Aim: To determine the immunoreactivity of somatostatin during the development of the human fetal pancreas and pancreatic ductal adenocarcinoma, given that, somatostatin-positive cells were demonstrated either into its embryonic anlage or into pancreatic cancer.
Methods: Tissue sections from 15 pancreatic fetal specimens, and an equal number of ductal adenocarcinoma specimens were assessed.
Results: The density of positive cells in the primitive exocrine ductal epithelium and endocrine epithelium was significantly different from the relevant density in the neoplastic pancreatic tissue of mixed (ductal-endocrine) and pure ductal type (P1=0.021 P2=0.001, P3<0.0001, P4=0.003 respectively). The above values were estimated from the 8th to 10th week. There was no significant difference in the density of positive cells in the mantle zone of the islets from the 13th to the 24th week, and the neoplastic tissue of mixed (P5=0.16) and pure ductal type (P6=0.65).
Conclusion: The immunostaining for somatostatin identifies a subgroup of pancreatic ductal adenocarcinomas with a neuroendocrine component, (initially considered as pure ductal tumors), and mixed ductal and neuroendocrine tumors. This pattern of expression in neoplasms recapitulates the normal pattern during the embryonal development of the organ, raising the question of therapeutic efficacy of somatostatin and analogues as monotherapy in pancreatic cancer management.
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http://dx.doi.org/10.1007/s10238-005-0073-4 | DOI Listing |
Tunis Med
January 2025
University of Sousse, Faculty of Medicine of Sousse, 4002, Farhat Hached University Hospital, Department of Endocrinology Diabetology, 4000, Sousse, Tunisia.
Introduction: Diabetes mellitus has emerged as a global public health issue due to its increasing prevalence and the increased risk of developing cancers. Pancreatic cancer is believed to be both a consequence of pre-existing diabetes and a potential cause of new-onset diabetes.
Aim: This study aims to compare the characteristics of patients with pancreatic ductal adenocarcinoma and newly diagnosed or long-standing diabetes mellitus.
Cancer Med
January 2025
Department of Hepatobiliary and Pancreatic Surgery, Zhongnan Hospital of Wuhan University, Wuhan, China.
Background: Early-stage pancreatic ductal adenocarcinoma (PDAC) is frequently misdiagnosed, contributing to its high mortality rate. Exosomal microRNAs (miRNAs) have emerged as potential biomarkers for the early detection of PDAC.
Aims: This study aimed to evaluate the feasibility of using exosomal miRNAs from PDAC tissues and serum as biomarkers for early detection and prognosis.
Extracell Vesicles Circ Nucl Acids
November 2024
Animal Physiology and Immunology, School of Life Sciences, Technical University of Munich, Freising 85354, Germany.
The recent study from the Pogge von Strandmann group published in , by Alashkar Alhamwe ., combined for the first time the Cre-LoxP recombination system with single-cell sequencing. The group monitored the tumor-derived extracellular vesicle (EV) uptake and the EV functions in the recipient non-malignant cells in a pancreatic ductal adenocarcinoma mouse model.
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January 2025
Department of Oncology, Sidney Kimmel Comprehensive Cancer Center, Johns Hopkins University School of Medicine, Baltimore, MD, USA.
Successful pancreatic ductal adenocarcinoma (PDAC) immunotherapy requires therapeutic combinations that induce quality T cells. Tumor microenvironment (TME) analysis following therapeutic interventions can identify response mechanisms, informing design of effective combinations. We provide a reference single-cell dataset from tumor-infiltrating leukocytes (TILs) from a human neoadjuvant clinical trial comparing the granulocyte-macrophage colony-stimulating factor (GM-CSF)-secreting allogeneic PDAC vaccine GVAX alone, in combination with anti-PD1 or with both anti-PD1 and CD137 agonist.
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January 2025
Department of Visceral, Vascular and Endocrine Surgery, Martin-Luther-University Halle-Wittenberg, University Medical Center Halle, 06120 Halle (Saale), Germany.
Pancreatic ductal adenocarcinoma (PDAC) is characterized by aggressive growth and metastasis, partly driven by fibroblast-mediated stromal interactions. Using RNA sequencing of fibroblasts from early-stage KPC mouse models, we identified significant upregulation of genes involved in adipogenesis, fatty acid metabolism, and the ROS pathway. ANGPTL4, a key adipogenesis regulator, was highly expressed in fibroblasts and promoted pancreatic cancer cell proliferation and migration through paracrine signaling.
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