Gastric cancer is diagnosed in nearly one million new patients each year and it remains the second leading cause of
cancer-related deaths worldwide. Although
gastric cancer represents a heterogeneous group of diseases, chronic
inflammation has been shown to play a role in
tumorigenesis.
Cancer development is a multistep process characterized by genetic and epigenetic alterations during tumour initiation and progression. The stromal microenvironment is important in maintaining normal tissue homeostasis or promoting tumour development. A plethora of immune cells (i.e., lymphocytes, macrophages, mast cells, monocytes, myeloid-derived suppressor cells, Treg cells, dendritic cells, neutrophils, eosinophils, natural killer (NK) and natural killer T (NKT) cells) are components of
gastric cancer microenvironment. Mast cell density is increased in
gastric cancer and there is a correlation with angiogenesis, the number of metastatic lymph nodes and the survival of these patients. Mast cells exert a protumorigenic role in
gastric cancer through the release of angiogenic (VEGF-A, CXCL8, MMP-9) and lymphangiogenic factors (
VEGF-C and
VEGF-F). Gastric mast cells express the programmed death
ligands (PD-L1 and PD-L2) which are relevant as immune checkpoints in
cancer. Several clinical undergoing trials targeting immune checkpoints could be an innovative therapeutic strategy in
gastric cancer. Elucidation of the role of subsets of mast cells in different human
gastric cancers will demand studies of increasing complexity beyond those assessing merely mast cell density and microlocalization.