Intestinal metaplasia (IM) and Helicobacter Pylori (HP) are major risk factors for gastric cancer (GC) [1], [2]. Throughout this development process, HP triggers the response by CD4 Th1 cells due to inflammation. Thus, macrophages and neutrophils soon reach this site and are stimulated by the release of reactive oxygen and reactive nitrogen products which cause DNA damage [3], [4]. HP is considered to trigger cause intestinal type GC with two major direct and indirect mechanisms. The indirect mechanism includes inflammation due to increased cell cycle and accumulation mitotic defects within a few decades. In this process called Correa hypothesis, AG occurs first, followed by IM, colonic metaplasia, dysplasia, and finally GC. The other mechanism is directly associated with DNA damage. Another feature of HP that makes it important as a carcinogen is that it can contain precancerous virulence factors (cytotoxin-associated gene A (CagA) and vacuolating cytotoxin A (VacA)). [3].

WNT signaling pathway which preserved in the evolutionary process have a role in important processes including development, differentiation, cell proliferation, mothology, mortality etc. [5], [6]. Therefore, functional genes on the WNT signaling pathway are important for carcinogenesis. The aberrant activation of the WNT signaling pathway is involved in the development and progression of a significant proportion of GC. Also, CTNNB1 and APC were listed as pivotal genes in the development of GC [7], [8], [9]. GC aggressiveness is dependent on WNT5A expression level [10]. WNT5A may help building favorable conditions for GC progression [11]. The RHOA gene in the WNT signaling pathway was described as both a potential therapeutic target and a biomarker for GC [12].

In this context, with this study, we aim to investigate the activity of WNT signaling pathway genes as diagnostic and prognostic markers in the presence and absence of HP in development process from IM to GC.