In the human gastric mucosa, Helicobacter pylori activates mechanisms that induce the preferential differentiation of regulatory T cells (Treg). Treg cells are CD4+, CD25+, and FOXP3+; have suppressive activity of inflammation and facilitate the immune escape of tumor cells.
Helicobacter pylori (H. pylori) infection is the main risk factor for gastric cancer, however, evidence is growing that infectious agents such as Epstein-Barr Virus (EBV) and Cytomegalovirus (CMV) are also related to this malignancy.
Gastric carcinoma (GC) is the third leading cause of cancer death among malignant tumors worldwide. It is considered a multifactorial disease, presenting high mortality rates in both sexes.
Latin America was affected by several human migratory waves during the colonisation period. Humans arrived at the continent with a new subset of Helicobacter pylori, which replaced the native species.
Volatile organic compound (VOC) detection in the exhaled air has a potential for gastric cancer screening. Questions of the VOC origin and their biological relevance still require to be answered.
Serum pepsinogen (Pg) I and the ratio between PgI and PgII (PgI/PgII) are related to the histological and functional status of the gastric mucosa. Low serum PgI and PgI/PgII values are biomarkers for atrophic gastritis.
