Abstract
Nowadays, gastric cancer is one of the most common neoplasms and the fourth cause of cancer-related death on the world. Regarding the age at the diagnosis it is divided into early-onset gastric carcinoma (45 years or younger) and conventional gastric cancer (older than 45). Gastric carcinomas are rarely observed in young population and rely mostly on genetic factors, therefore provide the unique model to study genetic and environmental alternations. The latest research on early-onset gastric cancer are trying to explain molecular and genetic basis, because young patients are less exposed to environmental factors predisposing to cancer. In the general population, Helicobacter pylori, has been particularly associated with intestinal subtype of gastric cancers. The significant association of Helicobacter pylori infection in young patients with gastric cancers suggests that the bacterium has an etiologic role in both diffuse and intestinal subtypes of early-onset gastric cancers. In this paper we would like to ascertain the possible role of Helicobacter pylori infection in the development of gastric carcinoma in young patients. The review summarizes recent literature on early-onset gastric cancers with special reference to Helicobacter pylori infection.
Highlights
Gastric cancer (GC) is a multifactorial disease in which both genetic and environmental factors are involved
In Western countries, mostly Latin America, the Middle East and Africa, the studies performed claim that individuals infected with m1 or s1 H. pylori strains have a chance for higher risk of developing gastric cancer or peptic ulcer in comparison to those underwent the infection with m2 or s2 strains [68, 69]
Considering genetic polymorphisms in gastric cancer and H.pylori infection, the growing interest in this field has become more expanded in recent years. In this process different cytokines take part e.g. IL-1, IL-17, tumor necrosis factor (TNF) α, tolllike receptors (TLRs) [77, 102,103,104,105,106,107,108,109,110,111,112,113,114]
Summary
Gastric cancer (GC) is a multifactorial disease in which both genetic and environmental factors are involved. Various geographic incidence in gastric cancer development might be explained, mainly by the occurrence of different H. pylori virulence agents, like CagA, VacA and OipA [57]. In Western countries, it has been postulated that cases infected with cagA-positive strains of H. pylori are displaying an increased risk of gastric cancer or peptic ulcer in comparison to those affected by cagA-negative strains [59, 60].
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