Pancreatology最新文献

{"title":"Risk assessment of multi-focal side-branch IPMNs: Long-term follow-up of one thousand patients.","authors":"Chase J Wehrle, Faheem Khan, Muhammad A Nadeem, Puneet Bansal, Breanna Perlmutter, Jenny H Chang, Divya Deverakonda, Noah X Tocci, Abby Gross, Rob Naples, Kathryn A Stackhouse, Samer Naffouje, Daniel Joyce, Toms Augustin, R Matthew Walsh, Robert Simon","doi":"10.1016/j.pan.2026.10.011","DOIUrl":"https://doi.org/10.1016/j.pan.2026.10.011","url":null,"abstract":"<p><strong>Background: </strong>While the natural history of solitary side-branch intraductal papillary mucinous neoplasms (SB-IPMNs) is increasingly well-described, the prevalence, disease course, and oncologic risk of multifocal disease remain poorly defined. It is unknown whether the presence of multiple cysts confers additional oncologic risk compared to solitary lesions. Our objective was to evaluate the natural history and oncologic risk associated with multifocal SB-IPMNs compared with solitary SB-IPMNs during long-term surveillance.</p><p><strong>Methods: </strong>Patients with side-branch intraductal papillary mucinous neoplasms (SB-IPMNs) undergoing non-operative surveillance with ≥2 cross-sectional imaging studies ≥6 months apart were included. The number of cysts at diagnosis and at most recent surveillance was recorded by an abdominal radiologist who was blinded to pathologic outcomes. The primary endpoint was high-risk pathology (high-grade dysplasia or invasive carcinoma). Secondary endpoints included clinically relevant (CR) progression, defined as development of guideline-based worrisome features or high-risk stigmata excluding cyst size and growth, development of new cysts, and need for surgical resection.</p><p><strong>Results: </strong>Of 1,000 patients, 370 (37%) had multifocal disease. Median follow-up was 6.6 years (IQR 3.0-10.3). Rates of CR-progression (developing worrisome features/high-risk stigmata) were similar between multifocal and solitary SB-IPMN patients (9.7% vs 9.4%, p = 0.849). High-risk pathology occurred in 43 patients (4.3%): 3.2% multifocal vs 4.8% solitary (p = 0.248). On multivariable analysis, multifocality was not associated with high-risk pathology, while CR-progression strongly predicted malignant potential (HR 31.3, 95% CI 16.3-62.1). Findings were unchanged in sensitivity analyses restricted to patients with MRI and using guideline-based progression criteria including cyst size and growth.</p><p><strong>Conclusion: </strong>Multiplicity of SB-IPMNs does not confer increased malignant risk at the patient level, despite nearly 40% of patients presenting with more than one cyst. These findings support a pancreas-wide susceptibility process (described as a \"field defect\") rather than a focal cyst-driven phenomenon. Accordingly, each cyst should be evaluated independently according to its own risk features.</p>","PeriodicalId":19976,"journal":{"name":"Pancreatology","volume":" ","pages":""},"PeriodicalIF":3.9,"publicationDate":"2026-10-14","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"149224757","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Pancreatic cancer cell and stellate cell-derived exosome crosstalk mediates pancreatic cancer-related diabetes.","authors":"Rohit Sarkar, Chamini J Perera, Md J Hossain, Victoria Tyma, Dinuki Perera, Tanzila Khan, Helen Binang, Parvathy Rajan, Alpha Raj Mekapogu, S M Zahid Hosen, Zhihong Xu, Joseph Yan-Wing Cheung, Jerry Greenfield, Suresh Chari, Kyle L Hoehn, Neil Horadagoda, Romano Pirola, Jeremy Wilson, Minoti Apte","doi":"10.1016/j.pan.2026.10.015","DOIUrl":"https://doi.org/10.1016/j.pan.2026.10.015","url":null,"abstract":"<p><strong>Background: </strong>Diabetes is a known risk factor, and a distinct form termed pancreatic cancer-related diabetes (PCRD) often precedes the diagnosis of cancer by 3-5 years, offering a potential window for intervention. We hypothesised that interactions between stromal pancreatic stellate cells (PSCs) and cancer cells trigger secretion of exosomal factors that impair islet function and insulin signalling, contributing to PCRD pathogenesis.