Published online Jan 15, 2022. doi: 10.4251/wjgo.v14.i1.153
Peer-review started: February 25, 2021
First decision: May 3, 2021
Revised: May 16, 2021
Accepted: December 9, 2021
Article in press: December 9, 2021
Published online: January 15, 2022
Processing time: 319 Days and 13.8 Hours
Approximately 8% of all non-Hodgkin lymphomas are extranodal marginal zone B cell lymphomas of mucosa-associated lymphoid tissue (MALT), also known as MALT lymphomas. These arise at a wide range of different extranodal sites, with most cases affecting the stomach, the lung, the ocular adnexa and the thyroid. The small intestine is involved in a lower percentage of cases. Lymphoma growth in the early stages is associated with long-lasting chronic inflammation provoked by bacterial infections (e.g., Helicobacter pylori or Chlamydia psittaci infections) or autoimmune conditions (e.g., Sjögren’s syndrome or Hashimoto thyroiditis). While these inflammatory processes trigger lymphoma cell proliferation and/or survival, they also shape the microenvironment. Thus, activated immune cells are actively recruited to the lymphoma, resulting in either direct lymphoma cell stimulation via surface receptor interactions and/or indirect lymphoma cell stimulation via secretion of soluble factors like cytokines. In addition, chronic inflammatory conditions cause the acquisition of genetic alterations resulting in autonomous lymphoma cell growth. Recently, novel agents targeting the microenvironment have been developed and clinically tested in MALT lymphomas as well as other lymphoid malignancies. In this review, we aim to describe the composition of the microenvironment of MALT lymphoma, the interaction of activated immune cells with lymphoma cells and novel therapeutic approaches in MALT lymphomas using immunomodulatory and/or microenvironment-targeting agents.
Core Tip: This review summarizes and discusses the major findings in extranodal mucosa-associated lymphoid tissue lymphomas with a focus on the microenvironment. It describes how long-lasting chronic inflammatory processes promote the growth of malignant cells, which can be directly mediated by bacteria and/or interaction with activated immune cells. In addition, major genetic alterations are summarized, and models of how these might be acquired are discussed. Finally, novel therapies targeting the microenvironment are described.