Detouring the Undesired Route of Helicobacter pylori-Induced Gastric Carcinogenesis

Abstract

Epidemiological and experimental evidence has emerged that a dysregulated inflammation is associated with most of the tumors, and many studies have begun to unravel the molecular pathways linking inflammation and cancer. As a typical example linking these associations, Helicobacter pylori (H. pylori) infection-associated atrophic gastritis has been recognized as precursor lesion of gastric cancer. The identification of transcription factors such as NF-κB and STAT3, and their gene products such as IL-8, COX-2, iNOS, cytokines, chemokines and their receptors, etc have laid the molecular foundation for our understanding of the decisive role of inflammation in carcinogenesis. In addition to the role as the initiator of cancer, inflammation contributes to survival and proliferation of malignant cells, tumor angiogenesis, and even metastasis. In this review, the fundamental mechanisms of H. pylori-induced carcinogenesis as well as the possibility of cancer prevention through suppressing H. pylori-induced inflammation are introduced. We infer that targeting inflammatory pathways have a potential role to detour the unpleasant journey to H. pylori-associated gastric carcinogenesis.

The Complex Network between Inflammation and Colorectal Cancer: A Systematic Review of the Literature

“…A strong link between inflammation and cancerogenesis was already presumed at the time of Hippocrates (460 B.C) and Galenus (129 A.D.) [ 40 ]. In 1863, Virchow added the “chronic” adjective to that link, described by Greek physicians, and was the first in medical history who discussed a lymphoreticular infiltrate in the tumor site [ 41 , 42 ]. Almost 30 years later, starting from the assumption that some microbial products could have anti-tumoral effects, W.B.…”

Untitled

“…GC is the fourth common cancer in men and the fifth common cancer in women 51 and is the third most common cause of death from cancer in the world 52,53 . From the first reports based on the role of HP with adenocarcinoma 54,55 , to recent studies, all confirmed the association between HP and adenocarcinoma 56,57 .…”

“…From the first reports based on the role of HP with adenocarcinoma 54,55 , to recent studies, all confirmed the association between HP and adenocarcinoma 56,57 . Finally in 1994, the International Agency for Research on Cancer classified HP as a type I carcinogen bacterium 52 .…”

From Diospyros kaki L. (Persimmon) Phytochemical Profile and Health Impact to New Product Perspectives and Waste Valorization

“…Furthermore, the enzyme urea amidohydrolase production increases H. pylori gastric acid resistance; urease hydrolyzes urea producing ammonia and carbon dioxide, and the end-products then nullify stomach acid to generate a pH environment fit for the establishment and proliferation of H. pylori [ 201 ]. According to an animal model experiment, H. pylori ’s urease knockout mutant does not seem to be responsible for causing gastric diseases [ 202 ]. As such, urease is thought to be a key focus for repressing H. pylori colonization [ 203 ].…”