Vescio F, Ammendola M, Currò G, Curcio S. Close relationship between mediators of inflammation and pancreatic cancer: Our experience. World J Gastroenterol 2024; 30(23): 2927-2930 [DOI: 10.3748/wjg.v30.i23.2927]
Corresponding Author of This Article
Michele Ammendola, MD, Professor, Science of Health Department, Digestive Surgery Unit, University “Magna Graecia” Medical School, University Hospital “R. Dulbecco”, Viale Europa Loc Germaneto, Catanzaro 88100, Italy. michele.ammendola@unicz.it
Research Domain of This Article
Surgery
Article-Type of This Article
Editorial
Open-Access Policy of This Article
This article is an open-access article which was selected by an in-house editor and fully peer-reviewed by external reviewers. It is distributed in accordance with the Creative Commons Attribution Non Commercial (CC BY-NC 4.0) license, which permits others to distribute, remix, adapt, build upon this work non-commercially, and license their derivative works on different terms, provided the original work is properly cited and the use is non-commercial. See: http://creativecommons.org/licenses/by-nc/4.0/
World J Gastroenterol. Jun 21, 2024; 30(23): 2927-2930 Published online Jun 21, 2024. doi: 10.3748/wjg.v30.i23.2927
Close relationship between mediators of inflammation and pancreatic cancer: Our experience
Francesca Vescio, Michele Ammendola, Giuseppe Currò, Silvia Curcio
Francesca Vescio, Giuseppe Currò, Silvia Curcio, Science of Health Department, General Surgery Unit, University “Magna Graecia” Medical School, University Hospital “R. Dulbecco”, Catanzaro 88100, Italy
Michele Ammendola, Science of Health Department, Digestive Surgery Unit, University “Magna Graecia” Medical School, University Hospital “R. Dulbecco”, Catanzaro 88100, Italy
Author contributions: Ammendola M initiated the idea of writing up the editorial; Vescio F and Curcio S contributed to the manuscript writing equally and performed the bibliographic search; Currò G revised the final paper; All authors have read and approved the final version of the manuscript.
Conflict-of-interest statement: All the authors report having no relevant conflicts of interest for this article.
Open-Access: This article is an open-access article that was selected by an in-house editor and fully peer-reviewed by external reviewers. It is distributed in accordance with the Creative Commons Attribution NonCommercial (CC BY-NC 4.0) license, which permits others to distribute, remix, adapt, build upon this work non-commercially, and license their derivative works on different terms, provided the original work is properly cited and the use is non-commercial. See: https://creativecommons.org/Licenses/by-nc/4.0/
Corresponding author: Michele Ammendola, MD, Professor, Science of Health Department, Digestive Surgery Unit, University “Magna Graecia” Medical School, University Hospital “R. Dulbecco”, Viale Europa Loc Germaneto, Catanzaro 88100, Italy. michele.ammendola@unicz.it
Received: January 13, 2024 Revised: May 4, 2024 Accepted: May 27, 2024 Published online: June 21, 2024 Processing time: 159 Days and 5.9 Hours
Abstract
In this editorial, we focus specifically on the mechanisms by which pancreatic inflammation affects pancreatic cancer. Cancer of the pancreas remains one of the deadliest cancer types. The highest incidence and mortality rates of pancreatic cancer are found in developed countries. Trends of pancreatic cancer incidence and mortality vary considerably worldwide. A better understanding of the etiology and identification of the risk factors is essential for the primary prevention of this disease. Pancreatic tumors are characterized by a complex microenvironment that orchestrates metabolic alterations and supports a milieu of interactions among various cell types within this niche. In this editorial, we highlight the foundational studies that have driven our understanding of these processes. In our experimental center, we have carefully studied the mechanisms of that link pancreatic inflammation and pancreatic cancer. We focused on the role of mast cells (MCs). MCs contain pro-angiogenic factors, including tryptase, that are associated with increased angiogenesis in various tumors. In this editorial, we address the role of MCs in angiogenesis in both pancreatic ductal adenocarcinoma tissue and adjacent normal tissue. The assessment includes the density of c-Kit receptor-positive MCs, the density of tryptase-positive MCs, the area of tryptase-positive MCs, and angiogenesis in terms of microvascularization density.
Core Tip: This editorial focuses on the mechanisms that link pancreatic inflammation to pancreatic cancer. Pancreatic cancer remains one of the most aggressive pathologies. A better understanding of its etiology and the identification of risk factors is essential for primary prevention. Mast cells (MCs) contain pro-angiogenic factors, particularly tryptase, that are associated with increased angiogenesis. We evaluated the role of MCs in angiogenesis in both pancreatic ductal adenocarcinoma tissue and adjacent normal tissue by assessing the density of c-Kit receptor-positive MCs, the density of tryptase-positive MCs, the area of tryptase-positive MCs, and microvascularization density.