</p><p><strong>Methods: </strong>KC (KrasLSL-G12D/+; Pdx1-Cre) mice were fed a high-fructose diet (HFrD) or control diet for 16 weeks. Exosomes were isolated from monocultures and co-cultures of cancer/PanIN cells with PSCs, characterised by nanoparticle tracking analysis and transmission electron microscopy, and incubated with mouse β-cells (MIN6) and peripheral cells (hepatocytes, adipocytes, skeletal myocytes). Effects on insulin secretion and insulin-signalling factors were examined. Exosomal glucose-6-phosphate dehydrogenase (G6PD) expression was modulated by siRNA to assess functional impact.</p><p><strong>Results: </strong>HFrD induced marked glucose intolerance in KC mice and was accompanied by enhanced PSC activation, macrophage infiltration, inflammation, and accelerated PanIN progression. Exosomes from PSCs, cancer cells, and co-cultures displayed typical morphology and marker expression and were efficiently internalised by β-cells and hepatocytes. Functionally, exosomes significantly impaired glucose-stimulated insulin secretion in mouse and human β-cells without altering insulin content. In hepatocytes, PSC-, cancer-, and co-culture-derived exosomes reduced key insulin-signalling components, including IR, IRS, AKT, FOXO1 and GLUT2, and inhibited glucose uptake. Silencing exosomal G6PD partially restored hepatocyte insulin signalling.</p><p><strong>Conclusion: </strong>This study identifies a potential contributor to PCRD and suggests a possible mechanistic role for exosomal G6PD in impaired insulin signalling associated with PCRD.</p>","PeriodicalId":19976,"journal":{"name":"Pancreatology","volume":" ","pages":""},"PeriodicalIF":3.9,"publicationDate":"2026-10-13","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"149195951","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Association of intrapancreatic fat deposition with coronary artery calcification burden.","authors":"Dingzhe Zhang, Yiping Zhang, Hao Zhou, Rui Yu, Jianhua Wang, Dongling Lv, Xiao Chen","doi":"10.1016/j.pan.2026.10.016","DOIUrl":"https://doi.org/10.1016/j.pan.2026.10.016","url":null,"abstract":"","PeriodicalId":19976,"journal":{"name":"Pancreatology","volume":" ","pages":""},"PeriodicalIF":3.9,"publicationDate":"2026-10-12","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"149183679","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Re: Impact of sarcopenia and myosteatosis on early and long-term survival after surgical resection of pancreatic ductal adenocarcinoma.","authors":"Gharbi Lassad","doi":"10.1016/j.pan.2026.10.001","DOIUrl":"https://doi.org/10.1016/j.pan.2026.10.001","url":null,"abstract":"","PeriodicalId":19976,"journal":{"name":"Pancreatology","volume":" ","pages":""},"PeriodicalIF":3.9,"publicationDate":"2026-10-10","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"149183701","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Response to: \"Impact of sarcopenia and myosteatosis on early and long-term survival after surgical resection of pancreatic ductal adenocarcinoma\".","authors":"Niels Siegel, Thomas Hank","doi":"10.1016/j.pan.2026.10.002","DOIUrl":"https://doi.org/10.1016/j.pan.2026.10.002","url":null,"abstract":"","PeriodicalId":19976,"journal":{"name":"Pancreatology","volume":" ","pages":""},"PeriodicalIF":3.9,"publicationDate":"2026-10-10","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"149183684","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Association of obstructive sleep apnea with pancreatic cancer in high-risk patients under surveillance in CAPS and PCYST cohorts.","authors":"Hassan Sinan, Emy Abou Sleiman, Amanda L Blackford, Takahiro Shinozuka, Dimitri Melki, Jad Saab, Michael Romanos, Kylie Ning, Michel Almardini, Andrea Castellino, Eun Ji Shin, Elham Afghani, Marcia Irene Canto, Michael Goggins","doi":"10.1016/j.pan.2026.10.013","DOIUrl":"https://doi.org/10.1016/j.pan.2026.10.013","url":null,"abstract":"<p><strong>Background: </strong>Obstructive sleep apnea (OSA) has been linked with increased cancer incidence and mortality. We hypothesized that OSA may be a risk factor for neoplastic progression among patients undergoing pancreatic cancer surveillance.