Pub Date : 2025-12-29DOI: 10.1016/j.pan.2025.12.023
Chris E Forsmark, Stephen Pandol
{"title":"The Consortium for the Study of Chronic Pancreatitis, Diabetes, and Pancreatic Cancer (CPDPC) 10 years of past accomplishments and looking forward to the next 5 years of the Chronic Pancreatitis Clinical Research Consortium (CPCRC).","authors":"Chris E Forsmark, Stephen Pandol","doi":"10.1016/j.pan.2025.12.023","DOIUrl":"https://doi.org/10.1016/j.pan.2025.12.023","url":null,"abstract":"","PeriodicalId":19976,"journal":{"name":"Pancreatology","volume":" ","pages":""},"PeriodicalIF":2.7,"publicationDate":"2025-12-29","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145896623","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}
Pub Date : 2025-12-29DOI: 10.1016/j.pan.2025.12.026
Kenichiro Okumura
{"title":"Comment on \"Focal pancreatic parenchymal atrophy could be a precursor of pancreatic cancer\" (Kikuyama et al., Pancreatology 2025).","authors":"Kenichiro Okumura","doi":"10.1016/j.pan.2025.12.026","DOIUrl":"https://doi.org/10.1016/j.pan.2025.12.026","url":null,"abstract":"","PeriodicalId":19976,"journal":{"name":"Pancreatology","volume":" ","pages":""},"PeriodicalIF":2.7,"publicationDate":"2025-12-29","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145889584","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":"Glucagon-like Peptide-1 receptor agonists rarely cause de novo acute pancreatitis but often result in serum lipase elevations of unclear clinical significance.","authors":"Jianing Li, Aditya Chandrashekar, Richu Ravikumar, Elham Afghani, Vikesh K Singh, Venkata Akshintala","doi":"10.1016/j.pan.2025.12.021","DOIUrl":"https://doi.org/10.1016/j.pan.2025.12.021","url":null,"abstract":"","PeriodicalId":19976,"journal":{"name":"Pancreatology","volume":" ","pages":""},"PeriodicalIF":2.7,"publicationDate":"2025-12-25","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145952653","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}
Pub Date : 2025-12-18DOI: 10.1016/j.pan.2025.12.012
Sirui Peng, Qiangxing Chen, Zixin Chen, Mengling Yao, Yunqiang Cai, Du He, Yu Cai, Ke Cheng, Jun Li, He Cai, Pan Gao, Xiafei Gu, Xin Wang, Yongbin Li, Man Zhang, Lingwei Meng, Qi Xia, Panpan Xu, Xie Dan, Jin Zhou, Zhong Wu, Bing Peng
Background: Intraductal papillary mucinous neoplasms (IPMNs) are known precancerous lesions whose malignant transformation to pancreatic ductal adenocarcinoma (PDAC) worsens prognosis. Current experimental models inadequately elucidate the molecular mechanisms driving this progression.
Methods: We performed spatial transcriptomics (ST) on three fresh tissue samples from the same patient including normal pancreas, high-grade IPMN, and invasive PDAC. We used Spatial inferCNV to profile the evolutionary clone trajectory. We utilize SpaCET to identify the tumor region and adjacent tumor microenvironment (TME) feature variation, as well as its crosstalk between tumor cells by CellChat.
Results: Our findings identified the master transcript factors and critical signaling pathways that might be involved in the progression of IPMN to invasive PDAC. Moreover, both IPMN and PDAC harbored the ELF3, MYC, and KLF4 amplification. We identified a significant heterogeneity among PDAC tissue with seven distinct subclones showing diverse functions, such as hypoxia, oxidative phosphorylation, and epithelial-mesenchymal Transition. Compared to IPMN, PDAC showed immune landscape remodeling: CD4+ T cells and dendritic cells depleted, while immunosuppressive M2 macrophages increased. In addition, cancer-associated fibroblasts (CAFs), particularly myofibroblastic CAFs, were enriched adjacent to invasive PDAC.
Conclusions: Our study integrates multiple computational approaches for spatial transcriptomics to identify ELF3/MYC/KLF4 amplifications during IPMN-to-PDAC progression, as well as 7 heterogeneous subclones with functions including hypoxia and EMT, alongside immune-stromal landscape remodeling and tumor-adjacent myofibroblastic CAF enrichment.
