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Pancreatic Disease: From Molecular Basis to Novel Therapies—2nd Edition

A special issue of International Journal of Molecular Sciences (ISSN 1422-0067). This special issue belongs to the section "Molecular Endocrinology and Metabolism".

Deadline for manuscript submissions: 30 November 2025 | Viewed by 674

Special Issue Editor


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Guest Editor
Department of Medicine, Renaissance School of Medicine at Stony Brook University, 101 Nicolls Road, Stony Brook, NY 11794, USA
Interests: transcription factors; Krüppel-like factor 4 (KLF4); Krüppel-Like Factor 5 (KLF5); intestinal biology; injury; inflammation; pancreatic neoplasia; pancreatic cancer
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Special Issue Information

Dear Colleagues,

This Special Issue is a continuation of our previous Special Issue titled “Pancreatic Disease: From Molecular Basis to Novel Therapies”. The pancreas, with its exocrine and endocrine functions, sits at the intersection of the body’s digestive and endocrine systems. Pancreatic acinar and ductal cells act in concordance to synthesize, store, and release digestive enzymes into pancreatic ducts, which drain into the duodenum. Pancreatic endocrine glands, called islets of Langerhans, regulate blood sugar levels by secreting two hormones into the blood: insulin and glucagon. The physiology of the pancreas is very tightly controlled, and disruptions result in pancreatitis (acute and chronic), pancreatic cancer, and Diabetes Mellitus (type 1 and 2). Several known perturbations induce acute pancreatitis, including the overactivation of trypsinogen, increased inflammatory cell infiltration, and the destruction of secretory cells. Recently, mitochondrial, lysosomal, and autophagic dysfunction, as well as calcium overload and increased endoplasmic reticulum stress, have been identified as drivers of pancreatitis progression. Chronic injury is characterized by fibro-inflammatory pathophysiology leading to the destruction of the pancreatic parenchyma. This is caused by genetic and environmental factors that are exacerbated by alcohol, nicotine, nutritional, and metabolic factors, to name a few. It has been shown that obesity, smoking, chronic pancreatitis, bacterial infections, and diabetes are the primary risk factors for pancreatic cancer development. Diabetes Mellitus is characterized by impaired sugar, protein, and fat metabolism resulting from insulin deficiency. Managing pancreatic diseases has yet to be very successful. Thus, novel interventions are required that can necessitate a better understanding of the mechanisms underlying the development of pancreatic pathologies. This Special Issue highlights recent progress in understanding the physiology and pathophysiology of the pancreas and therapeutic developments.

Dr. Agnieszka B. Bialkowska
Guest Editor

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Keywords

  • pancreatitis
  • acinar-to-ductal neoplasia
  • early pancreatic neoplasia
  • fibroinflammatory disease
  • pancreatic cancer
  • diabetes Mellitus

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Published Papers (1 paper)

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Research

14 pages, 1256 KB  
Article
Somatic Mutation Detection in Tumor Tissue and Matched Cell-Free DNA Using PCR-Based Methods in Pancreatic Cancer Patients Undergoing Upfront Resection
by Hana Zavrtanik Čarni, David Badovinac, Tanja Blagus, Katja Goričar, Branislava Ranković, Alenka Matjašič, Andrej Zupan, Aleš Tomažič and Vita Dolžan
Int. J. Mol. Sci. 2025, 26(17), 8518; https://doi.org/10.3390/ijms26178518 - 2 Sep 2025
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Abstract
Somatic mutations in KRAS and TP53 are among the most common genetic alterations in pancreatic ductal adenocarcinoma (PDAC). Advances in PCR-based technologies now enable the detection of these mutations in tumor tissue and cell-free DNA (cfDNA), providing a minimally invasive approach to assess [...] Read more.
Somatic mutations in KRAS and TP53 are among the most common genetic alterations in pancreatic ductal adenocarcinoma (PDAC). Advances in PCR-based technologies now enable the detection of these mutations in tumor tissue and cell-free DNA (cfDNA), providing a minimally invasive approach to assess tumor burden. However, in resectable PDAC, circulating tumor DNA (ctDNA) may represent less than 0.1% of total cfDNA, requiring highly sensitive detection methods. The aim of our study was to assess two PCR-based assays—competitive allele-specific PCR (castPCR) and digital PCR (dPCR)—for detecting selected somatic mutations in tumor tissue, cfDNA, and extracellular vesicle-associated DNA (EV-DNA) from plasma. Matched primary tumor and preoperative plasma samples were collected from 50 patients undergoing upfront resection for PDAC. CastPCR was used for detecting selected KRAS, TP53, SMAD4, and CDKN2A mutations in tumor DNA. Additionally, dPCR was used to analyze KRAS and TP53 mutations in tumor DNA as well as cfDNA and EV-DNA. The concordance between both platforms was 71.4% for KRAS p.G12D and 58.3% for the analysis of TP53 p.R273H mutations in tumor tissue. However, dPCR detected these mutations in an additional 28.6% and 39.6% of samples, respectively. In cfDNA, dPCR identified KRAS p.G12D in 10.2% and TP53 p.R273H in 2.0% of samples. Mutation detection in EV-DNA was limited by low DNA yield. Both platforms proved effective for tumor DNA analysis, with dPCR offering greater sensitivity. Somatic mutation detection from liquid biopsy using dPCR further supports its potential utility in the preoperative setting. Full article
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