</p><p><strong>Methods: </strong>Retrospective medical record review of two Johns Hopkins Hospital cohorts undergoing pancreas surveillance; patients with familial/genetic risk enrolled in the Cancer of the Pancreas Screening (CAPS) study and patients with incidentally detected pancreatic cysts, enrolled in the PCYST study. Time-to-progression to pancreatic ductal adenocarcinoma (PDAC) and neoplastic progression (either PDAC, high-grade dysplasia or pancreatic neuroendocrine tumor) were compared by OSA status, adjusting for covariates.</p><p><strong>Results: </strong>OSA was diagnosed prior to or during surveillance in 174 (19.5%) of 893 patients in CAPS and 376 (23.7%) of 1585 patients in the PCYST cohort. In the combined cohorts, OSA was associated with increased risk of progression to PDAC (unadjusted HR: 3.12, 95% CI: [1.82, 5.34], p < 0.001). OSA was also associated with male sex, higher BMI, fatty liver, fatty pancreas, diabetes, and history of smoking (all p < 0.01). After covariate adjustment, OSA remained associated with PDAC risk (adjusted HR: 2.56 [1.44, 4.55], p = 0.001). Factors associated with neoplastic progression included OSA (adjusted HR: 1.93 [1.25, 2.97], p = 0.003), increasing age (age-per 5-years adjusted HR: 1.14 [1.05, 1.24], p = 0.003), fatty liver (adjusted HR: 1.76 [1.19, 2.60], p = 0.005), and diabetes (adjusted HR: 1.77 [1.16, 2.71], p = 0.008).</p><p><strong>Conclusions: </strong>Patients undergoing pancreatic surveillance for their familial/genetic risk and/or incidentally detected pancreatic cysts have a greater likelihood of developing pancreatic cancer if they've been diagnosed with OSA.</p>","PeriodicalId":19976,"journal":{"name":"Pancreatology","volume":" ","pages":""},"PeriodicalIF":3.9,"publicationDate":"2026-10-09","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"149170749","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Healthcare expenditures across the care continuum of pancreatic cancer and resected precursor lesions.","authors":"Marloes Lja Sprij, Brenda J van Stigt, Albert G Siebers, Olivier R Busch, Niels G Venneman, Rogier P Voermans, Eva Kouw, Marco J Bruno, Djuna L Cahen, Iris Lansdorp-Vogelaar, Inge McM de Kok","doi":"10.1016/j.pan.2026.10.005","DOIUrl":"https://doi.org/10.1016/j.pan.2026.10.005","url":null,"abstract":"","PeriodicalId":19976,"journal":{"name":"Pancreatology","volume":" ","pages":""},"PeriodicalIF":3.9,"publicationDate":"2026-10-08","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"149183621","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"TRIM29 may facilitate progression of pancreatic ductal adenocarcinoma through immune remodeling.","authors":"Shuaiwu Luo, Yonghao Xu, Wenjun Liao, Jiakun Wang, Yong Li, Jun Yang, Pengcheng Zhou, Enliang Li, Rongshou Wu, Qi Chen, Linquan Wu","doi":"10.1016/j.pan.2026.10.006","DOIUrl":"https://doi.org/10.1016/j.pan.2026.10.006","url":null,"abstract":"<p><strong>Background: </strong>Pancreatic ductal adenocarcinoma (PDAC) is a highly lethal malignancy characterized by late diagnosis, aggressive progression, and an immunosuppressive tumor microenvironment. Biomarkers with both diagnostic value and biological relevance remain urgently needed.</p><p><strong>Methods: </strong>Five Gene Expression Omnibus cohorts comprising 548 pancreatic samples were analyzed using differential expression analysis, weighted gene co-expression network analysis, and machine learning. Spatial and single-cell transcriptomics, immune infiltration estimates, and survival analyses complemented biomarker screening. Tripartite motif-containing 29 (TRIM29) was evaluated in 80 paired clinical specimens, knockdown and re-expression experiments, and subcutaneous and orthotopic KPC tumor models.