Next Article in Journal
Histopathologic Features of Lymphedema: A Molecular Review
Previous Article in Journal
Peptides for Health Benefits 2019
Previous Article in Special Issue
Role of Metastasis-Related Genes in Cisplatin Chemoresistance in Gastric Cancer
Open AccessReview

Immunological Aspects of the Tumor Microenvironment and Epithelial-Mesenchymal Transition in Gastric Carcinogenesis

1
Chair and Department of Anatomy, Medical University of Lublin, 20-090 Lublin, Poland
2
Chair and Department of Forensic Medicine, Medical University of Lublin, 20-090 Lublin, Poland
3
Chair and 1st Department of Psychiatry, Psychotherapy and Early Intervention, Medical University of Lublin, Gluska Street 1, 20-439 Lublin, Poland
4
Clinica Medica “A. Murri”, Department of Biomedical Sciences and Human Oncology, University of Bari Aldo Moro, 70124 Bari, Italy
*
Author to whom correspondence should be addressed.
Int. J. Mol. Sci. 2020, 21(7), 2544; https://doi.org/10.3390/ijms21072544
Received: 9 March 2020 / Revised: 30 March 2020 / Accepted: 2 April 2020 / Published: 6 April 2020
(This article belongs to the Special Issue Gastric Cancers: Molecular Pathways and Candidate Biomarkers 3.0)
Infection with Helicobacter pylori, a Gram-negative, microaerophilic pathogen often results in gastric cancer in a subset of affected individuals. This explains why H. pylori is the only bacterium classified as a class I carcinogen by the World Health Organization. Several studies have pinpointed mechanisms by which H. pylori alters signaling pathways in the host cell to cause diseases. In this article, the authors have reviewed 234 studies conducted over a span of 18 years (2002–2020). The studies investigated the various mechanisms associated with gastric cancer induction. For the past 1.5 years, researchers have discovered new mechanisms contributing to gastric cancer linked to H. pylori etiology. Alongside alteration of the host signaling pathways using oncogenic CagA pathways, H. pylori induce DNA damage in the host and alter the methylation of DNA as a means of perturbing downstream signaling. Also, with H. pylori, several pathways in the host cell are activated, resulting in epithelial-to-mesenchymal transition (EMT), together with the induction of cell proliferation and survival. Studies have shown that H. pylori enhances gastric carcinogenesis via a multifactorial approach. What is intriguing is that most of the targeted mechanisms and pathways appear common with various forms of cancer. View Full-Text
Keywords: gastric cancer; epithelial-mesenchymal transition; immunology; immune cells; carcinogenesis; tumor microenvironment gastric cancer; epithelial-mesenchymal transition; immunology; immune cells; carcinogenesis; tumor microenvironment
Show Figures

Graphical abstract

MDPI and ACS Style

Baj, J.; Brzozowska, K.; Forma, A.; Maani, A.; Sitarz, E.; Portincasa, P. Immunological Aspects of the Tumor Microenvironment and Epithelial-Mesenchymal Transition in Gastric Carcinogenesis. Int. J. Mol. Sci. 2020, 21, 2544.

Show more citation formats Show less citations formats
Note that from the first issue of 2016, MDPI journals use article numbers instead of page numbers. See further details here.

Article Access Map by Country/Region

1
Search more from Scilit
 
Search
Back to TopTop