{"title":"Evolution of the Spatial transcriptomic landscape during the progression of high-grade pancreatic intraductal papillary mucinous neoplasms to invasive cancer.","authors":"Sirui Peng, Qiangxing Chen, Zixin Chen, Mengling Yao, Yunqiang Cai, Du He, Yu Cai, Ke Cheng, Jun Li, He Cai, Pan Gao, Xiafei Gu, Xin Wang, Yongbin Li, Man Zhang, Lingwei Meng, Qi Xia, Panpan Xu, Xie Dan, Jin Zhou, Zhong Wu, Bing Peng","doi":"10.1016/j.pan.2025.12.012","DOIUrl":"https://doi.org/10.1016/j.pan.2025.12.012","url":null,"abstract":"<p><strong>Background: </strong>Intraductal papillary mucinous neoplasms (IPMNs) are known precancerous lesions whose malignant transformation to pancreatic ductal adenocarcinoma (PDAC) worsens prognosis. Current experimental models inadequately elucidate the molecular mechanisms driving this progression.</p><p><strong>Methods: </strong>We performed spatial transcriptomics (ST) on three fresh tissue samples from the same patient including normal pancreas, high-grade IPMN, and invasive PDAC. We used Spatial inferCNV to profile the evolutionary clone trajectory. We utilize SpaCET to identify the tumor region and adjacent tumor microenvironment (TME) feature variation, as well as its crosstalk between tumor cells by CellChat.</p><p><strong>Results: </strong>Our findings identified the master transcript factors and critical signaling pathways that might be involved in the progression of IPMN to invasive PDAC. Moreover, both IPMN and PDAC harbored the ELF3, MYC, and KLF4 amplification. We identified a significant heterogeneity among PDAC tissue with seven distinct subclones showing diverse functions, such as hypoxia, oxidative phosphorylation, and epithelial-mesenchymal Transition. Compared to IPMN, PDAC showed immune landscape remodeling: CD4<sup>+</sup> T cells and dendritic cells depleted, while immunosuppressive M2 macrophages increased. In addition, cancer-associated fibroblasts (CAFs), particularly myofibroblastic CAFs, were enriched adjacent to invasive PDAC.</p><p><strong>Conclusions: </strong>Our study integrates multiple computational approaches for spatial transcriptomics to identify ELF3/MYC/KLF4 amplifications during IPMN-to-PDAC progression, as well as 7 heterogeneous subclones with functions including hypoxia and EMT, alongside immune-stromal landscape remodeling and tumor-adjacent myofibroblastic CAF enrichment.</p>","PeriodicalId":19976,"journal":{"name":"Pancreatology","volume":" ","pages":""},"PeriodicalIF":2.7,"publicationDate":"2025-12-18","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145846411","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}
Pub Date : 2025-12-13DOI: 10.1016/j.pan.2025.12.016
Naoki Ikenaga, Wenhui Luo, Takao Ohtsuka
{"title":"Positioning serum autoantibody signatures within the evolving landscape of early pancreatic cancer detection.","authors":"Naoki Ikenaga, Wenhui Luo, Takao Ohtsuka","doi":"10.1016/j.pan.2025.12.016","DOIUrl":"https://doi.org/10.1016/j.pan.2025.12.016","url":null,"abstract":"","PeriodicalId":19976,"journal":{"name":"Pancreatology","volume":" ","pages":""},"PeriodicalIF":2.7,"publicationDate":"2025-12-13","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145782470","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}
Pub Date : 2025-12-06DOI: 10.1016/j.pan.2025.12.004
Jiaqi Wang, Kaiyan Liu, Yaofang Zhang, Jie Li
{"title":"Comment on \"Effect of albumin infusion in patients with predicted severe acute pancreatitis: A randomized controlled trial\".","authors":"Jiaqi Wang, Kaiyan Liu, Yaofang Zhang, Jie Li","doi":"10.1016/j.pan.2025.12.004","DOIUrl":"https://doi.org/10.1016/j.pan.2025.12.004","url":null,"abstract":"","PeriodicalId":19976,"journal":{"name":"Pancreatology","volume":" ","pages":""},"PeriodicalIF":2.7,"publicationDate":"2025-12-06","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145889544","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}
Pub Date : 2025-12-01DOI: 10.1016/j.pan.2025.10.003
Rishi Das , Amir H. Davarpanah , Puneet Sharma , Steven Keilin , Preeti A. Reshamwala , Ram Subramanian , Field Willingham , Saurabh Chawla
{"title":"Association of pancreatic steatosis with Metabolic Dysfunction Associated Steatohepatitis using magnetic resonance imaging","authors":"Rishi Das , Amir H. Davarpanah , Puneet Sharma , Steven Keilin , Preeti A. Reshamwala , Ram Subramanian , Field Willingham , Saurabh Chawla","doi":"10.1016/j.pan.2025.10.003","DOIUrl":"10.1016/j.pan.2025.10.003","url":null,"abstract":"","PeriodicalId":19976,"journal":{"name":"Pancreatology","volume":"25 8","pages":"Pages 1489-1491"},"PeriodicalIF":2.7,"publicationDate":"2025-12-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145368520","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}
Pub Date : 2025-12-01DOI: 10.1016/j.pan.2025.10.012
Tianyi Li , Chao Ling , Yinjie Gao , Xiaosen Ma , Qiang Xu , Ruichen Gao , Anli Tong , Yuxiu Li
Background
Von Hippel-Lindau (VHL) disease is a heritable syndrome with multiorgan involvement. In this study, we describe the phenotype of pancreatic lesions and the genetic mutational profile of patients with VHL.