</p><p><strong>Results: </strong>Machine learning identified eight hub genes, including S100P, SFN, TMPRSS4, GJB2, GABRP, TRIM29, SERPINB5, and LAMB3, which showed favorable diagnostic performance across cohorts. Spatial transcriptomics revealed region-specific enrichment of these genes in PDAC tissues. Among them, TRIM29 was preferentially expressed in malignant epithelial cells, markedly upregulated in PDAC tissues, and associated with poor prognosis, reduced CD8⁺ T-cell infiltration, and activation of PI3K-AKT-mTOR signaling. Functionally, TRIM29/Trim29 knockdown suppressed PDAC cell proliferation, migration, and invasion, reduced AKT and mTOR phosphorylation, and increased CXCL10 transcript levels and extracellular protein concentrations. TRIM29 re-expression restored AKT and mTOR phosphorylation and reversed the increase in extracellular CXCL10 concentrations. In vivo, Trim29 knockdown suppressed tumor growth and increased CD8⁺ T-cell infiltration in orthotopic tumors.</p><p><strong>Conclusion: </strong>This study identifies TRIM29 as a machine learning-prioritized diagnostic biomarker and functional regulator of PDAC progression and immune remodeling, suggesting its potential value for biomarker-guided risk assessment and therapeutic exploration in PDAC.</p>","PeriodicalId":19976,"journal":{"name":"Pancreatology","volume":" ","pages":""},"PeriodicalIF":3.9,"publicationDate":"2026-10-07","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"149183633","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Utility of longitudinal changes in CA19-9 for detection of pancreatic ductal adenocarcinoma in patients with benign pancreatic diseases.","authors":"Toshiaki Abe, Tetsuya Takikawa, Kazuhiro Kikuta, Ryotaro Matsumoto, Yu Tanaka, Takanori Sano, Hidehiro Hayashi, Yasumasa Sekino, Yuichi Tanaka, Takayuki Masuo, Shungo Yaura, Takuma Takahashi, Hiroki Takei, Yoshiya Nagase, Shin Miura, Shin Hamada, Shuichi Aoki, Michiaki Unno, Atsushi Masamune","doi":"10.1016/j.pan.2026.10.007","DOIUrl":"https://doi.org/10.1016/j.pan.2026.10.007","url":null,"abstract":"<p><strong>Background/objective: </strong>Several benign pancreatic diseases are associated with an increased risk of PDAC; however, early detection remains challenging in these patients. We evaluated whether longitudinal changes in carbohydrate antigen 19-9 (CA19-9) could improve early detection of PDAC in patients with benign pancreatic diseases.</p><p><strong>Methods: </strong>We retrospectively reviewed 656 patients with benign pancreatic diseases (pancreatic cysts, intraductal papillary mucinous neoplasms, chronic pancreatitis, and autoimmune pancreatitis) who were regularly followed at our institution. Patients were classified into PDAC (n = 34) and control (n = 622) groups. Longitudinal changes in CA19-9 absolute values and percent changes were assessed at predefined time points up to 36 months before diagnosis. A logistic regression model incorporating these parameters was developed, and its discriminative ability and diagnostic performance were evaluated.</p><p><strong>Results: </strong>CA19-9 levels began to increase within the normal range as early as 12-18 months before PDAC diagnosis. From 12 to 18 months before diagnosis, the logistic regression model demonstrated higher AUC values than the conventional cutoff of 37 U/mL, with significant differences at 0-3 months (0.96 vs. 0.87, P = 0.003) and 12-18 months (0.69 vs. 0.56, P = 0.004). The model showed relatively high positive predictive values at 0-3 months (78.8%) and also at earlier time points, including 6-12 months (18.5%) and 12-18 months (12.0%). Similar trends were observed in patients with stage 0-II PDAC.</p><p><strong>Conclusions: </strong>Longitudinal assessment of CA19-9 may support earlier detection of PDAC in patients with benign pancreatic diseases.</p>","PeriodicalId":19976,"journal":{"name":"Pancreatology","volume":" ","pages":""},"PeriodicalIF":3.9,"publicationDate":"2026-10-07","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"149172219","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Closing the diagnostic gap in post-pancreatitis diabetes.","authors":"Cecillie Siggaard Knoph, Søren Schou Olesen","doi":"10.1016/j.pan.2026.10.003","DOIUrl":"https://doi.org/10.1016/j.pan.2026.10.003","url":null,"abstract":"","PeriodicalId":19976,"journal":{"name":"Pancreatology","volume":" ","pages":""},"PeriodicalIF":3.9,"publicationDate":"2026-10-07","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"149137933","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}