirated at the time of endoscopic retrograde cholangiopancreatography (ERCP), after Secretin stimulation, and was analyzed for protein in eight patients with proven adenocarcinoma of the pancreas and in 16 subjects of the same sex ratio and approximately matching ages, who had normal pancreatograms and pancreatic cytology, who served as controls. The albumin concentration, IgA, IgG, were all significantly greater in the pancreatic fluid of the cancer group, and the IgM and transferrin increase was of borderline significance. Many zymogen bands present in controls were either faintly present or absent in the cancer group at matching zymogen concentration. Cytology was positive or suspicious in eight of 11 cancer patients. The secretory protein abnormalities and cytology results in the cancer group did not depend on a particular tumor site or size, the smallest being 3 cm lesions. Hence, secretory abnormalities and gross tumor size and location are independent entities to a certain extent. It is possible that secretion changes may precede the development of gross tumor. Further study will be necessary before the actual significance of these findings for early diagnosis is known.

Adenocarcinoma↗
PubMed1979

Prospective evaluation of angiography in the diagnosis and management of patients suspected of having pancreatic cancer.

One hundred three patients suspected of having pancreatic cancer underwent celiac and superior mesenteric arteriography which was reported 'blind.' Final diagnosis, operative findings, and resectability of pancreatic cancers were correlated with angiography reports. Forty patients had pancreatic cancer. Thirty-seven of these underwent laparotomy, and 14 (37%) had resectable lesions. Sensitivity and specificity of arteriogrphy for pancreatic cancer were 72% (29/40) and 71% (45/63) respectively. Resectability was unrelated to the angiographic diagnosis. Nonresectability was related to an angiographic finding of definite tumor vessel (4/4), large-vessel encasement (14/7), and major venous pathology (8/11). Only the first of these was unique to pancreatic cancer. Hepatic metastases were detected in only six of 13 patients. Small-artery encasement, arterial occlusion, vessel displacement, and gallbladder distention were not indicators of diagnosis or extent of disease. Major anatomic anomaly of foregut vasulature was revealed in 25% of angiographic studies. Prior knowledge of such anomalies has important bearing on the operative approach to pancreatic resection. We conclude that angiography should be performed prior to laparotomy whenever a resectable pancreatic cancer is suspected from other investigations. When used prospectively, angiography is not a reliable diagnostic or prognostic tool for pancreatic cancer.

Adolescent↗
PubMed1978

Leucocyte adherence inhibition for detecting specific tumour immunity in early pancreatic cancer.

Tumour-specific immunity to pancreatic tumour antigens, assayed by an automated tube leucocyte-adherence inhibition assay (L.A.I.), was detected in 3 of 3 patients with localised pancreatic cancer and 3 of 8 patients with more extensive pancreatic cancer. Leucocytes from pancreatic cancer patients with L.A.I. reactivity did not react to antigens of stomach, colon, or lung tumours; leucocytes from patients with stomach, colon, or lung cancer of inflammatory disease of the pancreas and bowel did not show L.A.I. reactivity to pancreatic tumour antigens.

Adenoma, Islet Cell↗
PubMed2026

High-Sensitivity ctDNA Analysis Uncovers Relevant Signals Missed by NGS in Pancreatic Cancer.

PURPOSE: Pancreatic ductal adenocarcinoma (PDAC) carries high mortality despite multimodal therapy, and improved biomarkers are needed to guide perioperative care. This study evaluated the prognostic significance of Kirsten rat sarcoma virus (KRAS)-mutant circulating tumor DNA (ctDNA) detected by next-generation sequencing (NGS) and digital droplet PCR (ddPCR) in localized PDAC. EXPERIMENTAL DESIGN: In this prospective cohort study (2020-2024), patients with localized PDAC undergoing neoadjuvant chemotherapy (NAC) were enrolled across multiple sites within Northwestern Medicine. Blood samples for ctDNA were assessed at diagnosis, after NAC, and after resection using tumor-agnostic NGS and ddPCR targeting KRAS G12D/V/R mutations. Overall survival (OS) was assessed using Kaplan-Meier analysis. RESULTS: The cohort included 106 patients. At diagnosis, KRAS ctDNA was detected in 17.2% (17/99) by NGS and 64.9% (63/97) by ddPCR. Detection by both platforms was associated with shorter OS, with the higher-sensitivity ddPCR assay providing greater prognostic discrimination by identifying additional patients with poor outcomes not captured by NGS (NGS median OS 11.2 vs. 30.5 months, P < 0.001; ddPCR median OS 24.7 vs. 70.9 months, P = 0.004). Stratified by detection method, median OS was shortest in patients with ctDNA detected by both NGS and ddPCR (10.9 months), longest in those not detected by either platform (40.7 months), and intermediate in patients detected only by ddPCR (26.9 months; P < 0.001). CONCLUSIONS: In localized PDAC, KRAS-mutant ctDNA detected by NGS or ddPCR was associated with worse survival. ddPCR identified additional patients missed by NGS. Integrating ddPCR with NGS ctDNA measures may improve perioperative risk stratification, although validation is needed before clinical implementation.