Methods
We included 90 patients with VHL who were treated at a single center. Their clinical profile and types of pancreatic lesions were studied. In addition, genetic testing for mutations in the VHL gene was conducted using Sanger sequencing, covering all three exons and splicing sites of VHL. One patient with insulinoma underwent whole-exome sequencing (WES) and whole-genome sequencing (WGS).
Results
Of the 90 patients, 55 (61.1 %) had VHL disease-related pancreatic lesions (male: female, 29:26; mean age at diagnosis, 34 years). The lesions included simple cysts (n = 31, 56.4 %), serous cystadenoma (n = 4, 7.3 %), and neuroendocrine tumors (NETs) (n = 32, 58.2 %). Among the 32 NETs, one was an insulinoma, and the others were nonfunctional tumors. Of the 55 patients, 44 patients with pancreatic lesions underwent genetic testing for the VHL gene. Mutations were missense in 38 cases, nonsense in 2 cases, deletion in 3 cases, and a splicing site mutation in 1 case. 23 patients had mutations in either codon 161 or 167. NETs were statistically more frequent in patients with missense mutations in codons 161 and 167 compared to mutations in the rest of the VHL gene (21/23 vs. 7/15; P = 0.006). An amplification pattern of copy-number variation was found on the WGS in the insulinoma patient.
Conclusion
Pancreatic lesions are common in VHL disease. Mutations in codons 161 and 167 are hotspots in patients with pancreatic lesions, particularly NETs.
{"title":"Types of pancreatic lesions and the mutational landscape of the VHL gene in patients with von Hippel-Lindau disease","authors":"Tianyi Li , Chao Ling , Yinjie Gao , Xiaosen Ma , Qiang Xu , Ruichen Gao , Anli Tong , Yuxiu Li","doi":"10.1016/j.pan.2025.10.012","DOIUrl":"10.1016/j.pan.2025.10.012","url":null,"abstract":"<div><h3>Background</h3><div>Von Hippel-Lindau (VHL) disease is a heritable syndrome with multiorgan involvement. In this study, we describe the phenotype of pancreatic lesions and the genetic mutational profile of patients with VHL.</div></div><div><h3>Methods</h3><div>We included 90 patients with VHL who were treated at a single center. Their clinical profile and types of pancreatic lesions were studied. In addition, genetic testing for mutations in the <em>VHL</em> gene was conducted using Sanger sequencing, covering all three exons and splicing sites of <em>VHL</em>. One patient with insulinoma underwent whole-exome sequencing (WES) and whole-genome sequencing (WGS).</div></div><div><h3>Results</h3><div>Of the 90 patients, 55 (61.1 %) had VHL disease-related pancreatic lesions (male: female, 29:26; mean age at diagnosis, 34 years). The lesions included simple cysts (n = 31, 56.4 %), serous cystadenoma (n = 4, 7.3 %), and neuroendocrine tumors (NETs) (n = 32, 58.2 %). Among the 32 NETs, one was an insulinoma, and the others were nonfunctional tumors. Of the 55 patients, 44 patients with pancreatic lesions underwent genetic testing for the <em>VHL</em> gene. Mutations were missense in 38 cases, nonsense in 2 cases, deletion in 3 cases, and a splicing site mutation in 1 case. 23 patients had mutations in either codon 161 or 167. NETs were statistically more frequent in patients with missense mutations in codons 161 and 167 compared to mutations in the rest of the <em>VHL</em> gene (21/23 vs. 7/15; P = 0.006). An amplification pattern of copy-number variation was found on the WGS in the insulinoma patient.</div></div><div><h3>Conclusion</h3><div>Pancreatic lesions are common in VHL disease. Mutations in codons 161 and 167 are hotspots in patients with pancreatic lesions, particularly NETs.</div></div>","PeriodicalId":19976,"journal":{"name":"Pancreatology","volume":"25 8","pages":"Pages 1450-1455"},"PeriodicalIF":2.7,"publicationDate":"2025-12-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145505680","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}
Pub Date : 2025-12-01DOI: 10.1016/j.pan.2025.11.020
Evangelia Florou, Yoh Zen, Parthi Srinivasan, Andreas Prachalias
{"title":"Can negative lymph node involvement and resection-free margins (ypT1-3N0R0) complete the disease-free survival benefit of a pathologic complete response (ypT0N0R0) in resected pancreatic cancer post neoadjuvant treatment?","authors":"Evangelia Florou, Yoh Zen, Parthi Srinivasan, Andreas Prachalias","doi":"10.1016/j.pan.2025.11.020","DOIUrl":"https://doi.org/10.1016/j.pan.2025.11.020","url":null,"abstract":"","PeriodicalId":19976,"journal":{"name":"Pancreatology","volume":" ","pages":""},"PeriodicalIF":2.7,"publicationDate":"2025-12-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145687716","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}
Pub Date : 2025-12-01DOI: 10.1016/j.pan.2025.07.415
Joerg M. Steiner , Hana Algül , Dietrich A. Ruess , Ihsan Ekin Demir , Rickmer Braren , Sabine Schwamberger , Marina Lesina , Judith Reiser , Julia Werner , Tanja Groll , Thomas Metzler , Katja Steiger
Background/objectives
Acute necrotizing pancreatitis is a common disease in humans and leads to significant and world-wide morbidity and mortality. Exploration of new pharmaceutical agents for the treatment of this disease frequently rests on rodent models that may not be relevant for spontaneous human disease and also preclude collecting multiple blood samples. Goal of this project was to establish an experimental model for acute necrotizing pancreatitis in pigs that mirrors the development of systemic complications of acute pancreatitis in humans as a prelude to clinical trials in humans.
