Helicobacter pylori Infection, Chronic Inflammation, and Genomic Transformations in Gastric MALT Lymphoma

Abstract EN

Nowadays, it is believed that the main role in the development of gastric mucosa-associated lymphoid tissue (MALT) lymphoma plays Helicobacter pylori infection.

This world-wide distributed bacteria is in charge of most cases of not only upper gastrointestinal tract disorders but also some of extragastric problems.

Constant stimulation of the immune system causes a B-lymphocytes proliferation, which is considered to be responsible for the neoplastic transformation.

On the other hand, there are 10%–20% of patients who do not respond to Helicobacter pylori eradication treatment.

This group has often a chromosome translocation, which suggests that there is another unknown, so far, pathogenetic mechanism of MALT lymphoma.

Majority of genetic abnormalities are connected with nuclear factor-κB (NF-κB) pathway, which activates the uncontrolled proliferation of neoplastic cells.

Translocations already described in studies are t(11;18)(q21;q21), which is the most common, t(14;18)(q32;q21), t(14;18)(q32;q21), and t(3;14)(p14.1;q32).

This non-Hodgkin’s lymphoma is an indolent type originated outside lymph nodes.

In more than 50% of cases, it occurs in the stomach.

Occasionally, it can be found in salivary and thyroid gland, lung, breast, bladder, skin, or any other place in the human body.

This paper is a review of the current knowledge on etiology, pathogenesis, treatment, and follow-up of gastric MALT lymphoma.