Humans↗
PubMed2026

The Landmark Series: Mutation-Based Therapy of Pancreatic Cancer.

BACKGROUND: Pancreatic ductal adenocarcinoma (PDAC) remains a highly lethal malignancy with limited long-term survival despite advances in surgery and systemic therapy. PATIENTS: The population of interest comprises patients with PDAC characterized by targetable molecular alterations and biologically distinct transcriptomic subtypes. METHODS: We performed a narrative review of landmark and contemporary clinical trials, translational studies, and emerging molecular-classification platforms relevant to precision oncology in PDAC. RESULTS: Growing understanding of PDAC molecular biology has identified putative genetic mutations, including homologous recombination repair deficiency, mismatch repair deficiency, and mutated KRAS, enabling the development of targeted therapies and precision treatment strategies. Concurrently, transcriptomic profiling has revealed biologically distinct molecular subtypes associated with differences in prognosis and therapeutic response. Emerging tools such as molecular classifiers, deep learning models, and multiomic platforms may further refine patient selection and treatment personalization. CONCLUSIONS: This review highlights contemporary efforts of novel targeted therapies, ongoing advances in molecular subtyping, and the evolving role of precision oncology in improving outcomes for patients with PDAC.

Genomic alterations↗
PubMed2025

Propionyl-CoA carboxylase subunit B regulates anti-tumor T cells in a pancreatic cancer mouse model.

Most human pancreatic ductal adenocarcinoma (PDAC) are not infiltrated with cytotoxic T cells and are highly resistant to immunotherapy. Over 90% of PDAC have oncogenic KRAS mutations, and phosphoinositide 3-kinases (PI3Ks) are direct effectors of KRAS. Our previous study demonstrated that ablation of Pik3ca in KPC (KrasG12D; Trp53R172H; Pdx1-Cre) pancreatic cancer cells induced host T cells to infiltrate and completely eliminate the tumors in a syngeneic orthotopic implantation mouse model. Now, we show that implantation of Pik3ca-/- KPC (named &#x3b1;KO) cancer cells induces clonal enrichment of cytotoxic T cells infiltrating the pancreatic tumors. To identify potential molecules that can regulate the activity of these anti-tumor T cells, we conducted an in vivo genome-wide gene-deletion screen using &#x3b1;KO cells implanted in the mouse pancreas. The result shows that deletion of propionyl-CoA carboxylase subunit B gene (Pccb) in &#x3b1;KO cells (named p-&#x3b1;KO) leads to immune evasion, tumor progression, and death of host mice. Surprisingly, p-&#x3b1;KO tumors are still infiltrated with clonally enriched CD8+ T cells but they are inactive against tumor cells. However, blockade of PD-L1/PD1 interaction reactivated these clonally enriched T cells infiltrating p-&#x3b1;KO tumors, leading to slower tumor progression and improve survival of host mice. These results indicate that Pccb can modulate the activity of cytotoxic T cells infiltrating some pancreatic cancers and this understanding may lead to improvement in immunotherapy for this difficult-to-treat cancer.

Animals↗
PubMed2025

Elevated expression of transferrin receptor-1 in pancreatic cancer: clinical implications and prognostic significance.

PURPOSE: Many advanced-stage pancreatic cancers are fatal, highlighting the need for solid prognostic indicators. This study evaluates transferrin receptor-1 (TfR1) expression in pancreatic cancer tissues and cell lines for clinical and therapeutic potential. METHOD: The GuangRe database, which integrates mRNA data from The Cancer Genome Atlas (TCGA) and the Genotype-Tissue Expression (GTEx) project, was used to assess TFRC gene expression in pancreatic cancer and normal tissues. ROC curves and Kaplan-Meier and Log-rank tests were used to evaluate TFRC gene expression's diagnostic and survival efficacy. In vitro Western blotting and immunofluorescence experiments on pancreatic cancer cell lines assessed TfR1 expression. IHC staining was done on tissue samples from 90 patients to determine TfR1's clinical importance. RESULTS: The study found that TFRC mRNA levels were significantly higher in pancreatic cancer tissues compared to nearby normal tissues (P&#x2009;<&#x2009;0.05), with an AUC of 0.936. We found higher TfR1 protein levels in pancreatic cancer cell lines (P&#x2009;<&#x2009;0.01) using western blot and immunofluorescence studies. Immunohistochemistry showed that pancreatic cancer tissues expressed 30.1% TfR1 compared to paracancer (11.1%) (P&#x2009;=&#x2009;0.003). In COX regression analysis, increased TfR1 expression was related with lower overall survival (OS) and progression-free survival (PFS), making it an independent prognostic factor. CONCLUSION: Higher TfR1 expression is associated with poor pancreatic cancer outcomes, suggesting its potential as a prognostic biomarker and therapeutic target.

Humans↗