Gastric cancer is one of the most common causes of death worldwide. It is among the top 5 most frequently-diagnosed cancers globally and is the 3rd leading cause of cancer-related deaths. In its distribution, there are important geographical, ethnic, and socio-economic differences. Since patients are usually asymptomatic in the earlier stages, two thirds of the patients have inoperable disease at the time of diagnosis. Despite the advances in its treatment, prognosis is still poor [[1], [2], [3]].

Gastric adenocarcinoma has two main histological variants, namely diffuse and intestinal type. The most common variant is the “intestinal type” due to its morphological similarity to adenocarcinomas that occur in the intestinal tract. The sequence of molecular events underlying intestinal type GC (INT-GC) is not fully understood yet [4]. In a model of INT-GC, chronic persistent superficial gastritis caused by chronic HP infection, pernicious anemia, or possibly diets high-in-salt leads to chronic atrophic gastritis (CAG) and gastric intestinal metaplasia (GIM), which is ultimately followed by dysplasia and then adenocarcinoma [5,6]. Although there has been a recent debate as to whether cancer cells directly originate from intestinal metaplastic cells or GIM is a substitute marker of cancer, the presence of GIM has been associated with the development of INT-GC in epidemiological studies [7]. Although diffuse type GC (DIF-GC) can be induced by HP infection, there are significant differences between these two variants. Unlike INT-GC, DIF-GC does not have a previously-defined precancerous lesion, even in those associated with HP infection.

GIM is more common in the countries with higher GC incidence and is known to occur prior to GC development in experimental animal models [8,9]. The data obtained from human studies have supported that GIM is a precursor lesion for INT-GC. In a Chinese study, GIM was detected in about 33% of the population who lived in a region with high gastric cancer incidence [10]. In another study from Japan, it was advocated that the presence of GIM was the sole criterion associated with the development of INT-GC [11].

Given the poor prognosis of GC, it is important to determine prognostic markers for identifying the individual risk as well as staging the disease. In some studies and meta-analysis, HP-positive operated GC patients were found to have worse prognosis [12,13]. In our study, we aimed to investigate the possible negative effects of the presence of GIM, HP, and CAG in surgical specimen on long-term survival in operated INT-GC patients.