Villarroel-Espindola F, Ejsmentewicz T, Gonzalez-Stegmaier R, Jorquera RA, Salinas E. Intersections between innate immune response and gastric cancer development. World J Gastroenterol 2023; 29(15): 2222-2240 [PMID: 37124883 DOI: 10.3748/wjg.v29.i15.2222]
Corresponding Author of This Article
Franz Villarroel-Espindola, PhD, Director, Translational Medicine Unit, Instituto Oncologico Fundacion Arturo Lopez Perez, Rancagua 878, Providencia, Santiago 7500000, Metropolitan region, Chile. franz.villarroel@falp.org
Research Domain of This Article
Biochemistry & Molecular Biology
Article-Type of This Article
Review
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. Apr 21, 2023; 29(15): 2222-2240 Published online Apr 21, 2023. doi: 10.3748/wjg.v29.i15.2222
Intersections between innate immune response and gastric cancer development
Franz Villarroel-Espindola, Troy Ejsmentewicz, Roxana Gonzalez-Stegmaier, Roddy A Jorquera, Esteban Salinas
Franz Villarroel-Espindola, Troy Ejsmentewicz, Roxana Gonzalez-Stegmaier, Roddy A Jorquera, Esteban Salinas, Translational Medicine Unit, Instituto Oncologico Fundacion Arturo Lopez Perez, Santiago 7500000, Metropolitan region, Chile
Author contributions: Villarroel-Espíndola F contributed to the conceptualization, methodology, original draft preparation, writing, reviewing, editing, supervision and funding acquisition; Ejsmentewicz T and Salinas E contributed to the writing of the original draft; González-Stegmaier R contributed to the writing of the original draft, reviewing, editing and visualization; Jorquera R contributed to the writing, reviewing, editing and visualization.
Supported byInstituto Oncológico Fundación Arturo López Pérez, Santiago, Chile; National Research and Development Agency of Chile (ANID) and National Fund for Scientific and Technological Development (FONDECYT), No. 1221415 (to Villarroel-Espindola F).
Conflict-of-interest statement: Dr. F. Villarroel-Espindola has received compensation from Ilico SpA. and Gebrax-Chile for consulting services. Other authors declare having no conflict of interests, neither real nor perceivable, in relation to 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: Franz Villarroel-Espindola, PhD, Director, Translational Medicine Unit, Instituto Oncologico Fundacion Arturo Lopez Perez, Rancagua 878, Providencia, Santiago 7500000, Metropolitan region, Chile. franz.villarroel@falp.org
Received: September 20, 2022 Peer-review started: September 20, 2022 First decision: October 20, 2022 Revised: November 7, 2022 Accepted: March 9, 2023 Article in press: March 9, 2023 Published online: April 21, 2023 Processing time: 206 Days and 12.6 Hours
Abstract
Worldwide, gastric cancer (GC) is the fifth most commonly diagnosed malignancy. It has a reduced prevalence but has maintained its poor prognosis being the fourth leading cause of deaths related to cancer. The highest mortality rates occur in Asian and Latin American countries, where cases are usually diagnosed at advanced stages. Overall, GC is viewed as the consequence of a multifactorial process, involving the virulence of the Helicobacter pylori (H. pylori) strains, as well as some environmental factors, dietary habits, and host intrinsic factors. The tumor microenvironment in GC appears to be chronically inflamed which promotes tumor progression and reduces the therapeutic opportunities. It has been suggested that inflammation assessment needs to be measured qualitatively and quantitatively, considering cell-infiltration types, availability of receptors to detect damage and pathogens, and presence or absence of aggressive H. pylori strains. Gastrointestinal epithelial cells express several Toll-like receptors and determine the first defensive line against pathogens, and have been also described as mediators of tumorigenesis. However, other molecules, such as cytokines related to inflammation and innate immunity, including immune checkpoint molecules, interferon-gamma pathway and NETosis have been associated with an increased risk of GC. Therefore, this review will explore innate immune activation in the context of premalignant lesions of the gastric epithelium and established gastric tumors.
Core Tip: Premalignant cascade of gastric cancer starts with a chronic gastritis, and evolves to atrophic gastritis, intestinal metaplasia, dysplasia and finally the carcinoma. During the process, different immune responses contribute to inflammation of the gastric epithelium. Our work compiles studies related to the innate immune response with a focus on molecular and cellular features such as, Toll-like receptors, neutrophils, cytokines and socioeconomic factors, as crucial players during the precancerous cascade and the cancer onset.