Methods
The accessory pancreatic duct was surgically isolated in domestic pigs and 8 μmol/kg glycodeoxycholic acid were slowly injected into the duct, followed by ligation and cutting the duct. Pigs were repeatedly evaluated clinically and multiple blood samples were collected before the pigs were sacrificed and their organs histopathologically assessed after 1, 5, or 7 days.
Results
All pigs showed clinical and clinical pathological evidence of pancreatitis after induction of pancreatitis. Pigs showed histopathological evidence of acute necrotizing pancreatitis one day after induction of pancreatitis. At 7 days after induction of pancreatitis, dramatic regeneration could be observed in the pancreas. At 5 days after induction of pancreatitis, evidence of necrotizing pancreatitis was present with less evidence of regeneration.
Conclusions
The porcine model for acute necrotizing pancreatitis described here shows many parallels to spontaneous human disease and its systemic complications and may thus serve as a good model to assess the efficacy of novel pharmaceutical agents for the treatment of acute pancreatitis in humans.
{"title":"A porcine model of acute necrotizing pancreatitis","authors":"Joerg M. Steiner , Hana Algül , Dietrich A. Ruess , Ihsan Ekin Demir , Rickmer Braren , Sabine Schwamberger , Marina Lesina , Judith Reiser , Julia Werner , Tanja Groll , Thomas Metzler , Katja Steiger","doi":"10.1016/j.pan.2025.07.415","DOIUrl":"10.1016/j.pan.2025.07.415","url":null,"abstract":"<div><h3>Background/objectives</h3><div>Acute necrotizing pancreatitis is a common disease in humans and leads to significant and world-wide morbidity and mortality. Exploration of new pharmaceutical agents for the treatment of this disease frequently rests on rodent models that may not be relevant for spontaneous human disease and also preclude collecting multiple blood samples. Goal of this project was to establish an experimental model for acute necrotizing pancreatitis in pigs that mirrors the development of systemic complications of acute pancreatitis in humans as a prelude to clinical trials in humans.</div></div><div><h3>Methods</h3><div>The accessory pancreatic duct was surgically isolated in domestic pigs and 8 μmol/kg glycodeoxycholic acid were slowly injected into the duct, followed by ligation and cutting the duct. Pigs were repeatedly evaluated clinically and multiple blood samples were collected before the pigs were sacrificed and their organs histopathologically assessed after 1, 5, or 7 days.</div></div><div><h3>Results</h3><div>All pigs showed clinical and clinical pathological evidence of pancreatitis after induction of pancreatitis. Pigs showed histopathological evidence of acute necrotizing pancreatitis one day after induction of pancreatitis. At 7 days after induction of pancreatitis, dramatic regeneration could be observed in the pancreas. At 5 days after induction of pancreatitis, evidence of necrotizing pancreatitis was present with less evidence of regeneration.</div></div><div><h3>Conclusions</h3><div>The porcine model for acute necrotizing pancreatitis described here shows many parallels to spontaneous human disease and its systemic complications and may thus serve as a good model to assess the efficacy of novel pharmaceutical agents for the treatment of acute pancreatitis in humans.</div></div>","PeriodicalId":19976,"journal":{"name":"Pancreatology","volume":"25 8","pages":"Pages 1426-1433"},"PeriodicalIF":2.7,"publicationDate":"2025-12-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144812274","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}
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